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Legally blind:

April 28th, 2007

Judge turned against the Perth pair, threw out the baby with the bathwater

With Perth hobbled, perhaps conventional dissidents will be heard next time

Why Judge Sulan likes Gallo and we like John Moore

judge.jpgNews reports of the Adelaide judgement are coming through now, and they show the basis of Judge Sulan’s decision to disallow the appeal of Andre Chad Parenzee, 36, against being jailed for having sex with three women without informing them that he carries antibodies against HIV, a virus which according to the original papers of Robert Gallo in 1984 does not cause AIDS (not to mention that how such antibodies could be transmitted sexually is another unanswered question).

Quite simply, it is his contempt for the independent scholars from Perth.

Both in the media and in his comments, the two decent and thoughtful witnessess for the defense from the Perth Group are being trashed mercilessly for their challenges to orthodoxy, which the judge rates as foolish and inexpert. Their reputation is now mud. Ms Papadopulos-Eleopulos is quoted on her forthright willingness to sleep with an HIV positive man as if she was some kind of gang bang:

‘HIV does not exist’ appeal thrown out

By Todd Cardy

April 27, 2007 05:56pm

A HIV-positive man convicted for having unprotected sex with three women has lost an appeal, after a South Australian judge rejected defence claims the virus does not exist.

Andre Chad Parenzee, 36, was convicted on three counts of endangering life last January after one of the women, a mother of two, became infected with HIV.

Defence lawyers launched an appeal calling two Perth medical researchers – Eleni Papadopulos-Eleopulos and Dr Valendar Turner who testified in the South Australian Court of Appeal that the virus did not exist and could not be sexually transmitted.

The two AIDS-dissidents are members of the Perth Group, founded by Ms Papadopulos-Eleopulos, that believes HIV is not the cause of AIDS.

Justice John Sulan today dismissed the witnesses’ testimony, saying the pair lacked credibility and were advocates for a cause rather than independent experts.

He said the evidence that HIV existed was compelling and he rejected the application for a re-trial.

“I am satisfied that no jury would conclude that there is any doubt that the virus HIV exists,” he said in his judgment.

“I consider no jury would be left in any doubt that HIV is the cause of AIDS or that it is sexually transmissible.”

Justice Sulan said Ms Papadopoulos-Eleopulos, a physicist who works at the Royal Perth Hospital, relied upon opinions of others, which she often took out of context and misinterpreted.

He said claims that HIV testing methods were flawed were unfounded and the virus had been thoroughly studied by international experts.

Parenzee’s application for leave to appeal his conviction was the first time that the existence of HIV/AIDS had been tested in an Australian court.

The hearing spanned more than a year with controversy lining much of the witness testimony.

Under earlier cross-examination, Ms Papadopulos-Eleopulos was asked by the prosecution if she would have unprotected vaginal sex with a HIV-positive man.

“Any time,” she replied.

In other testimony, Ms Papadopulos-Eleopulos declared that Africa did not have an AIDS epidemic because HIV did not exist and efforts to curb the spread of the virus were merely political stunts.

To counter the claims, the prosecution called eight HIV experts including AIDS research pioneer Professor Robert Gallo.

Prof Gallo, who was one of the scientists who discovered AIDS in the early 1980s and linked HIV as the cause of the disease, testified via video-link from his home in Bethesda, Massachusetts.

He told the court the Perth Group members was misguided, inappropriate and delusional.

Parenzee was remanded in custody to be sentenced at a later date.

The bottom line is that the Perth Group pair made such a poor impression with their claim the virus didn’t exist that the Judge dismissed their authority and, unfortunately, any other arguments levelled against the HIV∫AIDS meme which no doubt took root in his brain many years ago.

It is unfortunate for Parenzee that his home is Australia. The defenders and promoters of HIV∫AIDS must have been delighted when they heard that the only defense witnesses appearing from the critics’ camp to undermine their cause were the two key figures of the nearby Perth Group.

They must have seen that as soon as the Perth pair started attacking the existence of the virus, the otherwise totally unpersuasive paradigm which is now an ideological given of government policy, charity, and culture around the world would get a free pass.

A better idea

Defense counsel Kevin Borick would have done better to arrange a video transmission from Berkeley to match the one from Bethesda, where Gallo testified by satellite. The judge valued hands on science as a qualification, and Duesberg is a classic lab retrovirologist.

For new arrivals to this disputed realm, we refer to the distinguished Berkeley scientist Peter Duesberg, who but for his personal integrity would now have a Nobel in hand for his priority in cancer research, and whose repeated demonstrations in peer reviewed journals that the claims of HIV∫AIDS scientists do not accord with the scientific literature of the field, including the studies which the leading scientists themselves carry out, are a lot harder to dismiss than the Perth Group’s claim that HIV does not exist despite its genetic cloning and different strains.

But perhaps Judge Sulan would dismiss Duesberg, and his repeated demonstrations in peer reviewed journals that the claims of HIV∫AIDS scientists do not accord with the scientific literature of the field, as insufficiently hands on as far as HIV is concerned.

So much for science critics

judgecartoon.jpegAfter all, he appears to have no respect whatsoever for independent examination of the scientific literature by attentive outsiders. This is how he dismisses Valendar Turner’s knowledge, despite his publications in peer reviewed journals:

His opinions are based on reading scientific literature, studying of scientific literature, and spending a considerable amount of time thinking.

That a Supreme Court judge can be so naive, and condemn the very process he lives by, is an embarrassment to the judiciary of Down Under, not to mention the entire nation.

Silver lining to Perth defeat

While the Judge’s contempt is a poor reward for their efforts to save humanity from despair over HIV, and we are sorry for them personally, a Perth retreat from the courts may be a good thing for the more conventional cause of correcting the science of HIV∫AIDS.

There has always been a danger that the Perth Group’s anachronistic and increasingly foolish claim that HIV does not exist would distract from the contradictions of the paradigm based on current scientific literature and label all dissidents as crackpot. Now it has happened.

The judge appears to have decided early that the Perth claim was unfounded and out of date (which it is now that genetic cloning and sequencing of HIV is a commonplace around the world) and that the credentials of the Perth pair were fatally flawed by their lack of hands on experience in the field.

I have found that Ms Papadopulos-Eleopulos and Dr Turner are not experts in the subject matter upon which they have given evidence. I have concluded that the witnesses called by the DPP are experts.

206 Because the witnesses called by the applicant are not expert, the opinion evidence which they gave is not admissible. I have noted above that the evidence given on whether HIV has been proved to exist, whether HIV is sexually transmissible, and whether it causes AIDS is opinion evidence. The finding that the witnesses for the applicant are not experts, and thus are not qualified to give expert opinion evidence, is, in my view, a sufficient basis upon which to refuse the application for permission to appeal.

judgecartoon.jpegSo he decided there was nothing in the rest of their claims, since Bob Gallo was so much more prominent in the science, famous and persuasive, and therefore reliable. The judge fawned on Gallo and the other mainstream authorities produced by the prosecution, as his comments on Gallo show:

When he gave his evidence he was forthright. At times, he was impatient with propositions that were being put to him. Mr Borick QC is critical of the manner in which Professor Gallo gave his evidence. He submits that Professor Gallo was not entirely frank and that his aggressive attitude towards the questioner was due to the fact that his opinions lacked credibility.

197 I reject that submission. I consider that Professor Gallo was a frank, forthright witness. Professor Gallo has been recognised throughout the world for his work. He is a pre-eminent expert in the field of virus identification and treatment. I accept his evidence and his opinions. I accept his evidence that the debate about HIV, whether it causes AIDS and whether it is sexually transmissible by heterosexual vaginal sexual intercourse, is a debate that was completed by the mid-1980s. I accept his evidence that the witnesses called by the applicant have misused material in support of their argument that HIV has not been proved to exist.

Here come de judge

All this can be seen recorded in detail in his lengthy and illuminating 82 page judgement, the Reasons for Decision of The Honourable Justice Sulan now available to the world for study. Reading through it we have to say it seems unlikely that the Perth Group will survive this lengthy public demolition of their reputation by an inattentive judge prejudiced in favor of power.

In one way this is a pity since they have done good work on the fundamental reasons why AIDS patients should suffer immune decline in the absence of any ascertainable influence from HIV. But their distracting claim that HIV has not been effectively isolated is a stale red herring whose odor attaches itself to all critics of the hypothesis that HIV causes AIDS, a claim which is genuinely unproven and contradicted by the scientific literature.

Peter Duesberg and other thoughtful scientists who can see that the paradigm is unjustified do not need to be associated with unprofessional quarrels with premises they do not challenge. It was always a danger that the Perth Group would break into the headlines and put paid to any chance that the valid scientific objections to the paradigm would be taken seriously by those outside the field.

Not to mention that Duesberg himself powerfully, cogently and conclusively dismissed the Perth Group’s reasoning ten years ago (see Virusmyth’s The Missing Virus section) on the existential issue, even as he respected their many contributions on other fronts, including the real nature of African AIDS, inaccuracies of HIV testing, and misconceptions about hemophilia and AIDS. In fact, he gave them the first two chapters of the scholarly volume that he edited, AIDS: Virus or Drug Induced, in 1996, for their invited expert reviews of HIV∫AIDS research distortions.


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SPECIAL NOTE: The Perth Group deserves respect, in the opinion of the editorial staff of NAR, and the strictures of Judge Sulan are ignorant calumny. The Perth Group’s identification of oxidative stress as one key mechanism in the kind of immune deficiency now labeled HIV∫AIDS is notable as one of the earliest contributions made (published in 1988, after more than five years research) to a correct diagnosis of AIDS and its underlying mechanism, a solution derailed in 1984 by the unfounded and still undemonstrated claim of Gallo that HIV was the culprit. Their analysis pointing out that oxidative stress caused by drugs, malnutrition and multiple infections can harm sensitive T cells is justified by much mainstream literature since, and has been endorsed by Luc Montagnier in his book “Virus”.

It should also be pointed out that their critique of Montagnier’s original experiments detecting the presence of HIV in the blood of AIDS patients (they said that he had failed to purify the virus) was endorsed in the Adelaide court room by none other than the satellite image of Bob Gallo himself, perhaps glad to draw attention away from his own lab sins which are legion (he is famous for making a fool of himself with contaminations of cultures). and Montagnier has conceded it. But this basis for challenging the very existence of the Virus grew out of date as labs all over the world cultured the Virus, duplicated its sequencing, and even distinguished between strains of the 9 kilobase wisp of RNA even as they failed to show its harmful effects.

The Perth Group would have been better off defending their analysis of the mechanism of immune deficiency against Gallo’s groundless challenge by pointing out, for example, that not only was finding HIV in 36%of AIDS patients, and antibodies to it in 88%, screamingly unconvincing, but the presence of cytomegalovirus, Epstein Barr virus and herpes virus in approaching 100% of patient blood samples indicated a theoretical bias on the part of Gallo that science cannot explain. All this is well exposed in Robert Root-Bernstein’s Rethinking AIDS, Chapter four.

Indeed the Group made very sharp points along these lines in the first paper, A Critical Analysis of the HIV-T4-cell-AIDS Hypothesis, they contributed to the Duesberg’s collection, AIDS: Virus or Drug Induced (1996). For example, they point out the little appreciated fact that Gallo’s original T cell culture of HIV was in a leukemia cell line, HT, which already happened to have the property of forming occasional giant cells with fused nuclei. This Gallo then interpreted as a cytopathic effect of HIV, his only evidence of supposed HIV cell killing in the one Science paper of his 1984 broadside to supposedly prove that HIV could kill cells.. “The virus positive cultures consistently showed a high proportion of round giant cells containing numerous nuclei (syncytia)”. But the syncytia was already happening before the presence of the harmless Deadly Virus.
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Now the loss of credibility due to arguing the Virus doesn’t exist has happened as feared in a court of law in Australia and sent an unfortunate man innocent of causing harm back to jail, because it meant that the very obvious proven fact in the literature (pace Nancy Padian, who now denies what she demonstrated) that HIV is effectively not transmissible in sex between heterosexuals could not be established in the Judge’s now closed mind.

But Kevin Borick, his lawyer who made the error of placing his bets on the Perth argument, says he will appeal anyway on other grounds, according to reports. And if this decision now fences off the Perth Group spoiler effect, it is all to the good.

Misdirected insults

blindbreast.jpegHowever, let’s not agree with the court in rejecting their case on the grounds that they are outsiders to the field of HIV∫AIDS without practical experience of the virus. This is naive if not absurd. Judge Sulan has no idea it seems of how often outsiders come up with advances in a field, especially on a theoretical level. His jeers at Papadopulos-Eleopulos along these lines are silly:

Ms Papadopulos-Eleopulos has no practical experience. She has never worked with patients who are said to be infected with HIV, or with any virus. She has never treated or diagnosed patients who have viruses. She has never worked in laboratories or conducted research. She has no practical experience.

133 She has given evidence on the topics of virology, immunology, epidemiology, microbiology and microscopy. She has no practical experience and she has never worked in any of the areas.

134 Although Ms Papadopulos-Eleopulos demonstrated a superficial understanding of a number of the areas, I consider that her knowledge is limited to her reading. She has what one might describe as a textbook understanding of the science of viruses, but she has no depth of knowledge or understanding and she simply relies upon written material. She did not demonstrate any understanding or knowledge similar to that demonstrated by the witnesses called by the DPP.

135 I conclude that she does not have expertise in the various disciplines in which expertise is required. In my opinion, she is not qualified to express opinions about the existence of HIV, or whether it has been established that it causes AIDS. Nor has she expertise to express opinions about whether the virus is transmissible. Nor is she qualified to express opinions about the tests that have been developed to diagnose the virus.

136 Even if I were to conclude that Ms Papadopulos-Eleopulos had some expertise to express opinions about the methodology for determining whether HIV exists, I consider her opinions to be so out of line with the prevailing opinions and the prevailing evidence which supports the existence of the virus, that no jury could rely upon her opinions. In my view, no weight could be given to her evidence. That is a relevant factor in considering whether permission to appeal should be granted.

137 Ms Papadopulos-Eleopulos lacks independence. She is an advocate for a cause. She chooses to rely upon opinions of others which she often takes out of context and misinterprets. She lacks objectivity. If faced with evidence which does not support her views, she simply refuses to acknowledge it, or dismisses it without any basis for so doing. Examples of her refusal to acknowledge evidence which does not support her views include her response to the epidemiological evidence which she says is not proof and which she dismisses as unreliable.[81]

Of course, he had the good lady in front of him, so for all we know she does give a poor impression in public. She certainly fails to speak very good English, according to the transcript, although Gallo’s grammatical structures are not much better. We suspect that if Judge Sulan had been able to see Gallo in person rather than on video he might have got a different impression, also.

Here is what he thought about Turner:

Dr Turner’s knowledge of the subject matter is limited to reading. He has no formal qualifications to give expert opinions about the virus. He has no practical experience in the treatment of viral diseases. He has no practical experience in the disciplines of virology, immunology or epidemiology.

143 His opinions are based on reading scientific literature, studying of scientific literature, and spending a considerable amount of time thinking.

144 I conclude that Dr Turner is not qualified to advance expert opinion about virus isolation, antibody tests, viral load tests, or sexual transmission of the virus. His knowledge of these subjects is limited to having read a number of publications. He relies entirely on his interpretation of various studies in the specialised disciplines of virology, epidemiology, microbiology, immunology, pathology or infectious diseases, in none of which he has qualifications beyond his medical degree. He has no practical experience, and has performed no research which has been published.

This is an extraordinarily clear statement that no one but insiders are qualified to read and understand the literature of a field. The Gallo-Fauci-Moore defense team must be chortling.

How rebels are handicapped

blindjudge.jpegIn this way, the task of critics who detect a flaw in conventional wisdom is made difficult. The first accusation is that they don’t know what they are talking about, because they don’t have the inside knowledge needed to make a good decision. If for example you disagree with George W. Bush’s upcoming decision to drop bombs on Iran, the first counter is, you are not in possession of secret information about how close they are to making a nuclear weapon.

Then it is also a fairly clear principle in cases where independent scholars and critics tilt at mainstream shibboleths that the critics are likely to be eccentrics in personality and behavior, and the defenders at the top of the establishment much more acceptable in their smooth conformity to the conventions of dressa and behavior, since that is partly how they got to the top of the pyramid and stay there. The critics, meanwhile often have all the earmarks of the crackpot, or at least can easily be painted as such.

That is why we thank Destiny for the existence of John P. Moore, one of the greatest assets of the movement to reexamine HIV∫AIDS science in his non conformist behavior in speech and writing, and in the inaccurate and ad hominem style of his website AIDSTruth.org

Unlike Anthony Fauci of NIAID, he is neither stylish in dress nor smooth in behavior. He and Robert Gallo, the ebullient roguish initiator of this gigantic mess, have in common the tendency to let loose verbally or in print and on line (in the case of Moore) if they get a chance.

Quick way to tell who’s right on HIV∫AIDS

For a change, we have colorful individuals on both sides of this debate, and that is as it should be. For after all, these are disputes about scientific theory and interpretation, and the quality of the ideas that are expressed are highly dependent on the qualities of the man or woman expressing them.

In fact, we have often thought it is not really necessary for any outsider who comes upon this debate to read very far into it to know who is almost certain to be right.

All one has to do is line up Robert Gallo, Anthony Fauci, Mark Wainberg and John Moore and compare them with Peter Duesberg, Harvey Bialy, Celia Farber and Rebecca Culshaw.

It would be pretty clear even to a distinguished but mentally myopic, meme ridden, power worshipping Australian Supreme Court judge who are the salesmen heavily invested in the paradigm, and who are the independent minded, public spirited, self sacrificial critics.

Addition: While we were posting this a very fine Comment by the inimitable MacDonald has been attached to the previous post, but is highly relevant here for its deft exposure of the Judge’s bias against the Perth Group as revealed in his Reasons for Decision, in which his Reasons for Bias against the Perth Group are in fact, as MacDonald aptly points out, much better as Reasons to Reject the Testimony of Robert Gallo, to whom they apply in spades. (Later moved to Comments under this post. – Ed.)

Adelaide a bust

April 27th, 2007

Judge Sulan turns down Parenzee appeal of jail sentence

HIV∫AIDS meme triumphs on legal front

kangcloseup.jpegBad news for human rationality from Adelaide. Australia, where after ruminating for two or three months Judge Sulan of the Supreme Court of Southern Australia has decided the fate of the unfortunate Chad Parenzee, jailed earlier for having sex without confessing that he was, according to the science of Robert Gallo, harboring antibodies to the HIV virus.

Despite a court hearing where it was plain to all intelligent observers present or who afterwards read the transcript, that Gallo’s HIV∫AIDS science was exposed as senseless, being both inconsistent in theory and without good evidence of any kind, an impression most clearly conveyed by the great man himself, Gallo having testified by video transmission from his home in the USA, the Judge decided an hour ago as of this writing that Parenzee’s appeal should be denied.

On what grounds he justified this opinion we do not yet know, but we have a very good idea that the efforts of the courageous Perth Group pair (see previous post on this topic) to challenge Gallo and his fellow Australian HIV∫AIDS promoters on their science went for nought, simply because this was a political game and not a legal or scientific one.

Immovable meme

We imagine that the Judge despite showing one or two moments of Aussie feistiness and independent spirit during the case, notably when Gallo was giving his testimony, was not able to overcome the HIV∫AIDS meme which must have set up residence in his brain some twenty two years ago, and have ruled it ever since.

kangaroofighter.jpegMost of the testimony which showed that there were serious questions that could be asked about the HIV∫AIDS paradigm probably went over his head, and even if they didn’t, the insistence of the Perth pair in challenging the very existence of the virus probably lost them the case as soon as they testified. This kind of allegation has no chance against the meme once it is in the brain of a judge or anyone else.

However, their other points about the inconsistency, incredible claims, and lack of evidence for the paradigm probably showed him that there was a valid controversy behind the scenes and in a world ruled by sense should have persuaded him, during the month or two he has taken to review the case, to allow the appeal.

What the decision shows, in our opinion, is that it is politics and economics that decides this kind of case, not science, even if Judge Sulan was the sharpest of cookies and saw through the babble that Gallo produced in testifying, as he read it through again in the quiet of his chambers.

Running from buffalo

We imagine that the good Judge actually spent a fair amount of time on the phone and at lunches, dinners and parties sounding out the other influential people in his city, which is the capital of Australia, and in other centers of influence, who have to do with governing medical matters, and finding out who would approve what. A Supreme Court judge in Adelaide did not achieve his prominent post without a good bit of discreet clubmanship and subtle approval negotiation, you can be sure of that.

Far better that a no account gay man should languish in jail a few years for flouting the law, even if it was based on flawed establishment science, that the Judge should have to deal with all the social fallout for taking a stand against the thundering herd of buffalo heading in the wrong direction. Can you imagine the comment he would be exposed to in the press and at parties of the ruling classes of Adelaide? His wife surely imagined it for him.

Stand up, and stand for, or you stand still, say the idealists from their encampment outside the gates of power. On the other side of the moat, drawbridge and walls of the castle that keeps them out, however, everyone but the servants knows that the real ruling principle is observe the weathercock at all times, and know which way the wind is blowing.

kangaroo.jpegTime will tell

Perhaps Judge Sulan took his time because he was wrestling with his conscience. We like to think so. Or perhaps he hesitated, appalled at the idea of playing the provincial handmaiden to a bunch of carpetbagging crooks whose congame was all too apparent via video when Gallo testified.

But one way or another, it was probably the naivete of those who deal in ideas and in truth that made them think for a moment that the decision could run any other way. The game is politics, not science, and only political influence and celebrity wattage of the William Jefferson Clinton level can really move the mountain, we see now.

Luckily that does not seem impossible. Sooner or later, some kid of some megarich couple in a society where top hedge fund managers are now paid $2.4 billion a year – the USA – will run into the trap of HIV∫AIDS positivity one way or another, and Daddy will fork up enough money to fight the case in an American court and win.

But meanwhile John Moore of Cornell will crow, and those who can read the scientific literature for themselves and see how it contradicts the public claims of the scientists who write it, will have to remain patient.

Well, we can promise them a consolation prize soon – a post showing how Dr Moore himself is one of the staunchest witnesses for the prosecution of his own paradigm, simply by quoting his own papers.

Guessing game

Meanwhile, it is of interest to note that a straw poll taken in recent days among the most active critics of HIV∫AIDS found that most were unwilling to guess the outcome, but those that did broke about 50/50.

aussiesupremecourt.jpegWe are embarrassed to admit that we thought the good Judge, being full of down to earth Aussie spirit, and rebelling against the influence of carpetbaggers from the US, would allow the appeal.

Most accurate was the cynical satirist and 911 conspiracy theorist Marcel Girodian, who wrote to us:

I’m quite sure that he will not allow the appeal, because the international ramifications of that would be too destabilizing to established order. I am also sure that he has been “talked to” by the powers that be, and it has been made clear to him that he is not to allow the appeal.

Now if i’m wrong , i’ll very delightedly eat my hat. But i doubt that i’m wrong.

Democracy is just a fantasy that they use to keep the people from realizing they are slaves. All the structures of democracy are easily manipulated and corrupted, and have been so for centuries.

On the other side was the more idealist Marcos, from South America. He wrote:

I´ve been reading the testimonies and I think that the existence of a scientific controversy has become so clear that that only for itself should be proof enough for the judge to aknowledge a reasonable doubt and allow the appeal.
I see it that way.Therefore, I´m confident.
I`m not saying that the judge will take any sides in the controversy. It´s not his job.
On the other hand, if this thing doesn´t turn out to be a winner, well I won´t care… I´ll keep on and on fighting for the truth to come out. That´s the message I think we should send out to everyone.

We like to believe that the tide of history runs from Marcel to Marcos, from cynicism and disappointment to success and truth. In the end. But it may be that, as Max Planck observed, we have to wait for the retirement and even death of the current rulers before that rennaissance of science to where it should be.

“Science advances funeral by funeral,” was his rueful thought.

Potshot at Duesberg

April 27th, 2007

Surgeon-biologist Orac tackles Duesberg’s cancer idea with limited respect

Hostile to Duesberg on AIDS, he labors to rescue oncogenes from the aneuploidy gold rush

The first attempt at a public critique of Peter Duesberg’s cancer initiative, his leadership of a return to exploring the aneuploidy which marks all cancer cells (their excess chromosomes, sometimes even double the normal number), has been made. Orac, whose blog on Seed magazine’s Science Blogs site, is Insolence, has managed quite a lengthy treatment, laboriously raising objections to Duesberg’s explanation in Scientific American (earlier post).

The post attempts to save oncogenes from the stampede over to aneuploidy, reminding us that Duesberg both pioneered the field of cancer genes and repudiated it soon afterwards. Thus the first section of the Duesberg article, which is being carried by You Bet Your Life in the form of a pdf , mentions how Duesberg found the first example of ‘oncogenes’‘, the quickly fashionable cancer field that he afterwards rejected and now is threatening to replace with more productive aneuploidy research.

Chromosomal Chaos and Cancer

Current wisdom on the role of genes in malignancy may not explain some features of cancer, but stepping back to look at the bigger picture inside cells reveals a view that just might

By Peter Duesberg

When I first began to study cancer as a young postdoctoral fellow in the early 1960s, it looked to leading scientists as though viruses could be the cause of most, if not all, malignancies. That idea was based on the discovery of several tumor- and leukemia-producing viruses that could infect a host cell and insert their own genetic material into its genome, sparking a cancerous transformation and proliferation of the cell. I was optimistic and naive enough to hope that if researchers could understand the exact molecular mechanisms by which such viruses caused cancer, we could develop vaccines to eliminate one of humanity’s most dreaded diseases.

My own contribution to that pursuit came in 1970, when my colleagues, Michael Lai and Peter Vogt, and I managed to isolate a specific gene, src, which was suspected to be the tumor-initiating culprit in avian Rous sarcoma virus. Within a few years, more creative scientific minds than mine had followed this lead to a realization that a closely related gene was already present in the normal DNA of animals, including humans. And a new cancer model was born: it proposed that some triggering event, such as a mutation in a human cell’s own version of src, could ignite tumorigenic powers like those possessed by its viral counterpart. The cancer-promoting potential of such a time bomb buried in our personal genomes earned it the title of “proto-oncogene.” Once the mutation occurred, it would become a full-fledged oncogene. …. (cont. in Scientific American or on the pdf copy of the Duesberg article here

Here is a Wall Street Journal blog note on the appearance of the piece:

A Cancer Theory From a Controversial Scientist

Researchers have been looking in the wrong place in the body for cancer’s origins, writes Peter Duesberg in Scientific American (subscription required). What makes the publication of his theory remarkable is that the magazine’s editors felt obliged to include a note disavowing the work Mr. Duesberg is most famous for—his claim that HIV doesn’t cause AIDS. While Mr. Duesberg is “surely wrong” about HIV, the magazine’s editors write, his work on a new theory about cancer—that an aberration in chromosomes, not genes, ignites malignant cells—has gained enough traction in the scientific world that it merits publication.

Mr. Duesberg, a professor of molecular and cell biology at the University of California, Berkeley, is treated as a pariah in the scientific community for his ideas about HIV and AIDS. At the same time, he has carried out groundbreaking cancer research and gained fame in 1970 for being the first virologist to identify a cancer-causing gene.

In the late 1960s and 1970s, Mr. Duesberg and others began looking into the role of mutations in a few key genes that regulate cell function. He has since shifted the hunt for cancer’s origins one level up in the cell, to chromosomes, rod-like structures made up of thousands of genes. Unlike genes, chromosomes barely vary across a species. The smallest difference in them can be catastrophic. In cancer cells, chromosomes are scrambled. Mr. Duesberg suggests these chromosomal disruptions unbalance the way thousands of genes regulate cell function and reproduction, eventually leading to cancerous cells.

The chromosome hypothesis avoids some difficulties with the gene theory of cancer, Mr. Duesberg says. Some of the most potent carcinogens, like asbestos or tar, don’t cause genetic mutations. But the chromosomes of cells treated with cancer-causing doses of carcinogens become unstable. Few children get cancer, but Mr. Duesberg notes that the rare cases of those who do also suffer from or are susceptible to chromosomal abnormalities. — Robin Moroney
Permalink | Trackback URL: http://blogs.wsj.com/informedreader/2007/04/16/a-cancer-theory-from-a-controversial-scientist/trackback/

For additional understanding of the value of Duesberg’s approach – and the scientific weakness of the oncogene paradigm which has ruled for nearly three decades in cancer research – see Harvey Bialy’s book, “Oncogenes, Aneuploidy and AIDS: A Scientific Life and Times of Peter H. Duesberg” (North Atlantic Book, 2004).

Then you can have fun reading and dissecting the blog critique, which task Dr Bialy, Duesberg’s sharp witted champion in this as well as in the soggy science of HIV∫AIDS, says is beneath him, according to a recent communication referring to “gibberish read only by pod people”. It is hard not to agree with him.

It is also hard to stomach the demons of illwill and disrespect let loose by the witchcraft of the Web and attached to every comment by “Adele” and other witless riders of Orac’s self-confessedly “insolent” coat tails, or those of epidemiologist Tara Smith, the svelte bathing beauty and blogging genius also at Science Blogs to whom Duesberg’s errors are also transparent at first glance. It is amazing that knowledgeable posters such as Ky Sanderson are prepared to punt in this verbal sewer, where they have as little effect trying to correct the prejudices of the lynch mob as pouring a single bottle of Listerine into the subterranean tunnels of waste disposal under Manhattan.

Here is the self-description of the blogger:

Who (or what) is Orac?

Orac is the nom de blog of a humble pseudonymous surgeon/scientist with an ego just big enough to delude himself that someone, somewhere might actually give a rodent’s posterior about his miscellaneous verbal meanderings, but just barely small enough to admit to himself that few will. (Continued here)
…I’m not only a cancer surgeon (which in and of itself is not enough to qualify me to comment on this topic) but rather because I’m also a cancer researcher and a molecular biologist (which, I submit, does make me qualified to comment on this topic).

This is the well qualified fellow who now has the effrontery to decorate his text in his long post with the following prejudicial statements (errors in bold) about Duesberg’s incorrectness (as he sees it) on HIV∫AIDS”, reminding us that one of the many crosses the distinguished Berkeley professor has had to bear in trying to enlighten the elite as to the scientific three card monte shuffle perpetrated upon them for 22 years by Robert Gallo, Anthony Fauci and now John Moore is the smug prejudice of the lay defenders of the faith, who intuitively know that he is wrong even though his many hostile peer reviewers were by definition unable to show it:

Peter Duesberg, as you may know, is the controversial scientist who is perhaps the foremost advocate of the discredited hypothesis that HIV does not cause AIDS.

(A rhetorical statement) “The one that first comes to mind as particularly relevant to Peter and AIDS is that it does seem impossible that a man who is clearly so utterly wrong concerning something as now scientifically straightforward as whether AIDS is caused by HIV could actually be correct about something as complex as the genetic basis of malignancy.”

Yet they think nothing conflating the scientific validity of Duesberg’s ideas concerning cancer, which might indeed be partially or mostly correct, with his discredited hypothesis that HIV does not cause AIDS, implying that because he might be correct about cancer implies that he is correct about AIDS. It doesn’t

I do not plan on discussing why Duesberg’s ideas regarding HIV are wrong, even though the results of such HIV/AIDS denialism leads to quackery and has serious real-world consequences for real people. Tara and Nick have done far more than my minor efforts to critically examine such wingnuttery.

I think Duesberg’s an utter crank and pseudoscientist when it comes to his HIV/AIDS denialism,

Clearly, this is a man in whose brain the AIDS meme has taken up residence and cuckoo-like, has kicked out any semblance of openmindedness on that score, and so probably one who appoaches Duesberg’s new ideas with equal lack of self assessment.

That characteristic is always the most amazing attribute of the host of otherwise intelligent, combative and self promoting bloggers that have mushroomed with the advent of the Web. Why is it that they never turn their critical eye on themselves and their own thinking? Self-editing is not the greatest talent of Orac, that’s for sure. Does he not consider that if in his view Duesberg’s hypothesis is “argued poorly”, it may be his own understanding which is lacking? After all, it has been Duesberg’s career interest and project for many years, and if it has made headway against so much prejudice against him it must make very good sense.

But Orac is such a clogged thinker himself that it may be he is simply confused. For example, he says “implying that because he might be correct about cancer implies that he is correct about AIDS. It doesn’t. Sorry, but the two issues are at best peripherally and weakly related and at most not related at all. ” Here he seems unable to grasp the point, which is not that the two fields are closely related but that Duesberg is a very good mind in science, one of the best in the business. who has initiated two fashionable fields of research.

Similarly, he writes that

Now, potential chromosomal causes are again being looked at, and for whatever part Duesberg’s advocacy had in spurring this he is to be acknowledged, even if his boosters do have an annoying tendency to make it sound as though scientists would have zero interest in studying chromosomal causes of cancer were it not for Duesberg, which, given the attention shown to this topic at recent meetings that I’ve attended, is ridiculous.

without seeming to think of the possibility that without Duesberg’s pathbreaking efforts over many years the dominant paradigm (cancer through individual gene mutation) would reign on undisturbed, and that he has every reason to take credit that it is now a hot topic.

It is by now abundantly clear that Orac’s research methods lean heavily on the “Ask John” approach.

However, he begins with a nice enough statement of the core idea of aneuploidy – excess chromosomes in the cell – and its history starting with Boveri and sea urchins.

It has been known for many many decades that most cancer cells are aneuploid. This means that, instead of having the correct number of chromosomes (in the human, 46 chromosomes, two matched sets of 22, plus the sex chromosomes, either XX or XY). In some diseases, such as Down syndrome (known as trisomy-21), there are either missing or extra chromosomes. In the case of Down syndrome, there is a third copy of chromosome 21. Such abnormal chromosomal numbers come about when, during meisosis (cell division that produce germ cells), the newly copied chromosomes don’t segregate properly to the two daughter cells, one to each. Instead, both go to one or the other cell. In cancer cells, the situation is much worse; such missegregation during mitosis can lead to aneuploidy that is much more severe, to the point where some cancer cells can have 70 chromosomes or more. Because certain genetic mutations, for example in DNA damage repair genes, can lead to chromosomal instability that can in turn lead to aneuploidy, the basic argument has been over the relative importance of the roles of aneuploidy and the accumulation of genetic mutations as leading to cancer. On the one extreme, there is the argument that aneuploidy is the primary cause of cancer, causing the accumulation of genetic mutations through breaks in chromosomes. On the other extreme is the argument that aneuploidy is a consequence, not a cause, of cancer. Duesberg, as you may guess, takes the extreme version of the former view. These days, most other scientists studying this question tend to consider both important to varying degrees in the development of cancer.

This is an introduction to a post which in theme is presumably the product of Orac’s “Ask John” research, where he has checked with anyone around in the hospital who might know to find out what the current paradigm’s cancer research is all about. Anyone who has read “Oncogenes, Aneuploidy and AIDS” knows what kind of briefing he has received. Leading scientists in the field are desperate to make sure that even if aneuploidy continues to prove out as a productive field it won’t replace the oncogenes paradigm they have invested in for three decades.

Now master blogger Orac sounds the same theme: aneuploidy is “intriguing” and may even be “primary” but let’s allow oncogenes to keep their place on the stage also. Never mind that Duesberg – who founded the field of oncogenes, no less, when he discovered the first example of a cancer causing gene in the Rous sarcoma virus – has always rejected that paradigm as well the HIV∫AIDS story as unsound, and Orac doesn’t seem to know why.

The concept that aneuploidy may play a major and, in some cases, primary role in carcinogenesis is a legitimate scientific idea with scientific evidence to support it. It doesn’t need to be defended or argued using such bad arguments, but Duesberg can’t seem to help himself. The problem is, Duesberg’s thinking is black-and-white, all-or-nothing. He can’t seem to fathom the concept that both aneuploidy and genetic mutations might feed upon each other. In addition, he also almost totally neglects other evidence implicating other causes or important factors in the progression of cancer, such as cancer stem cells, tumor angiogenesis, or even the metabolic hypothesis ( i.e., the Warburg effect), which, like the chromosomal hypothesis, is also enjoying a resurgence. Cancer is a complex set of diseases, likely with multiple causes contributing to the development of different cancers in different proportions, which is why my skeptical antennae start twitching whenever I hear someone like Duesberg (or anyone else, for that matter) postulate in essence a single cause for all cancer.

Still, he is obviously persuaded persuaded that Duesberg’s approach is productive, even if he spends much time emphasizing that Duesberg didn’t think of it first:

It is clear to me that epigenetics (cellular factors other than genes that regulate gene activity) and chromosome structure are very important in carcinogenesis, more so than had been appreciated before

All in all, not too disrespectful a treatment, and a useful collection of possible objections to aneuploidy that will come from the blog world. There are endless jabs at the supposed idiocy of one of the world’s great scientists for flouting the assumption of the blogger that HIV∫AIDS must be as valid as its global support indicates. But these don’t erase the new if split respect that Orac seems to have for Duesberg now that the Scientific American has endorsed aneuploidy and him in this fashion.

The Comments that follow include a priceless articulation of the hostile prejudice against Duesberg that now sprinkles the floor of the Web forest like toadstools:

I agree with you, this almost seems to be a presage to even more crankery from Duesberg. I can just see that as time goes on and this hypothesis is balanced out by other findings that show every cancer can’t simply be housed under the umbrella of aneuploidy if he’ll once again just dig in and refuse to accept evolving facts. When Duesberg suggested that HIV causing AIDS was based on mostly correlative evidence in 1987 (and Science published it), he kind of had a point. It wasn’t a particularly good, or useful point, but within the year there was excellent evidence from studies of AZT, as well as responses to Duesberg’s criticisms that really should have had those ideas tossed, and certainly by about 1993 or so the science was settled. These days given what we know about the HIV proteins, mechanisms of latency and entry in CD4 cells, it’s frankly just embarrassing he didn’t give up decades ago, I wonder if he’ll do the same here if things don’t turn out his way.

I will continue to disagree, however, that this wasn’t a mistake for Sci Am. I believe in the scientific death sentence – that is, if you are proven untrustworthy, you shouldn’t be allowed to contribute to the literature anymore. So what if he’s changed fields, he demonstrated himself to be a dishonest crank so badly and for so long why should we risk the literature with contributions from this guy? I don’t find his so-called dissident status cute or funny, it results in bad science, bad policy and ultimately death as these bizarre ideas take hold in Africa (especially S. Africa) and even in the United States as with the HARM people. I’m all for the black list for cranks too because I believe cranks are fundamentally deceptive and untrustworthy contributors to scientific debate, and all of his subsequent (thankfully rejected) internet publications on HIV/AIDS are really just a pack of lies.

I simply wouldn’t trust this guy again, ever.

Posted by: Mark | April 25, 2007 03:50 PM

Established publications used to keep this kind of rant out of the letters column, but now we see it given permanent form on the servers of the Web, rather like a madman used to have to work very hard to get hold of a weapon, but now a Mr Cho can kill 32 people with a Glock bought at a sports store.

One always wonders what the writer – Mark, in this case – will feel when he is older, and Duesberg is vindicated, but his juvenile post is still cached by Google for all his grandchildren to see,

(Orac’s post)

Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly

Category: Cancer • Medicine • Science • Skepticism/critical thinking
Posted on: April 25, 2007 9:01 AM, by Orac

A lot of readers (well, a couple, anyway) have been asking me about the recent article by Peter Duesberg in the most recent issue of Scientific American entitled Chromosomal Chaos and Cancer. I suppose it’s because I’m not only a cancer surgeon (which in and of itself is not enough to qualify me to comment on this topic) but rather because I’m also a cancer researcher and a molecular biologist (which, I submit, does make me qualified to comment on this topic). Peter Duesberg, as you may know, is the controversial scientist who is perhaps the foremost advocate of the discredited hypothesis that HIV does not cause AIDS. I had been tempted to comment on Dueseberg’s hypothesis based on the orgasmic reaction of Duesberg’s sycophants in the HIV/AIDS “dissident” community to the recent publication of an article on it by Duesberg in Scientific American. One such booster, even went so far as to say:

The one that first comes to mind as particularly relevant to Peter and AIDS is that it does seem impossible that a man who might just be correct concerning something as complicated as the genetic basis of malignancy could be so totally wrong about something as straightforward as whether HIV kills T-cells.

This is perhaps the dumbest thing I’ve heard said about evaluating Duesberg’s aneuploidy hypothesis of cancer. To demonstrate why, let me recast the question a bit to: “The one that first comes to mind as particularly relevant to Peter and AIDS is that it does seem impossible that a man who is clearly so utterly wrong concerning something as now scientifically straightforward as whether AIDS is caused by HIV could actually be correct about something as complex as the genetic basis of malignancy.”

HIV/AIDS denialists would be screaming bloody murder about such a question were I to pose it as anything other than a rhetorical device, and they would have a point to some extent. Yet they think nothing conflating the scientific validity of Duesberg’s ideas concerning cancer, which might indeed be partially or mostly correct, with his discredited hypothesis that HIV does not cause AIDS, implying that because he might be correct about cancer implies that he is correct about AIDS. It doesn’t. Sorry, but the two issues are at best peripherally and weakly related and at most not related at all. That is why I do not plan on discussing why Duesberg’s ideas regarding HIV are wrong, even though the results of such HIV/AIDS denialism leads to quackery and has serious real-world consequences for real people. Tara and Nick have done far more than my minor efforts to critically examine such wingnuttery. Instead, I decided simply to ask the question about Duesberg’s chromosomal chaos hypothesis as the cause of cancer and ask: Is there any “there” there? It’s a question I’ve asked myself before but never written about, and this seemed like an opportune time to discuss the issue.

The first thing that struck me about the Scientific American article is that it looked very much like a popular version of two very similar recent review/opinion articles that Duesberg published in 2005 and 2006. I’m mainly going to discuss the Scientific American article because it’s basically the same message in a form more palatable to the educated lay reader. But, before I begin, I’d like to point out a couple of things. First, the concept that chromosomal abnormalities cause cancer dates back at least to 1914, when the German zoologist Theodor Boveri, based on studies of sea urchin development, first suggested it. Indeed, this featured prominently as a milestone in cancer research in a display in at the recent 100th anniversary meeting of the American Association for Cancer Research. Thus, the basis of Duesberg’s idea is quite old. Indeed, the concept that chromosomal derangements caused cancer predominated for 40-50 years, until the solution to the structure of DNA, the elucidation of the genetic code, and study of genetics led to an emphasis on genetic causes of cancer. Combined with the observation that tumor cells are genetically unstable, leading to many mutations, the genetic hypothesis led to the discovery of oncogenes and tumor suppressors. Now, potential chromosomal causes are again being looked at, and for whatever part Duesberg’s advocacy had in spurring this he is to be acknowledged, even if his boosters do have an annoying tendency to make it sound as though scientists would have zero interest in studying chromosomal causes of cancer were it not for Duesberg, which, given the attention shown to this topic at recent meetings that I’ve attended, is ridiculous.

It has been known for many many decades that most cancer cells are aneuploid. This means that, instead of having the correct number of chromosomes (in the human, 46 chromosomes, two matched sets of 22, plus the sex chromosomes, either XX or XY). In some diseases, such as Down syndrome (known as trisomy-21), there are either missing or extra chromosomes. In the case of Down syndrome, there is a third copy of chromosome 21. Such abnormal chromosomal numbers come about when, during meisosis (cell division that produce germ cells), the newly copied chromosomes don’t segregate properly to the two daughter cells, one to each. Instead, both go to one or the other cell. In cancer cells, the situation is much worse; such missegregation during mitosis can lead to aneuploidy that is much more severe, to the point where some cancer cells can have 70 chromosomes or more. Because certain genetic mutations, for example in DNA damage repair genes, can lead to chromosomal instability that can in turn lead to aneuploidy, the basic argument has been over the relative importance of the roles of aneuploidy and the accumulation of genetic mutations as leading to cancer. On the one extreme, there is the argument that aneuploidy is the primary cause of cancer, causing the accumulation of genetic mutations through breaks in chromosomes. On the other extreme is the argument that aneuploidy is a consequence, not a cause, of cancer. Duesberg, as you may guess, takes the extreme version of the former view. These days, most other scientists studying this question tend to consider both important to varying degrees in the development of cancer, the present pressing scientific question being: Which causes which and how? It’s very much a chicken-or-the-egg problem. Does mutation lead to aneuploidy or aneuploidy lead to large numbers of genetic derangements that lead to cancer? Or are both aneuploidy and mutation responsible in differing proportions depending on the cancer?

Unfortunately, although he describes how tumors evolve under the selective pressures of the organs in which they arise, acquiring the ability to proliferate, evade apoptosis, become insensitive to normal growth arrest signals, and metastasize, Duesberg seems unable to restrain himself from overselling his case and lapsing into straw men arguments about rival hypotheses. He’s very frustrating that way. The concept that aneuploidy may play a major and, in some cases, primary role in carcinogenesis is a legitimate scientific idea with scientific evidence to support it. It doesn’t need to be defended or argued using such bad arguments, but Duesberg can’t seem to help himself. The problem is, Duesberg’s thinking is black-and-white, all-or-nothing. He can’t seem to fathom the concept that both aneuploidy and genetic mutations might feed upon each other. In addition, he also almost totally neglects other evidence implicating other causes or important factors in the progression of cancer, such as cancer stem cells, tumor angiogenesis, or even the metabolic hypothesis ( i.e., the Warburg effect), which, like the chromosomal hypothesis, is also enjoying a resurgence. Cancer is a complex set of diseases, likely with multiple causes contributing to the development of different cancers in different proportions, which is why my skeptical antennae start twitching whenever I hear someone like Duesberg (or anyone else, for that matter) postulate in essence a single cause for all cancer.

Let’s look at what Duesberg argues. In essence, he argues that aneuploidy comes first and is the prime inciting event that starts the cascade of genetic changes that lead to malignancy. DNA is damaged, either through mutagens or other causes, and then, through what becomes a self-catalyzing process, aneuploidy leads to progressive chromosomal alterations that lead to increasingly widespread genetic alterations in a process that feeds on itself, leading to chromosomal instability and cancer. Indeed, Duesberg postulates that carcinogens work as “aneuploidogens” rather than as mutagens.
464314423_92c662218e.jpg

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Grrlscientist has posted a concise summary of Duesberg’s arguments here, and Hank Barnes has a copy here. (I’m guessing that Duesberg or Harvey Bialy gave him the PDF.)

So, here we have a scientific hypothesis with a moderate degree of plausibility based on what we know. What arguments can Duesberg marshal in its favor? Disappointingly, most of his arguments leave much to be desired. Let’s start with Duesberg’s first argument, which is so bad that it needs to be quoted extensively to be appreciated:

Cancer risk grows with age. Lamentably common, cancer afflicts about one in three people at some point in their lives, but mostly after the age of 50, which is when chances for malignancy soar. Thus, cancer is, by and large, a disease of old age. The gene mutation theory of cancer’s origins, however, predicts that the disease should be quite common in newborns. If, as that hypothesis holds, about half a dozen mutations to critical genes were necessary to ignite malignancy, certainly some of those mutations would accumulate like SNPs over the course of generations in the genomes of many individuals. A baby could thus inherit three of six hypothetical colon cancer mutations from her mother, for example, and two from her father and be at extremely high risk of cancer from picking up the missing sixth mutation in any one of her billions of colon cells. Some babies might even be born with colon cancer from inheriting all six hypothetical colon cancer mutations from their parents. But colon cancer is never seen in children. Indeed, even laboratory mice intentionally engineered to carry an assortment of ostensibly carcinogenic mutations from birth can live and propagate happily, with no higher risk of developing tumors than normal lab mice.

[…]

Interestingly, among the rare exceptions to cancer’s age bias are children with congenital aneuploidy, as in Down syndrome, or with inherited chromosome instability syndromes, such as the disease known as mosaic variegated aneuploidy (MVA), which also causes severe mental retardation. Defects of mitotic spindle assembly in the cells of children with MVA produce random aneuploidies throughout their bodies, and nearly one third develop leukemia or unusual solid cancers.

Being born aneuploid, or prone to aneuploidy, clearly accelerates processes that lead to cancer. Indeed, the inherent instability of aneuploid cells would explain why most aneuploid embryos, as Boveri observed 100 years ago, would not be viable at all and thus why newborns are cancer-free and cancer is not heritable.

This argument is a strawman and neglects other factors, to boot. For one thing, contrary to what Duesberg states, the “gene mutation theory of cancer” does not necessarily predict that cancer should be quite common in newborns. Quite frankly, I don’t know what Duesberg was smoking when he wrote that and don’t see his rationale for arguing that. For one thing, it’s not true that colon cancer is never seen in children. It’s quite rare, to be sure, but in families with genetic mutations that predispose to colon cancer, the disease can appear in children as young as 5 or 6. I presume that Duesberg picked colon cancer because the genetic sequence of mutations that occur as the lining of the colon goes from dysplasia, to polyps, to noninvasive cancer, to invasive cancer was worked out so elegantly by Burt Vogelstein back in the early 1990’s. In addition, it is true that patients with Down syndrome are more susceptible to certain cancers, specifically hematopoietic (blood) cancers, but it also turns out that they are less susceptible to solid tumors, thanks to high levels of the antiangiogenic factor endostatin, the gene for the precursor of which happens to reside on chromosome 21 and is expressed at a higher level because there are three copies rather than two. Second, Duesberg neglects to notice that oncogenes and tumor suppressors cause dysregulated growth and morphogenesis, the sine qua non of cancer. Although it is true that deleting some tumor suppressors results in viable mice who appear normal other than a predisposition to cancer, such potent growth dysregulation could cause embryonic lethality just as easily as aneuploidy could, depending on the specific gene.

Indeed, although it’s not as obvious, Duesberg’s making in essence the same mistake as Dr. Egnor: confusing selective mechanisms in germ line cells with those in somatic cells. A basic consideration of evolutionary theory makes it obvious that there would be major selective pressure against mutations that result in cancer in babies and children, because the cancer would kill the child before reproductive age. In contrast, cancer-predisposing genes that are either neutral before reproductive age or confer some advantage (as has been postulated, for example, for some mutations in the BRCA1 gene, which predisposes to breast cancer), may not be selected against and could remain in the germline at a high frequency in the population. Thus, from a strictly evolutionary perspective, it is not at all surprising that inherited cancers are rare in newborns and young children, even if we postulate, for the sake of this argument, that aneuploidy has nothing to do with cancer and the “genetic mutation theory” of cancer is 100% correct. Duesberg should know this, given his invocation of selective pressures leading to increased aneuploidy in cancer.

Finally, Duesberg tries to argue that mutations don’t occur at a sufficient frequency under normal conditions to account for the increasing rate of cancer with age, but does not address the shortening of telomeres or that it may only take one or two mutations in key genes, such as those involved in DNA damage repair, to make the a single cell deficient in repairing its own DNA, which can then lead to an increased mutation rate, leading both to mutations and increased aneuploidy. Indeed, it has been postulated that the prerequisite for some cancers is what is termed a “mutator phenotype,” in which a much higher rate of mutation is observed. In any case, aneuploidy is easier to detect than mutations, assays for which can only look at a small fraction of the genome at one time and are not sensitive enough to detect mutated cells in a background of normal cells. In contrast, small numbers of aneuploid cells can be detected in a normal background. The bottom line is that chromosomal instability is a feature of virtually all cancers but the evidence that it is driven by primarily aneuploidy is conflicting and nowhere near the slam dunk that Duesberg seems to think; in essence, it’s unclear whether it is primarily aneuploidy that drives mutation or primarily mutation that leads to aneuploidy.

Here’s the next bad argument:

Carcinogens take a very long time to cause cancer. Numerous chemicals and forms of radiation have been shown to be carcinogenic in animals or established as the source of occupational or accidental cancers in humans. But even the strongest carcinogens at the highest survivable doses never cause cancer right away. Instead the disease emerges only after delays lasting years or even decades. In contrast, when substances known to cause gene mutations are administered to bacteria, the cells begin displaying new phenotypes within hours; in larger organisms such as flies, the effect is seen within days. A gene mutation scenario therefore does not explain why cells exposed to carcinogenic agents become cancer cells…

Does anyone see the flaw in an argument comparing humans to bacteria or flies in this manner? Let’s look at flies, because they are eukaryotes. The average lifespan of, for example, Drosophila is much shorter than a human’s, on the order of 30 days or so. Carcinogens generally require cellular replication before cancer can develop. So, let’s see, a latency period for cancer after exposure to carcinogens of few days in the life of a fruit fly like Drosophila is not unlike a latency period of a couple of decades in a human, if you compare it to the organism’s overall life span. Bacteria reproduce amazingly rapidly; so it is not surprising that they respond to chemicals even faster. As for strong carcinogens not causing cancer right away, nothing in the genetic mutation theory of cancer demands that they must, particularly given that strong doses may result in more deleterious mutations and that the ability of a normal cell to repair its own DNA is quite prodigious. It may ultimately be shown experimentally to be true that aneuploidy is a better explanation for the long latency period of human cancers, but there is nothing in the mutation theory that demands that there must be a short latency period after a tumor cell is exposed to a carcinogenic agent, especially since it is now understood that “multiple hits” are usually required occurring in a single cell to result in cancer.

Here’s the next Duesberg argument:

Carcinogens, whether or not they cause gene mutations, induce aneuploidy. Scientists have looked for the immediate genetic effects of carcinogens on cells, expecting to see mutations in many crucial genes, but instead have found that some of the most potent carcinogens known induce no mutations at all. Examples include asbestos, tar, aromatic hydrocarbons, nickel, arsenic, lead, plastic and metallic prosthetic implants, certain dyes, urethane and dioxin. Moreover, the dose of carcinogen needed to initiate the process that forms malignant tumors years later was found to be less than one-thousandth the dose required to mutate any specific gene. In all cases, however, the chromosomes of cells treated with cancer-causing doses of carcinogens were unstable–that is, displaying higher than usual rates of breakage and disruption.

Sure, carcinogens induce aneuploidy, but just because some carcinogens do not directly damage DNA does not necessarily mean that the induction of aneuploidy must be the mechanism by which they cause cancer. It might be, but it doesn’t necessarily have to be. For example, part of the mechanism by which asbestos is thought to cause cancer is by causing chronic inflammation, which chronically stimulates nearby cells to divide, while at the same time exposing them to a milieu containing numerous inflammatory cytokines secreted by white blood cells that invade the area. In the case of dioxin, for example, there appears to be a receptor to which dioxin binds that stimulates cell survival pathways. Either of these mechanisms, and others, could be at play in the carcinogenesis due compounds that do not cause extensive DNA damage and could account for the long latency period between exposure to carcinogen and cancer.

The rest of Duesberg’s arguments range from the “so what?” to the more intriguing. For example, he points out that different patterns of aneuploidy are seen in different tumors. Given the known genetic heterogeneity of cancers, this is not at all surprising and doesn’t necessarily mean that aneuploidy is the primary cause of cancer. For example, the Philadelphia chromosome, the result of a reciprocal translocation, an exchange of genetic material, between chromosomes 9 and 22. It is very common, virtually pathognomonic for chronic myelogenous leukemia. This is associated with the excessive production of an oncogene (Bcr-Abl), which activates cell cycle genes and induces genomic instability. Certainly, there must be some sort of aspect to the structure of these two chromosomes that make this particular translocation as common as it is, but the end result that drives CML is a mutation that results in the excessive production of an oncogene. Indeed, molecularly targeting this oncogene has resulted in a very effective drug against CML called Gleevec. In fact, targeting single gene abnormalities, although it hasn’t resulted in a cure for cancer, has resulted in several very effective treatments, such as Herceptin, which is directed against the Her-2/neu oncogene. Finally, lots of single gene mutations in transcription factors, DNA repair enzymes, or cell signaling molecules can alter the expression of dozens or hundreds of downstream (or even thousands) of genes in predictable ways. Large scale chromosomal breaks are not necessary to account for such globally deranged gene expression.

Duesberg next argues that “gratuitous traits do not contribute to cancer survival,” referring specifically to genes for metastasis and drug resistance, oddly enough. The problem with this argument is that a subset of the genes for carcinogenesis are not infrequently also genes involved in metastasis. Similarly, genes involved in drug resistance often have other functions than just drug resistance. For example, the mdr1 multidrug resistance gene product is an ATP-dependent channel that extrudes a variety of substances, not just chemotherapeutic agents, from a cell, an excellent example of how evolution can coopt the function of an existing protein to do another function. Finally, Duesberg appeals to the ability of cancer cells to change their phenotype rapidly, supposedly much faster than genes can mutate. This may indeed be true, and it may indeed be possible that aneuploidy contributes to this, given its ability to cause wholesale rearrangements of chromosomes and hundreds (or even thousands) of genes in one fell swoop. However, all it takes is selection by drug for tumor cells that express ever-increasing amounts of mdr1; chromosomal rearrangements, although they certainly may contribute to drug resistance, do not appear to be strictly necessary for it. Moreover, once again, Duesberg cannot resist overselling his case:

Once this vicious cycle is under way, the fact that every cell would be randomly generating its own new phenotypes could explain an observation made decades ago by Leslie Foulds of the Royal Cancer Hospital in London that “no two tumors are exactly alike … even when they originate from the same tissue … and have been induced experimentally in the same way.” Such individuality is yet another hallmark of cancer that cannot be explained by the activity or inactivity of specific genes, which would be expected to have consistent effects each time and in each cell.

The problem with this argument is that it’s only partially correct. Using the “gene chip,” which now allows scientists to assay the levels of every gene in the human genome at the same time, we now know that tumors often have a surprisingly similar pattern of expression of thousands of genes. Indeed, one of the most startling findings early in the use of such gene chips was that nearly all breast cancer could be divided on the basis of gene chip experiments into a small number of distinct subtypes, the main ones of which include the “basal” (more aggressive) or “luminal” (less aggressive) phenotype. Moreover, the expression of the Her-2/neu oncogene leads to a distinct, identifiable, reproducible gene expression pattern, in direct contradiction to Duesberg’s claims above. Indeed, tests based on such gene chips are already making their way into the clinic to estimate a patient’s risk of recurrence and guide chemotherapy decisions.

Lest one think that I’m hostile to Duesberg’s hypothesis, let me disabuse you of the notion right now. Although I think Duesberg’s an utter crank and pseudoscientist when it comes to his HIV/AIDS denialism, I find some of his work in cancer intriguing, and I disagree with Mark and Larry that it was such a horrible thing to feature him in an article in Scientific American, especially given the disclaimer. It is clear to me that epigenetics (cellular factors other than genes that regulate gene activity) and chromosome structure are very important in carcinogenesis, more so than had been appreciated before. However, contrary to how Duesberg’s sycophants like to portray the chromosomal hypothesis of cancer as an epic battle that’s all about Duesberg, who is portrayed as the lone voice arguing for the hypothesis that aneuploidy is the cause of cancer, in reality it’s nothing more than yet another scientific controversy that is, fortunately, no more nasty than a lot of other controversies in science, such as, for example, the hypothesis that changes in cell metabolism are the cause of, not a consequence of, carcinogenesis. It’s also nowhere near as clear as Duesberg claims whether aneuploidy is a cause or a consequence of carcinogenesis. For one thing, there are at least two examples that I’m aware of (which means there are probably more than that) of groups generating tumor cells that do not have significant or widespread aneuploidy, demonstrating that aneuploidy may not be a prerequisite for carcinogenesis, in direct conflict with Duesberg’s hypothesis. In addition, there’s a very interesting article from Don Cleveland’s lab in the January Cancer Cell that suggests that aneuploidy can promote carcinogenesis under some circumstances (an observation that seems supportive of Duesberg’s hypothesis) and act as a tumor suppressor under others (an observation that is arguably not).

What really irks me about Duesberg with respect to his ideas about cancer is that he may be on to something, but he can’t seem to stop himself from the same black-and-white, either-or thinking that apparently led him down the road of HIV crankery, nor can he seem to resist massively overselling his hypothesis as the be-all and end-all hypothesis to explain cancer initiation and progression. As I said at the beginning of my post, whenever someone postulates theirs as The One True Cause of Cancer, my skeptical antennae start twitching, and Duesberg’s aneuploidy hypothesis is no exception. Cancer is a complex and resourceful foe, not to mention that it’s hundreds of different diseases, not a single disease. Duesberg neglects a variety of other new hypotheses for causes of carcinogenesis that hold equal or greater promise than the chromosomal chaos hypothesis. Among these are cancer stem cells, tumor angiogenesis, and the aforementioned metabolic hypothesis of cancer (a.k.a. the Warburg effect). He even neglects what I consider to be a far more fascinating and sophisticated version of the chromosomal hypothesis, specifically Tom Misteli’s concept that derangements in the higher order three dimensional structure of chromosome territories can lead to cancer by alterations in gene expression.

Duesberg’s supporters may look at the relative neglect of chromosomal structure as a controller of gene expression and a potential cause of cancer and wonder why it was neglected for so long. The analogy I like to make is to politics. It is said that politics is the art of the possible. To me, science is the study of what it is possible to study. Two to three decades ago, we figured out how to study individual genes; so that’s what we studied, even though we soon realized that such reductionist techniques did not give the complete picture of cancer. Less than 10 years ago, gene chips, coupled with improvements in statistical analysis and increases in computing power that made it possible to analyze the data produced from such huge experiments, allowed us to look at the expression of the entire genome at once, leading to a richer understanding of the changes in gene expression that occur during cancer. The more sophisticated techniques and understanding did not invalidate what we had learned before; it complemented and extended it. Similarly, we now have the tools to probe chromatin structure at a level of detail never before possible; consequently we are now looking at chromatin structure in cancer. Our increasing ability to probe the detailed structure of chromosomes will likely now complement and extend what we have learned about cancer through the study of mutations in individual genes. Walter Giaretti asks:

…I would like to pose the question if the “aneuploidy theory” of cancer in relationship with the “mutation theory” still remains as controversial as in the near past. Don’t we have now enough experimental evidence that cancer originates and progresses with the contribution of both gene mutations and aneuploidy?

Duesberg’s failure is that he doesn’t seem willing to accept that the answer to this question is almost certainly “yes.” As Giaretti puts it:

It is likely that new studies directly comparing DNA copy number and gene expression will be performed in the near future on the role of aneuploidy in cancer, on what genetic events may induce chromosomal instability and on the validation of novel criteria for early diagnosis. It is predictable that these studies will vanish the conflicting views that either aneuploidy or gene mutations are a unique cause of the origin and progression of cancer negating the role of the alternative mechanism. Today, these conflicting interpretations are increasingly being abandoned to let a more complex mixed paradigm take over from previous concepts. In brief, ideas stemming from the old Boveri theory and from the modern theories may soon be seen as cooperative and equally important to cancer.

There are indeed deficiencies in our current understanding of cancer initiation and progression, but there’s no reason that gene mutations and aneuploidy couldn’t both contribute to these processes. Indeed, I’d be surprised if it were otherwise. Duesberg seems too dogmatic and wedded to his hypothesis to see the big picture.

(TrackBack URL for this entry: http://scienceblogs.com/mt/pings/38968)
* Ky Sanderson on Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly
* Kristjan Wager on Wiley & Sons: When “fair use” equals “no use”
* Mustafa Mond, FCD on “Woo-omics” at NCCAM
* Dale on Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly
* TheProbe on Wiley & Sons: When “fair use” equals “no use”
* Ky Sanderson on Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly
* Orac on Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly
* Adele on Peter Duesberg, chromosomal chaos, and cancer: An intriguing hypothesis argued poorly
* ordinarygirl on Ever wonder what happened to Roger Ebert?
* Luna_the_cat on Who perpetrated the “Holohoax”? Tell us!

Comments

Just how central is Duesberg to the latest research in aneuploidy and cancer. I read Bialy whining somewhere that Duesberg was not cited in a recent review of aneuploidy and cancer. I get the impression that Duesberg (or at least Bialy) is overselling his role. Certainly Duesberg’s sycophants seem to believe that Duesberg is the centre of the world.

The one thing that Duesberg is doing that others aren’t is taking an extreme position.

Posted by: Chris Noble | April 25, 2007 10:43 AM

Gene mutations, aneuploidy, epigenetic processes, tumor environment and anything else that alters gene expression. Duesberg is far too dogmatic.

The cynic in me thinks that flogging Duesberg’s role in popularizing interest in the role of aneuploidy in cancer may just be a way of drumming up business for this company that he, Bialy and Rasnick are associated with that is marketing or attempting to market this Anucyte cancer detection system? http://www.primenewswire.com/newsroom/news.html?d=112649

Posted by: Dale | April 25, 2007 11:10 AM

Isn’t Down syndrome due to a non-disjunction event in the second meiotic division, not mitosis? In that sense, it’s different than aneuploid cancer lineages which arise due to mitotic non-disjunction.

I may have missed this, but is the main chromosomal abnormality in Duesberg’s article aneuploidy? What about other aberrations (fusions, translocations, inversions, duplications, deletions, etc)? Aren’t there a lot of cancers associated with chromosomal defects other than aneuploidy?

Posted by: RPM | April 25, 2007 12:50 PM

Retinoblastoma.

Posted by: mark | April 25, 2007 01:16 PM

Not to be too cryptic, but as far as kids not getting cancer? Nope.

As far as chromosomal defects yes. In particular, it’s not the aneuploidy of a huge number of translocations seen in leukemias and lymphomas but the creation of fusion genes and inappropriately expressed genes from the transformation (a promiscuous promoter driving an oncogene for instance) that results in specific types of cancer.

Orac is right. Duesberg is being to simplistic and rigid.

Posted by: mark | April 25, 2007 01:22 PM

Acute promyelocytic leukemia.

The majority of cases of acute myelogenous leukemia.

Posted by: Abel Pharmboy | April 25, 2007 01:34 PM

sn’t Down syndrome due to a non-disjunction event in the second meiotic division, not mitosis? In that sense, it’s different than aneuploid cancer lineages which arise due to mitotic non-disjunction.

Fixed.

In these epic posts, the occasional screwup does occur. Mea culpa. It’s kind of like the scene in Animal House:

Bluto: Over? Did you say “over”? Nothing is over until we decide it is! Was it over when the Germans bombed Pearl Harbor? Hell no!

Otter: Germans?

Boon: Forget it, he’s on a roll.

I was on a roll.

Posted by: Orac | April 25, 2007 01:47 PM

Orac,

Thanks for a typically smart and insightful criticism of Duesberg’s article, not to mention an admirably reasonable reaction to the fact of Duesberg’s authorship.

At the risk of seeming unappreciative: Scientific American’s lawyers do usually frown on the use of its graphics without permission–strictly speaking, it isn’t a violation of our rights so much as it is of the artist’s. I don’t think she’d mind in this case, but can I offer a shout of appreciation to the terrific Jen Christiansen, who drew that illustration?

Posted by: John Rennie | April 25, 2007 03:18 PM

Finally got to read the whole thing, it was a bit epic.

I agree with you, this almost seems to be a presage to even more crankery from Duesberg. I can just see that as time goes on and this hypothesis is balanced out by other findings that show every cancer can’t simply be housed under the umbrella of aneuploidy if he’ll once again just dig in and refuse to accept evolving facts. When Duesberg suggested that HIV causing AIDS was based on mostly correlative evidence in 1987 (and Science published it), he kind of had a point. It wasn’t a particularly good, or useful point, but within the year there was excellent evidence from studies of AZT, as well as responses to Duesberg’s criticisms that really should have had those ideas tossed, and certainly by about 1993 or so the science was settled. These days given what we know about the HIV proteins, mechanisms of latency and entry in CD4 cells, it’s frankly just embarrassing he didn’t give up decades ago, I wonder if he’ll do the same here if things don’t turn out his way.

I will continue to disagree, however, that this wasn’t a mistake for Sci Am. I believe in the scientific death sentence – that is, if you are proven untrustworthy, you shouldn’t be allowed to contribute to the literature anymore. So what if he’s changed fields, he demonstrated himself to be a dishonest crank so badly and for so long why should we risk the literature with contributions from this guy? I don’t find his so-called dissident status cute or funny, it results in bad science, bad policy and ultimately death as these bizarre ideas take hold in Africa (especially S. Africa) and even in the United States as with the HARM people. I’m all for the black list for cranks too because I believe cranks are fundamentally deceptive and untrustworthy contributors to scientific debate, and all of his subsequent (thankfully rejected) internet publications on HIV/AIDS are really just a pack of lies.

I simply wouldn’t trust this guy again, ever.

Posted by: Mark | April 25, 2007 03:50 PM

John Rennie,

I salute you, Sir, for publishing the article by Dr. Peter Duesberg on aneuploidy and cancer. His hypothesis is clearly testable: produce a diploid tumor, somewhere, somehow.

I disagree, though, that Orac’s criticism is “smart” or “insightful.” Rather, it is a mess. It could never be published anywhere — he intersperses irrelevant issues (Egnor and creationism), spends half the time talking about Duesberg and his supporters, carping on strawman HIV issues, and in typical verbose fashion misses the import of the issue.

Cancer kills over 500,000 Americans each year. Most families have lost a loved one to cancer. Aside from the success in lung cancer (smoking reduction) and some leukemias (a few new drugs), cancer prevalence rates haven’t budged since the 1950s.

So, what clinical benefits or societal benefits has the “oncogene” theory of cancer produced in nearly 40 years? I submit –zero.

That’s why the Duesberg article is important — old wine in a new bottle as Nature Biotechnology once wrote.

Let’s not lose sight of the objective — to cure cancer. To cure something, one has to properly determine its cause. Since aneuploidy, apparently, is found in every solid tumor, it certainly must be explained — not explained away as Orac in typical smarmy fashion seeks to do.

Posted by: Ky Sanderson | April 25, 2007 04:10 PM

Sanderson, you nut-job, why not read what Orac wrote before you piss on it? Then you would know that Orac doesn’t explain away aneuploidy at all. He actually supports Duesberg on this one.
You might also learn something about cancer. Like about Herceptin and Gleevec, drugs that wouldn’t work at all if there weren’t some truth to the oncogene hypothesis.
Why don’t you go and hang out with your three denialist friends. Maybe you can teach each other how to read.

Posted by: Adele | April 25, 2007 04:43 PM

In my opinion, what has driven interest in the role of genomic instability and aneuploidy in cancer isn’t Duesberg but the technological advances of the early 90s (like fluorescent in situ hybridization) that have enabled investigators to examine ploidy in tumors in far more detail than was possible prior to the 90s. Also my opinion – aneuploidy and mutations both contribute to cancer but aneuploidy is more obvious in tumors than mutations are because it’s easier to detect.

Posted by: Dale | April 25, 2007 05:10 PM

I’m not sure what the fine print of the “fair use” law says, but I really feel that Orac is ripping SciAm off a bit here. From my vantage point, I’d fully support a recommendation from SciAm that Orac remove the pictures in this blog. They go beyond fair use, unless Orac’s post was along the lines of “SciAm used artwork which gives a misleading impression…” (that is, the pictures were a cornerstone of the point Orac was making).

I think that a more appropriate treatement from Orac would be a summary of the article with perhaps a selected quote or two, and a comment along the lines of “the ideas are very elegantly presented in artwork accompanying the SciAm article” (with a link to the paid-for article).

Posted by: Kevin | April 25, 2007 05:16 PM

Sadly typical of Duesberg. Can’t accept that the concept isn’t exactly novel, can’t accept that other theories have validity, can’t accept supporting role instead of leading man.

Posted by: Robster, FCD | April 25, 2007 06:06 PM

Dear Dr.

For a different view of cancer, you might want to see the article shown on the cover of The American Journal of Pathology in this month’s MAY issue. (http://ajp.amjpathol.org/) (Tone Sandal, Klara Valyi-Nagy, Virginia A. Spencer, Robert Folberg, Mina J. Bissell, and Andrew J. Maniotis.

Epigenetic Reversion of Breast Carcinoma Phenotype Is Accompanied by Changes in DNA Sequestration as Measured by AluI Restriction Enzyme. Am J Pathol 2007 170: 1739-1749.) I’ll send you the entire PDF if you send me an address where I can email it.

I read your assessment of Peter’s SCi Am. article on aneuploidy, and agree with you about the excitement regarding the renaissance of global changes in higher order structure, and cancer, that similar to aneuploidy, involve entire genomic structural changes. You might want to look at what others as well as I have written regarding this issue of “mechanogenomics,” as I called it.

Stein GS.Am J Pathol. Mechanogenomic control of DNA exposure and sequestration. 2005 Apr;166(4):959-62.

Maniotis AJ, Valyi-Nagy K, Karavitis J, Moses J, Boddipali V, Wang Y, Nuñez R, Setty S, Arbieva Z, Bissell MJ, and Folberg R: Chromatin organization measured by Alu I restriction enzyme changes with malignancy and is regulated by the extracellular matrix and the cytoskeleton. Am J Pathol 166: No. 4 April 2005.

Folberg R, Arbieva Z, Moses J, Hayee A, Sandal T, Kadkol S, Lin AY, Valyi-Nagy K, Setty S, Leach L, Chevez-Barrios P, Larsen P, Majumdar D, Pe’er J, Maniotis AJ.
Tumor cell plasticity in uveal melanoma: microenvironment directed dampening of the invasive and metastatic genotype and phenotype accompanies the generation of vasculogenic mimicry patterns. Am J Pathol. Oct;169(4):1376-89, 2006.

Valyi-Nagy K., Folberg R., Valyi-Nagy T. Andrew Maniotis. Role of tumor invasiveness, the extracellular matrix, and chromatin sequestration in the susceptibility of uveal melanoma to herpes simplex virus type 1. Experimental Eye Research 84 (2007) 991-1000.

Mechnogenomic control of DNA exposure and sequestration.

Drawings from 100 years ago of Galeoti’s, Hertwig’s, and Hanseman’s comparisons of cancer cell and normal cell chromosomes illustrated gross differences in chromatin structure and chromosome numbers in human tissue harboring a tumor (1). But how higher order chromatin structure is controlled and maintained by the cancer cell and its microenvironment has remained beyond our reach. The work presented by Maniotis et al. in this issue presents new data that shows there are striking differences in restriction enzyme sensitivity between tumor cell and normal cell genomes. The work shows in addition, that these differences depend upon chromatin-associated proteins rich in disulfide bonds, specific molecules present in the extracellular matrix (ECM) environment, and the cytoskeleton, whose organization permits or impedes sequestration and exposure of specific sites along DNA. The work advances the idea that the mechanical contiguity of these components may work in concert to form a cytoarchitectural resistance mechanism that may constitute a basis for a paradigm shift in both the contexts of normal cellular physiology, and in cancer.

It had been established by a previous generation of tumor biologists using DNase digestions and nick-end labeling techniques, that in order for a gene to become expressed, it had to be “exposed.” Moreover, Puck et al., (2) had shown that transformed tumor cells that were “reverse transformed” to a normal phenotype with various chemical compounds exhibited a shift in their nuclei’s sensitivity to DNAase I, and also exhibited changes in cell shape and cytoskeletal organization.

Maniotis et al. in this issue show data that compared the extent of exposure or sequestration of a well-characterized collection of highly invasive, poorly invasive, and normal human cell genomes to specific restriction enzymes. Restriction enzyme digests on intact genomes untreated with other chemical agents showed that Alu I and Msp I both could distinguish normal cells from tumor cells of different degrees of invasiveness. Highly invasive cell nuclei always resisted digestion with these enzymes compared to poorly invasive or normal cells. Also, through comparisons of mitotic chromosomes microsurgically extracted as complete genomes (3,4), with interphase nuclei from the same cell types, differences in chromatin digestibility were shown to be independent of the cell cycle, and localized to chromosomes, without the possibility of enzyme access contributing to the differential digestive effects observed in different cell types. The different relative sensitivities of chromatin or chromosomes to restriction enzymes was also demonstrated to be independent of ploidy, but sensitive to oncogene insertions on the same genetic background. Moreover, the differences in chromatin and chromosome stability in comparisons of highly invasive, poorly invasive, and normal cells was also found to involve proteins rich in disulfide bonds. This phenomenon was demonstrated by adding DTT or ß-mercaptoethanol to the digestion reactions and rendering the highly invasive cell genomes sensitive to Alu I.

In the second part of the work, a systematic search was initiated to test if growth factors, or soluble and polymerized ECM molecules also induce cells to alter their sequestration or exposure of DNA, and to test if there was any specificity to the influence of different ECM molecule types on Alu site exposure or sequestration. These experiments showed that soluble laminin and RGD-C were both capable of rapidly and profoundly causing all cell types that were tested to sequester their DNA from the digestive effects of Alu I. However, sequestration induced by these ECM molecules was always more intense among increasing grades of cellular invasiveness. Serum, fibronectin, bFGF, EGF, and type I collagen exerted no effect on the seqestration of Alu I sensitive sites. The same results were obtained with polymerized extracellular matrix conditions. In addition, when polymerized ECM preparations were prepared such that ECM molecules were deposited in specific regions of a surface, the contrast in chromatin sensitivity could be easily observed between cells touching the extracellular matrix compared to the same cells that did not touch ECM deposits.

These studies suggest several novel biological concepts: through comparisons of the sensitivities of chromosomes derived from a chromatin extraction method that preserves the native structure of chromatin with digestion of specific Alu I and Msp I sites with digestions of interphase cells of the same type that are exposed or not exposed to defined matrices, a more accurate picture is provided as to how global chromatin structure exists and is controlled under physiological ion conditions, and how the organization, mechanics, and function of different types of genomes are linked to DNA sequestration, and exposure, and how these processes might occur at the level of tissue.

These findings have special relevance in tumor biology. It is now known that laminin is a principal component of extravascular matrix-rich vasculogenic mimicry patterns, or fluid-conducting meshworks that conduct plasma within tumors that probably arises from leaky vessels disturbed by invasive tumor cells (5-11), and whose presence designates how patients harboring melanomas and other tumors will progress (see Ref. 12). The fact that laminin and RGD-C sequester the Alu sites in both normal and tumor cells in only 30 minutes is remarkable because it suggests that specific ECM moieties present in the environments of malignant tumors can rapidly and profoundly induce a complete reorganization of the higher order structure of the genome to sequester Alu sites. However, these observations also suggest that perfusion itself, by whatever route (eg. tumor angiogenesis, vasculogenic mimicry, vessel cooption, etc.) may be a small part of the story regarding how factors get into cells of highly invasive tumors. These data would suggest that the highly invasive cells themselves, owing to their abnormal organizational characteristics, may be the principal directors for both nutrient access, and many of the nucleic acid-disrupting drugs used in cancer chemotherapy.

Furthermore, it is clear that conceptual frameworks advanced to explain how prokaryotic genomes are controlled cannot explain how the regulatory machinery controlling higher order chromatin structure coordinates large regions of the eukaryotic genome along with its batteries of hundreds, or perhaps thousands of genes and gene networks. For instance, it has been established that even among single cell eukaryotes such as yeast, the majority (>95%) of single-gene mutations in yeast affect not only the expression of the mutant gene, but also the expression of many other genes (13).

In multicellular organisms, in addition, the cytoskeleton and extracellular matrix (ECM) are known to play a fundamental role in determining cellular behaviors. To test if different cytoskeletal fiber systems influenced the sequestration or exposed the Alu I sites, a variety of cytoskeleton-disrupting drugs were then employed to determine if the higher order structure of chromatin was controlled by actin, microtubules, or intermediate filaments. It had been previously established that a tug to an integrin receptor could alter the molecular alignment of intranuclear molecules in 1 second, and each cytoskeletal system had been shown to exert different stabilizing effects on both nuclear structure, and force transduction (14). The results of these experiments showed that indeed, as with the force-transduction experiments on integrin receptors, each cytoskeletal fiber system contributed profoundly to the sequestration or exposure effect, such that actin disruption decreased sequestration, while microtubule or intermediate filament disruption increased sequestration.

These findings raise and experimentally address new questions regarding the fundamental way genetic information is controlled by proteins containing disulfide-rich bonds, by the extracellular matrix microenvironment, and by the cytoskeleton. The work also has contributed several new approaches that can be used as diagnostic tools that use the differences in the sensitivities of DNA to distinguish differing degrees of malignancy that do not depend on molecular markers which have been shown to be highly variable in the context of vasculogenic mimicry, and which manifests as molecular mimicry in tissue sections of the most invasive types of tumors (5,15,16). These factors working separately, or in concert, may have relevance to the “resistance” of malignant cells, and have implications regarding how drug resistance of the most malignant types of tumor cells may be induced by the presence of specific types of extracellular matrix moieties. It appears the architecture of cytoplasm and nuclei themselves, induced by the extracellular matrix, dictates how DNA is sequestered or exposed. Models of higher order chromatin structure and gene control in higher eukaryotic cells must be considered contextual and hierarchical with respect to the ECM environment and the cytoskeleton (17). In this context, and as suggested by the authors, tensional integrity (tensegrity) may be a useful conceptual framework to account for how molecules can function collectively as components of integrated, hierarchical systems, in the physical context of living cells and tissues (18).

References
1. Wilson EB. The Cell in Development and Inheritance. Pathological mitosis in cancer cells, pps. 68,69. Reprinted from the New York Edition of 1896. The sources of Science # 30, Johnson Reprint Corporation, New York and London, 1966.

2. Puck TT, Krystosek A, Chan DC. Genome regulation in mammalian cells. Somat Cell Mol Genet 1990 16: 257-265.

3. Maniotis, A., Bojanowski, K., Ingber, D. Mechanical continuity and reversible chromosome disassembly within intact genomes removed from living cells. J. Cellular Biochem. Vol 65: 114-130, 1997.
4. Bojanowski, K., Maniotis, A., Ingber, D. DNA toposiomerase ll can control chromatin topology and drive chromosome condensation without enzymatically modifying DNA. J. Cellular Biochem. Vol. 69:127-142, 1998.
5. Maniotis A., Folberg R., Hess A., Seftor E., Gardner L., Pe’er J., Trent J., Meltzer P., Hendrix M. Vascular channel formation by human uveal melanoma cells in vivo and in vitro: Vasculogenic mimicry. Amer. J. Path. Vol. I55, No 3, pps. 739-752, September,1999.

6. Andrew Maniotis, Xue Chen, Christopher Garcia, Phillip J. DeChristopher, Ding Wu, Jacob Pe’er, Robert Folberg. Control of Melanoma Morphogenesis Endothelial Survival, and Perfusion By Extracellular Matrix. Lab Investigation. Vol. 82 No. 8 p.1083-1092, 2002.

7. Shirakawa K, Tsuda H, Heike Y, Kato K, Asada R, Inomata M, Sasaki H, Kasumi F, Yoshimoto M, Iwanaga T, Konishi F, Terada M, and Wakasugi H. Absence of Endothelial Cells, Central Necrosis, and Fibrosis Are Associated with Aggressive Inflammatory Breast Cancer. Cancer Research 61, 445-451, January 15, 2001.

8. Shirakawa K, Kobayashi H, Heike Y, Kawamoto S, Brechbiel M, Kasumi F, Iwanaga T, Konishi F, Terada M, Wakasugi H. Hemodynamics in Vasculogenic Mimicry and Angiogenesis of Inflammatory Breast Cancer Xenograft. Cancer Research 62, 560-
566, January 15, 2002.

9. Kobayashi H, Shirakawa K, Kawamoto S, Saga T, Sato N, Hiraga A, Watanabe I, Heike Y, Togashi K, Konishi J, Brechbiel MW, Wakasugi H. Rapid accumulation and internalization of radiolabeled herceptin in an inflammatory breast cancer xenograft with vasculogenic mimicry predicted by the contrast-enhanced dynamic MRI with the macromolecular contrast agent G6-(1B4M-Gd)(256). Cancer Res. 2002 Feb 1;62(3):860-6.

10. Shirakawa K, Kobayashi H, Sobajima J, Hashimoto D, Shimizu A, Wakasugi H. Inflammatory breast cancer: vasculogenic mimicry and its hemodynamics of an inflammatory breast cancer xenograft model. Breast Cancer Res. 2003;5(3):136-9. Mar 06, 2003.

11. Clarijs R. Otte-Holler I, Ruiter, de Waal MW. Presence of a fluid-conduting meshwork in xenografted cutaneous and primary human uveal melanoma. Investigative Ophthalmology and Visual Science: Vol. 43 No 4 2002.

12. Folberg R, Maniotis AJ. Vasculogenic mimicry. Acta Pathologica, Microbiologica, et Immunologica, Scandinavica. Jul;112 (7-8):508-525,. 2004.

13. Featherstone DE, Broadie K. Wrestling with pleiotropy: genomic and topological analysis of the yeast gene expression network. Bioessays. Mar;24(3):267-74, 2002.
14. Maniotis, A., Chen, C., Ingber, D. Demonstration of mechanical interconnections between integrins, cytoskeletal filaments, and nuclear scaffolds that stabilize nuclear structure. Proc. Nat. Acad. Sci . Vol. 94 pp.849-854, 1997.

15. Chen X, Maniotis AJ, Majumdar D, Pe’er J, Folberg R: Uveal melanoma cell staining for CD34 and the assessment of tumor vascularity. Invest Ophthalmol Vis Sci. Aug; 43(8): 2533-9. 2002.

16. Seftor EA, Meltzer PS, Kirschmann DA, Pe’er J, Maniotis AJ, Trent JM, Folberg R, Hendrix MJ. Molecular determinants of human uveal melanoma invasion and m
metastasis. Clin Exp Metastasis. 2002;19(3):233-46.

17. Roskelley CD, Srebrow A, and Bissell MJ: A hierarchy of ECM-mediated signaling regulates tissue-specific gene expression. Curr Opin Cell Biol 7: 736-747, 1995.

18. Ingber DE. The Architecture of Life. Scientific American, January, pp 48-57, 1998: see also Ingber DE. Tensegrity II. How structural networks influence cellular information processing networks. Journal of Cell Science 116, 1397-1408, 2003.

Posted by: Andrew Maniotis | April 26, 2007 05:22 AM

Trying to blow your own trumpet again, Andrew? Perhaps more people might read what you write if you presented it in smaller digestible chunks, and more might listen to what you have to say if you dropped the dogmatic and anti-scientific approach that you share with Duesberg in refusing to be open to alternative hypotheses and willing to accept when you have been shown to be wrong (as you both have in relation to your AIDS denial).

Posted by: DT | April 26, 2007 09:53 AM

Wow, Dr. Maniotis, nice work! I just have to wonder how you justify your work with “Alu I”. Because I personally don’t believe it exists.

Do you have electron micrographs of Alu I in the act, cutting DNA? Have you confirmed this with crystal structures? Are your Alu I preps 100% pure? Are you sure the DNA isn’t just being cut by endogenous restriction enzymes activated by oxidative stress when you add your inevitably impure “Alu I”? Did you check the redox environment of the cells? Isn’t it possible that the DNA in cancer cells is more sensitive to “Alu I” digestion because of their different redox state?
Another thing I notice is you use the T4-2 breast cancer cell line. You know better than anyone, “to culture is to alter.” So what’s the relevance? Why didn’t you do this work in situ in patients? Cancer has been around forever, and there’s still no work on Alu I sensitivity directly in patients? Unbelievable.

Obviously, AluI doesn’t exist. And now I’m not even sure about cancer.

Posted by: Adele | April 26, 2007 10:57 AM

Methinks Dr. Maniotis would like me to blog his latest article. A little bit excessively self-promoting, but what the heck? I might even be willing to oblige him as long as it’s not a Wiley & Sons publisher, where I might have to worry about being sued if I were to do a selective quotation or two or appropriate a smaller version of one of his figures for “fair use.” I’m always happy to talk science, as opposed to pseudoscience like HIV/AIDS denialism, and I’m equally happy that Dr. Maniotis refrained from mentioning his views on HIV/AIDS, given that he is a signatory to a letter by the Perth Group stating that HIV doesn’t cause AIDS.

As long as we stick to cancer, I don’t see why we couldn’t have a fruitful discussion, and I don’t see why I couldn’t have a fruitful discussion even with Duesberg himself. For one thing, I’d be interested in knowing Dr. Maniotis’ thoughts on Dr. Duesberg’s arguments, as presented in the SciAm article and a couple of recent scientific reviews, particularly bad arguments such as “babies don’t get cancer.”

Posted by: Orac | April 26, 2007 11:57 AM

I would like to see a fruitful discussion on cancer between Orac and Dr. Maniotis. However, could you shorten it a bit? Not every scientific argument has to be “War and Peace”

Posted by: Ky Sanderson | April 26, 2007 12:14 PM

Adele, As you are no doubt aware there are still ethical questions about the circumstances under which Watson and Crick obtained Rosalind Franklin’s crystallographic data of DNA structure. I think to be on the safe side you should add DNA to your list of things whose existence must be questioned.

Posted by: Dale | April 26, 2007 12:33 PM

Orac:

You state that would like to address “particularly bad arguments such as “babies don’t get cancer.” But, Dr. Duesberg didn’t write that and you know it.

He wrote:

Lamentably common, cancer afflicts about one in three people at some point in their lives, but mostly after the age of 50, which is when chances for malignancy soar. Thus, cancer is, by and large, a disease of old age.

How can anyone dispute this? He then wrote:

But colon cancer is never seen in children., which you deliberately misinterpreted this narrow quote to include cancer in general.

So, back to the properly framed issue:

If you can produce babies with colon cancer, then your point is well-taken and Dr. Duesberg is in error. If not, then your point is not well-taken, and you are in error.

Here’s a paper from the NCI on colon cancer.

It’s pretty good, but doesn’t mention any babies getting colon cancer, so it doesn’t quite answer the question.

Here’s a SEER Fact Sheet, also from the NCI. It states:

From 2000-2004, the median age at diagnosis for cancer of the colon and rectum was 71 years of age. Approximately 0.0% were diagnosed under age 20.

So, according to these authorities, Duesberg is right: babies don’t get colon cancer. At least from 2000 – 2004. Do you have any comment on these facts?

Posted by: Ky Sanderson | April 26, 2007 01:29 PM

Duesberg’s elegant reply

April 22nd, 2007

delaneyp.jpgThe drug company financed activist and HIV enthusiast Martin Delaney of Project Inform has seen fit to write a little diatribe against the distnguished scientist Peter Duesberg, as we noted a couple of posts earlier.

This piece of confused literature has been posted by his distinguished colleague, Cornell researcher and HIV∫AIDS streetfighter John P. Moore, Goon show character manque and now chief poster of accusations of homophobia on Moore’s website AIDSTruth.org, under the title “Peter Duesberg and homophobia”.

As we pointed out earlier, these words together in the one title form a self-contradictory phrase, since homophobia and Duesberg are as far apart as a sewer and the Golden Gate bridge, or a tin of Athlete’s Foot powder and a $4000 pair of crocodile Manolo Blahnik stillettos.

The heading is oxymoronic since Duesberg’s whole effort in correcting bad science serves to save the lives of any of the gay lemmings that Delaney is leading over the precipice in HIV∫AIDS who will listen to him.

Duesberg spears Delaney’s balloon

This is why Duesberg has now sent the following letter to Delaney, which says it all:

Dear Martin Delaney,

I understand from Harvey Bialy and Anthony Liversidge that you are sending out messages on websites that I am “homophobe”.

Assuming that you as a director or ex-director of “Project Inform” are interested in verifiable information, I invite you to come to my office here at Donner Lab at UCB and check my email correspondence for the huge, indeed very huge numbers of emails I have sent out responding to self-identified gay men asking me for information about HIV, DNA chain terminators and protease inhibitors currently prescribed as anti-HIV drugs.

Based on my information of the primary consequences of these drugs on the livelihood of human cells and organisms, I typically discourage gay men and others from using these drugs. In the light of the biochemical effects these drugs were designed for my advice is: These drugs are AIDS by prescription.

On the same grounds, I would, however, encourage people to take these drugs, if I really disliked or hated them.

So – if you practice freedom of information at Project Inform, you may end up offering me a part time job after reviewing my email files.

Let me know when you come over.

Sincerely,

Peter D.

Peter Duesberg
Dept. Mol. & Cell Biol.
Stanley Hall
UC Berkeley
BERKELEY CA 94720

Touche, as they say in educated circles. Not much left for Delaney or Moore to say, unless they want to try bleating “But HIV causes AIDS” for the umpteenth time. We advise Moore not to bother, since we have discovered the paper he wrote recently showing that it doesn’t and can’t from about six points of view, which we shall post shortly.

Project Misinform, AIDS Truthiness

Why did Moore display Delaney’s delusional diatribe so prominently? Why all the accusations of homophobia on his site recently?

Presumably this editorial placement, along with other accusations of homophobia directed at prominent HIV∫AIDS critics, including this obscure blogger, is for lack of anything more substantial to deflect the scientifically based bunker busters of paradigm criticism directed against him by the AIDS “denialists”, his name for those who believe it is more important to review the lack of substance and success of the basic assumptions of HIV∫AIDS than it is for him to get more funding for his microbicide research at Cornell painting the undersides of macaques, which sadly has been severely called into question by a recent study that suggested microbicides actually enhanced the transmission of HIV.

From the point of view of anybody who cares about the lives and welfare of HIV∫AIDS patients of any sex or color it can only be said that there is as much useful information from Project Inform as there is truth at AIDSTruth, but what is most prominently missing from both is plain good sense.

How could a man – Martin Delaney – who is gay and presumably cares for his fellow gays – not already know how grateful so many gays are for the work of Peter Duesberg, without whom they never would have known of the sixty reasons not to believe that HIV causes AIDS, which John Moore has now confirmed, in the paper we are about to present for the delectation of all who appreciate hypocrisy, inner conflict and true “denial” at the highest level, that is, in the schizophrenic mind of Moore, a man whose assistance in making the HIV∫AIDS critics look good, and himself and his cronies bad, is beginning to look like the actions of a double agent, one who secretly agrees with the critics of HIV∫AIDS and because he is prevented by economics and politics from coming out and saying so in public -which would result in the instant loss of his position at Cornell – has to show it somehow.

This is why we urge “denialists” to go easy on John P. Moore, who may yet prove to be one of them. And indeed, a man who despite every financial pressure aids the cause of truth deserves the prize he will no doubt get in the end, possibly joining Robert Gallo (the first man to show that HIV does not cause AIDS) and Anthony Fauci (the first man to point out publicly that HIV is the best vaccine against AIDS, because it excites the production of more T cells rather than less) and Duesberg at Stockholm for defeating AIDS.

But since you cannot share a Nobel among more than three people, it may well be that he will share it with Gallo and Duesberg, so we urge him not to annoy Anthony Fauci any further by making a public nuisance of himself with silly and low level insults of his critics on the non scientific level, since Fauci will not be pleased when we reveal to the world why Moore’s claim to fame and favor with Stockholm deserves to take precedence over the director of the NIAID.

AIDS as Jonestown

April 22nd, 2007

The “dream became a nightmare”, as Jones’s crowd of followers was led over the cliff

From Jonestown and Virginia Tech to HIV∫AIDS, large groups can’t easily shed shared assumptions

Plenty of warning signs

jimjones.jpeg“White night! White night!’ That phrase, loudly announced on the loudspeakers accompanied by an air raid siren, was the signal for an emergency meeting at the remote jungle plantation of Jonestown, a call for the unfortunate Marxist socialist Utopian members of the People’s Temple to gather, sometimes all night, to discuss how to repel threats from outside to their paradise.

In the end the proposals included discussions of mass nurder-suicide. Drills were conducted for it. There were people with guns and rifles surrounding the assembly, an armed encampment, the guns pointing inside as well as out, says one inmate who survived.

“I was not free to leave, nor was anyone” says another. “He was punished so severely that he was literally frightened out of his mind,” says one survivor of another, who tried to escape but never did succeed. “I didn’t trust anyone. Everyone was watching everyone”.

Misled by a paranoid

Jim Jones’ rants are being replayed on the History Channel, which is carrying a program this weekend, Paradise Lost, revisiting the last days of Jonestown, Guyana in 1978 with testimony from a few who escaped the final mass suicide. From the perspective of any viewer now Jones’s speeches, taped or acted, are obviously those of a drug taking paranoid.

But once a crowd takes you as a guru, and are sufficiently oppressed and punished, this history reminds us, you can rant as insanely as you like and they will swallow it all whole. Perhaps the alternative is too hard for an individual to face – that you have followed a cheat and a madman. But it is also group pressure. “I really cared what the others would think of me, “says a defector.

It is also that the followers grasp at the straws offered them by the leader, who provides the rationale for reversing reality. “I have never understood how people could lie with such freedom and conviction”, Jones told NBC. Thus it was other people who lied, and not the guru, even to those that lived in the encampment and experienced it for themselves.

How easy the con game is

In the end Jones controlled 913 people so effectively that they took his Kool Aid laced with cyanide voluntarily, and even murdered their kids first. One or two people resisted and were forced, and a grandmother hid successfully under her bed, but when she crawled out the next day, there were bodies of the deluded lying still everywhere.

Congressman Ryan flew to Guiana with Don Harris from NBC and Tim Reiterman from the San Francisco Examiner, all of them supposedly sophisticated in politics and human behavior, but they did not realize till the very end they were in danger of their lives from a man whose mind behind his habitual dark glasses was murderously paranoid.

“We are under the protection of Congress,” reasoned the hapless Congressman, who ended up shot on the tarmac as he was trying to leave in his plane, his body joining four others including those of the newsmen.

The best thing ever

Earlier, Ryan had addressed the crowd soon after arrival and talking to Jones. According to the reenactment, he said with a reassuring smile that he could see there were people here “who thought this was the best thing that had ever happened to them in their whole lives.” He himself only wised up to the reality of the situation when leaving, when he was attacked with a knife by a Jones fanatic, whose blood spattered his shirt.

Stephen Jones’ son could see his father was a drug crazed nut case long before it all happened. “Anybody is capable of putting a bullet into your head”, his father informed him helpfully, as he left to play in a basketball tournament. His mother seemed to feel a disaster was in the offing. Some members had wanted to leave the community as soon as they arrived. Yet on the flimsiest of pretexts, Jones was able to led 913 people to their doom. Only a handful left with Ryan to the airport, 15 in all. They were shot by a truckload of Jones riflemen, who killed five and wounded others, some of whom escaped into the jungle.

Motivations of a leader

Of course, the motivation of Jones is all important here too. “Every hour of the day Jim Jones knew he was a fraud. he knew he was a bad guy. He just didn’t want anyone else to know about it,” says his son. The bottom line was that Jones didn’t want to die alone. He was afraid of exposure. He was afraid of being abandoned by his group of followers. He was nothing without them. He didn’t fancy taking the Kool-Aid himself, however. He had himself shot in the head.

To all who attend the topic of this blog, all this remind you of anybody? Seems to us all of these factors apply to Anthony Fauci, Robert Gallo and John Moore, except they are not ready to get shot just yet.

What Cho showed

If you read the Times today (Sun April 22) you will also find Benedict Carey’s discussion “When a Group is Wise”, in The Week In Review. His topic is Seung-Hui Cho, the Virgina Tech mass killer, and how the community that surrounded him noticed his strangeness and tried to establish communication. Cho’s teetering on the edge of insanity was obvious to many he encountered, and upset many of them enough to be discussed and/or action taken.

Carey seems to think all this should satisfy the concerns of those who worry that his potential as a killer was overlooked until too late. Yet surely the story of Cho only confirms how difficult it is for people to beak away from the basic feel good assumptions of the group they are in, which in this case was the university community and its ruling presumption that a paid up member is not nuts, however violent his writings and isolated his behavior. This assumption stubbornly resisted replacement in the face of all the warning signs, and nobody saw the possibility of another deluded mass killer, even though the police were brought in.

Can you say “inviolable illusion”?

Both these stories of disillusion seem to us to have great bearing on the story of HIV∫AIDS science so far, which as professional psychologists and theorists of the psyche like Caspar Schmidt, Mark Biernbaum and others have pointed out, is a story in which individual and mass delusion plays a large part, not only among patients and the general public but among the scientists who ignore the scientific literature and Peter Duesberg’s reviews, and insist on remaining loyal to their leaders even when their claims are unreasonable, illogical, flout common sense and established science, and even contradict the literature they themselves write and publish in scientific journals.

It seems pretty clear that Robert Gallo, Anthony Fauci, and John Moore could tell their community that the Virus was made of gorgonzola cheese and transmissible by anyone eating it who wiped their knife on the back of a dog owned by a Portuguese sailor with a wooden leg, and the claim would be treated as Biblical text worthy of being researched to the tune of $1 billion dollars a year.

The Jonestown of science

In fact, it is hard to see how the grotesque saga of Jonestown differs in any significant way from the tale of HIV∫AIDS now sweeping the world.

There is the same phenomenon of a leader or leaders peddling an impossible fairy tale, the same deluded followers willing to assume they know what they are talking about, the same crowd being punished and abused into a slavery of the mind, the same rewrite of this unhappy and dangerous treatment as kind and beneficial, the same Kool-Aid being administered to avoid exposure of what is really going on, the same penalties being visited upon defectors, the same ranting paranoia when faced with critics, the same goon squad ready to do violence on truthseekers.

Could it be that the spirit of Jim Jones somehow found its way into the souls of the leaders of HIV∫AIDS?

Surely not. HIV∫AIDS self destruction is simply the typical insanity of the crowd in all matters ideological, here harnessed by those who have turned a science into a religion where they are the self-serving gurus, no matter who is sacrificed to their ambition.

Jynona Norwood, who lost 27 relatives in Jonestown, questions whether Jones was ever motivated by benevolence.

“Everybody wants to paint these pretty stories about how it started off OK. I personally believe that Jim had deep hatred in his heart from Day One.”

Californian Fred Lewis lost his wife and seven children at Jonestown.

“I blame myself. I blame my wife,” he told CNN. He also blames Jim Jones. “He was a con artist all the way.”

But don’t blame the victims, said one speaker at a memorial service held Tuesday at St. Mary’s Cathedral in San Francisco.

“Remember the people of Jonestown, not for their horrible deaths, but for who they were — people in search of a better world.”

CNN 1998 Jonestown Anniversary Report:

CNN
Jonestown massacre + 20: Questions linger
November 18, 1998

SAN FRANCISCO (CNN) — Twenty years after the world was shocked by the mass murder-suicide in the supposedly utopian community known as Jonestown, the questions linger: How and why did 913 people die? Some believe answers may lie in more than 5,000 pages of information the U.S. government has kept secret.

“Twenty years later, it would be nice to know what went down,” said J. Gordon Melton, founder and director of the Institute for the Study of American Religion.
Time to declassify?

Over the years, there have been rumors of CIA involvement. Some people believe CIA agents were posing as members of the Peoples Temple cult to gather information; others suggest the agency was conducting a mind-control experiment.

In 1980, the House Select Committee on Intelligence determined that the CIA had no advance knowledge of the mass murder-suicide. The year before, the House Foreign Affairs Committee had concluded that cult leader Jim Jones “suffered extreme paranoia.”

The committee — now known as international relations — released a 782-page report, but kept more than 5,000 other pages secret.

Without those documents, it’s hard to confirm or refute the speculations that have sprung up around Jonestown, said Melton, who planned to be in Washington Wednesday to ask for the documents’ release.

George Berdes, chief consultant to the committee at the time of the investigation, told the San Francisco Chronicle the papers were classified to assure sources’ confidentiality, but he thinks it is time to declassify them.
Paradise becomes a prison

What is known about the end of Jonestown is that on November 18, 1978, Jones ordered more than 900 of his followers to drink cyanide-poisoned punch. He told guards to shoot anyone who refused or tried to escape. Among the dead: more than 270 children.

Only two years before, Jones — the charismatic leader of the Peoples Temple, an interracial organization that helped the desperate — was the toast of San Francisco’s political circles.

But after an August 1977 magazine article detailed ex-members’ stories of beatings and forced donations, Jones abruptly moved his flock to Jonestown, a settlement in the jungle of Guyana, an Idaho-sized country on South America’s northern coast.

The plan was to create an egalitarian agricultural community. But Peoples Temple members who worked the fields and subsisted mostly on rice soon learned it was more like a prison, recalls Jonestown defector Deborah Layton.

Dissent was unthinkable, she says. Offenders sweltered in “The Box,” a 6-by-4-foot (1.8-by-1.2-meter) underground enclosure. Misbehaving children were dangled head-first into the well late at night. Loudspeakers broadcast Jones’ voice at all hours.
‘Time for us to meet in another place’
Layton
Layton: “It was like walking into a leper colony”
(Audio 179 K/15 sec. AIFF or WAV sound)

In May 1978, Layton, a trusted financial lieutenant for Jones, slipped out of Guyana. She went to the U.S. consulate and later to newspapers with a warning: Jones was conducting drills for a mass murder-suicide.

But there was little official government action until November 1978, when U.S. Rep. Leo Ryan, who had been contacted by a number of people worried about their relatives in the Peoples Temple, decided to lead a delegation of reporters and relatives to Jonestown.

Ryan’s group arrived on November 17. Their visit began happily enough, but the mood soured after some Jonestown residents indicated they wanted to defect. The group was ambushed the next day as they tried to leave at a nearby airstrip. Ryan and four others were killed.

Later that night, Jones told his followers “the time has come for us to meet in another place,” as the mass suicide began. He was found shot through the head.
‘Jim had deep hatred in his heart’

Jynona Norwood, who lost 27 relatives in Jonestown, questions whether Jones was ever motivated by benevolence.

“Everybody wants to paint these pretty stories about how it started off OK. I personally believe that Jim had deep hatred in his heart from Day One.”

Californian Fred Lewis lost his wife and seven children at Jonestown.

“I blame myself. I blame my wife,” he told CNN. He also blames Jim Jones. “He was a con artist all the way.”

But don’t blame the victims, said one speaker at a memorial service held Tuesday at St. Mary’s Cathedral in San Francisco.

“Remember the people of Jonestown, not for their horrible deaths, but for who they were — people in search of a better world.”

Correspondent Don Knapp and The Associated Press contributed to this report.

Homophobia twists AIDS

April 18th, 2007

John Moore teaches us leadership

stophomophobWe are in receipt of an email from the distinguished Cornell researcher, John P. Moore, who may be one of the most combative and unthinking of paradigm proponents in the endlessly compromised field of HIV∫AIDS, but is thoughtful and has his heart in the right place on one topic, that’s for sure. He is a strong opponent of verbal homophobia, even in private email, and has written to us to deplore our apparent tolerance of this style of bullying in two of the most distinguished of his opponents in the HIV∫AIDS dispute, as recorded here in our previous post.

John P. Moore, implacable foe of HIV∫AIDS reviewersWe capitalized on the brou-ha-ha, he told us, without taking a stand against the sin. He was right. We were trying to keep out of that complicated social issue – in this case whether the written homophobic insults were inherently disgraceful, or merely the excesses of a private spat where insults are used to lash the recipient into paying careful attention, somewhat illogically – since it was not directly involved in the scientific debate about whether HIV caused AIDS or not, and it was up to the reader to decide where he/she stood on the particular example, and it was none of our business, and we preferred not to get in the middle of a catfight between two tigers.

John Moore wrote to tell us we were wrong, and it was important to take a stand, and we belatedly realized he was right. The only thing necessary to ensure the triumph of evil is that good men do nothing, a saying someone has well applied to the Nazi genocide. We apologize. As Don Imus has belatedly realized too the use of hatefilled terms in argument is such a breach of decency and the use of bullying verbal violence of that kind is so hurtful to those who fear and have experienced worse along the same lines that nothing can excuse it.

To overlook it is to condone it, and the state of society is always improved by anyone’s objection to such things, and not objecting to it is to waste an opportunity to raise the level of discourse back to where it should be, after so many thousands of years of evolution, that is, free of bullying and violence.

But Moore needs to rethink, too

Our only excuse is that we were preoccupied with psychologist Mark Biernbaum’s telling email reminder to Moore that his bullying support of HIV∫AIDS conventional wisdom was more damaging by far to gays than any verbal abuse.

As long as the can of worms that is HIV∫AIDS remains sealed and efforts to open it are kept from the public eye by the strenuous efforts of John Moore and his cohorts on AIDSTruth and elsewhere, it is lives which will continue to be damaged and lost, not merely the peace of mind of a gay man in an email exchange where mutual understanding and a positive outcome are destroyed by such hostile language.

So we ask John P. Moore in his turn, if he feels so sensitive and solicitous about the welfare of a gay man attacked in private email with gayhating barbs, how can he reconcile himself to his denial of a public voice to those who bring to his attention the uncountable flaws in his favorite paradigm?

We are not even saying he knows he is wrong to think that HIV causes AIDS, although we know of at least one paper from 2004 where he pretty much admits that the difficulties of accepting that it does are insoluble. We’ll post that soon.

But how can he truly love gays as much as any other human beings and yet deny a voice to critics of HIV∫AIDS, some of them far higher in the pantheon of great scientists than he is as yet, when this leaves the fate of gays and other people hinging on his assumption that he is right without review, without a free public debate, and without free coverage from investigative reporters of the issue (he said in Montreal he wanted to ban coverage by journalists of the topic), which is the only way to ensure his judgement is sound, when so much of the scientific literature speaks against it?

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So we ask John P. Moore in his turn, if he feels so sensitive and solicitous about the welfare of a gay man attacked in private email with gayhating barbs, how can he reconcile himself to his denial of a public voice to those who bring to his attention the uncountable flaws in his favorite paradigm?
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And incidentally, we have an email in hand from Harvey Bialy, whose life has been devoted to truthful science in his roles as editor and scholar, saying quite forthrightly that he is not homophobic, but homophiliac, as anyone who knows him knows. If you want to read the whole exchange, pop over to the group blog You Bet Your Life and check out the new Bad manners and Good Gossip side box down on the left, a parking spot for “Potential contributions, of either original “good gossip”, or comments on pre-existing items, (which) may be sent to the managing editor.”

bialysunbig.jpgThe renowned independent scholar and fierce guard dog of science who spends much of his time with his sharp teeth clamped on the trousers of a terrified HIV∫AIDS paradigm promoter attempts to explain in his introduction why he habitually sends out scathingly sulphuric email that leaves its recipients with third degree burns:

Contrary to perhaps widely spread opinion (an expression with three ambiguous words), I am extremely thoughtful about everything I write whether it is intended for publication, private with the understanding that it is confidential, or private with the expectation that its recipient might wish to use its coarse language (or apparent betrayals of trust) against me at some future time on the wild and wooly way outset west ever, called The Internet.

And being a mischievous sort by nature and nombre (although as all who know me know, never malicious, no matter how “wicked” the mischief might appear), often these private emails of the third category wind up being extremely provocative, and often cause me considerably more “wasted time” (an ambiguous two word, common expression) than I bargained for in the initial, often improperly spell-checked, electronic missives, which are impulsive only in that restricted, technical sense.

Nonetheless, one cannot grumble about the fruits of the seeds of one’s own planting to any profit (although many try often to do so, at least to my experience), and so I bear the ignominies that come my way with the best good humor I am able to muster at the moment they come, life being quite a complex progression of connected temporal stimuli of all varieties from inside as well as out, and although each reducible to
“chemistry”, the temporal wholeness is a great deal more than the sum of its chemical parts. (I know, none of the above is either bad manners or good gossip…patience…we
will get there soon enough.)

We urge any readers who can extract from this extended riff exactly what the justification is supposed to be to please explain in Comments below.

Delusional Delaney

shirtBack to the topic of homophobia, which experts on CNN’s Anderson Cooper broadcast are already detecting in the Virginia Tech shooter, as one who feared he wasn’t as attracted to women as he wanted to be (see shirt at left). Whether this is true or not, self-hatred appears to be a common theme in discussions of this kind, whether heterosexual or homosexual. Could it be that certain well known promoters of the HIV∫AIDS paradigm suffer from this mental imbalance?

Certainly it is true that as many have pointed out gays have been their own worst enemy in HIV∫AIDS, many of them being led by activists often financed by the drug companies into deploring the critics of HIV∫AIDS who might have rescued them from an ideology not justified by the scientific literature.

delaneyp.jpgOne of the best examples of that is the post just put up at AIDSTruth by Martin Delaney, which begins by attacking Peter Duesberg as having no background in AIDS and thus no authority in reviewing the paradigm and rejecting it. Here it is with spelling corrected:

Peter Duesberg and homophobia
by Martin Delaney
April 15, 2007

More than a decade and a half ago we on the frontlines in the fight against HIV/AIDS concluded that Peter Duesberg was bitterly homophobic. Long before there were many anti-viral drugs for him to blame, he clearly blamed AIDS on the gay men who contracted it, arguing that it was the product of a life of promiscuity and drug abuse. In the earliest days, a lot of people suspected that, but studies were soon done by Ascher and others that disproved the theory. Only Duesberg continued to promote the belief, despite studies of thousands of drug using men, controlled for the presence or absence of HIV. Only the presence of HIV correlated with death and major immune deficiency. Drug use and promiscuity were indeed a risk factor for contracting HIV, but by themselves were never shown capable of producing AIDS-like symptoms. Despite this evidence, Duesberg continued to blame AIDS on the behavior of the men, not the viral infection they acquired. This was the same nonsense mouthed by right wing fundamentalists, minus the religious overtones. It still came down to blaming the victim for the disease. In my opinion Duesberg always was, and continues to be, a major homophobe. For a while, he tried to counter this view by hanging around with leather-clad gay men, trying to show some affiliation, but these men were simply a first wave of denialists among the gay community. They were notorious themselves for denigrating others in the gay community, accusing people with AIDS of promiscuity and drug abuse. Their presence in no way cleansed Duesberg of his homophobia.

In all his efforts to blame the victim for the disease, Duesberg has always overlooked the fact that there were plenty of gay men who died of AIDS who never had a history of either promiscuity or drug use. Whenever confronted with this information, Duesberg simply accused people of lying or being in denial.

While I am not aware of explicit homophobic words on record by Duesberg (unlike his friend and business colleague Harvey Bialy, though both are known to use racial slurs), his explanations about AIDS makes it clear what he thinks of gay people in general – contrary to clear, controlled studies, Duesberg insists that AIDS is the fault of the immorality of its victims.

As anyone informed knows, Duesberg has in fact a record of

a) having written a series of the most extensive and comprehensive reviews of HIV’s role in AIDS,on which he became the best informed man in the world,

b) he mapped the sequences of not one but about ten retroviruses

c) he has written about 15 grant proposals for the NIH on researching HIV and AIDS , all rejected for so little reason that even the past editor of Science complained (Dan Koshland) after supporting one in vain and

d) he demonstrated the toxicity of AZT before it was acknowledged as indeed the cause of many needless deaths before the mid nineties, when the dose was reduced by two thirds.

If he is right in his judgement, tempered and tested in the white heat of hostile reaction and penalties, from his peers and scientific ignoramuses both, and produced by more careful study of the literature than anybody else in the world, he has thus saved many gay men’s lives, and continues to try and save more, even as they continue to insist, under the leadership of Martin Delaney and other activists funded by the drug manufacturers (computers still working well, Martin?), in taking a little AZT and ARV’s in a cocktail which has no party spirit in it at all, in fact, causes the drug symptoms which half the deaths of AIDS patients in the US are now attributed to.

As one informed observer has recently pointed out here, the predicament of gays who take high doses of recreational drugs and/or are overly strenuous in cleaning themselves and thus stripping their digestive systems of protective flora and fauna, are by every logic and paper in the relevant literature endangering themselves, and if Duesberg is responsible for pointing that out he is hardly homophobic.

As so many distinguished contributors have pointed out here in Comments, gay men have largely ignored this advice, instead developing a reflex hostility towards it for political and emotional reasons, Figures like Martin Delaney are among those who have to take prime responsibility for fostering those political and emotional motivations, which have persuaded so many to ignore reason and the message of the scientific literature, which tells us that HIV is the last thing that might cause immune system dysfunction, and the partying habits of many gays the first thing that should be considered instead.

The “plenty of gay men who died of AIDS who never had a history of either promiscuity or drug use” are without much doubt those who took AZT or the later cocktails, since the only improvement that has resulted from spoonfeeding them standard medications over two decades to date not surprisingly coincides with the reduction in AZT dose in the early nineties. There has been no improvement since, as we learned last summer.

The question Martin Delaney and John Moore have to answer is, do they really think there is no question to answer?

Or are they overcome with some kind of bias in favor of the status quo which prevents them from even considering the alternative, a bias so strong that they wish to prevent others from considering it also?

Whether that bias stems from other factors or from homophobia, there is no doubt that is has a seriously homophobic effect, the illness and death of those that trust their leadership.

That. at least, is what the scientific literature tells the few people who read it without preconceptions.

SciAm editors explain

April 16th, 2007

Editorial expands on Jekyll-Hyde theme as best defense of giving a “pariah” a platform

Good science as numbers game, rather than best interpretation of evidence

Guess we spoke too soon in wholly admiring the Scientific American editors unusual spirit of standing up and standing for good science in providing a platform for Peter Duesberg to explain his breakthrough ideas on how cancer is generated.cat_on_a_hot_bin_roof_jackie_fleming.jpg
(Pic is Cat on a Hot Bin Roof by Jacqueline Fleming)
“Cat on a Hot Bin Roof” is based on the expression “Cat on a hot tin roof”. An acrylic on canvas 21 x 16 Inches (Width x Height). Painted in 2005. The painting is part of a baby and children series that incorporates nursery rhymes, childhood themes and stories. Jackie brings these tales to life in brilliant colors with vivid figures and humoristic characters that appeal to all ages. All paintings are one of a kind, signed by Jacqueline Fleming. Jackie is based in Santa Fe, New Mexico. (To buy, go to MostOriginal)

In a depressing exhibition of how elite editors are forced to kowtow to the prejudice of the scientific herd, the Scientific American editorial in this issue, When Pariahs Have Good Ideas, tries to head off criticism and counter attack from John P. Moore types anxious to condemn any sign of respecting the scientific analysis and judgement of Peter Duesberg, in case the spotlight is brought to bear once again on whether he may be right after all about the laughably inconsistent paradigm on which they stand insecurely in HIV∫AIDS.

As wrong as Duesberg surely is about HIV, there is at least a chance that he is significantly right about cancer. We consider the case worthy of bringing to your attention, with the article beginning on page 52.

It’s not Duesberg who is shaky on HIV∫AIDS

“Laughably inconsistent”, that is, with logic, reason, evidence and common sense, and out of kilter with its own mainstream literature, by which proponents have persuaded the world that a Virus which cannot generally be found at all in “HIV positive” patients even with PCR is going somehow inexplicably to reappear and surge after years and kill them, an unprecedented feat for a retrovirus or indeed any microbe at all which has been successfully banished from the body by antibodies, which is what HIV tests test for, since there is so little HIV to be found, if any at all, in AIDS patients, even dying ones, and anyway there is no explanation of how it could possibly kill T cells even if there was any solid evidence that it did so, indeed there is an abundance of data showing it does not, and in fact is as harmless to cells as any other retrovirus among the multitude that inhabit the body without any effect whatsoever on the host.

Not to mention the fact that mainstream studies show with brilliant clarity, despite the brazen denial of the ever politick authors themselves, that the Virus in question is not infectious between heterosexuals, so how there can be a worldwide pandemic racing across Africa and Asia to kill millions on this basis is not easily accounted for in scientific terms, though it is very well explained in terms of political and economic advantage for the purveyors of the paradigm and its drugs.

Heading off the backlash

Unhappily the Scientific American editors are forced to do the same, having to explain themselves politically rather than scientifically to anticipate and parry the response of Robert Gallo, John P. Moore, Anthony Fauci and other scientific pr hit men who may strike back on behalf of their politically and financially beloved but increasingly scientifically shaky HIV∫AIDS paradigm, which even their mainstream literature now constantly calls into question with its latest results. sciameditorial.jpg

Readers may therefore be shocked to see Duesberg as an author in this month’s issue. He is not here because we have misgivings about the HIV-AIDS link.

So instead of celebrating their gumption in providing a place for this superior scientific mind to explain his valuable initiative in cancer, which now boasts many followers around the world at high institutions, we have to observe it and good science compromised by a somewhat weaseling editorial which joins the bulk of the scientific community in mistaking science for a democracy, where votes decide the truth and to go against the unthinking mainstream for too long labels one a crank.

To the dissidents, Duesberg is Galileo, oppressed for proclaiming scientific truth against biomedical dogma. A far larger number of AIDS activists, physicians and researchers, however, think Duesberg has become a crank who refuses to accept abundant proof that he is wrong. To them, he is at best a nuisance and at worst a source of dangerous disinformation on public health.

Science as a numbers game

Do the editors of Scientific American really think that the “far larger number” is a guide as to who is right in a fierce paradigm dispute where all the perks, power, profit and position are on the paradigm side, and all the literature of the field on the other? Let’s hope not.

The Ask John research route

But perhaps like so many people who participate in science and its story, including it seems the smartly tailored Anthony Fauci, who apparently (unless he is invested in Tamiflu) remains unaware that Vitamin A is the simple answer to bird flu, according to study papers we pointed to a year ago, they have not bothered to check PubMed for the real dope, but merely called up a pet senior scientist for his opinion, often one not even in the field concerned.

Of course, this is the preferred way in forming scientific judgement because it is the one which prevails, and anybody who actually reads the literature of science in a disputed field and realizes that the paradigm is a crock, as indicated in HIV∫AIDS by the papers and book chapters which the scientists in residence at the top of the hill write quietly for their friends and not for public consumption, will have a very hard time not being labeled a crank by the Scientific American editors, most other scientists and the public at large, a public which has not been informed by the New York Times that any other reality than indicated by its mantra “HIV, the virus that causes AIDS”, is being discussed by anybody, other than by the one highly misleading Op Ed by John P. Moore last year dismissing Duesberg and his often well credentialed supporters as “Deadly Quackery”.

It is an approach that we have characterized in the past as the “Ask John” style of checking facts, and it is sad to see the Scientific American editorial writer writing an apology for featuring Duesberg based on a complete misunderstanding of how science works to replace paradigms with better ones. Science is not a democracy, and nor is it led exclusively by accomplished scientists who embrace novelty and change as if it was welcome, since it will displace them and the beliefs on which their careers were founded and flourished.

Science is a study which like any other in the academy is ruled by people who are mostly anxious to retain their position and funding till their retirement, and don’t particularly relish any young whipper snapper interfering with their quietly sailing into the sunset, and certainly not a senior colleague who should know better how to behave in the club.

Kicking dissidents down the hill

For proof of this phenomenon ask any Nobel prize winner what it was like when they first came up with their world view flipping idea. They will have nothing good to report in most cases. First publication was almost always very troublesome.
Meanwhile, the bulk of scientists are journeymen who labor in the fields below the lowest slopes of Mount Olympus, and their opinion about any paradigm which governs their work is a follower’s opinion borrowed from the leaders of the field. This is especially true today as the influx of giant sums from investors and corporations has turned science into a profession rather than a vocation, and even a business in many cases.

Whatever the reason, the fact is that scientific opinion is formed among those in and outside a field mostly by the social necessity of getting into lockstep for social reasons extraneous to scientific concerns, and with some $7 billion a year in Federal funds devoted to this paradigm he who pays the piper calls the tune, even for otherwise enlightened and well informed scientific periodicals.

This editorial is a sorry example of this influence at work, which anybody who has read Peter Duesberg’s work on HIV∫AIDS will find irritating but will forgive as a leadership weakness inherent in running any science oriented institution these days.

When we look at submitted manuscripts from scientists, we consider it a reassuring sign when the authors forthrightly acknowledge both their collaborators and their competitors and note potential conflicts of interest before we ask. If we see that they are describing the science of their rivals fairly, we can have more confidence that they are being similarly candid about their own work. (Still, the old nuclear disarmament treaty maxim applies: trust, but verify.) We typically steer away from controversial ideas too new to have much supporting evidence. Those that have lasted for years and accumulated some substantiation have earned consideration. Our judgments are imperfect, but they tend to mirror those of the scientific community.

Blots on a researcher’s history often should bear on regard for his or her new work. Scientists who have intentionally published fraudulent papers, as the stem cell researcher Woo Suk Hwang so notoriously did two years ago, may be irredeemably tainted. But to dismiss a scientist solely for holding some wrong or controversial views risks sweeping away valuable nuggets of truth. We respect the opinions of any readers who may criticize our choice to publish Duesberg in this case but hope they will nonetheless evaluate his ideas about cancer on their own merits.

“Evaluate his ideas about cancer on their own merits?” Is there any reason why this novel principle cannot be applied to Duesberg’s ideas about HIV∫AIDS also?

We can’t think of one.

Here is the whole editorial song and dance, choreographed by a cat on a hot tin roof:

April 15, 2007

When Pariahs Have Good Ideas

By The Editors

Even mentioning the name Peter Duesberg inflames strong feelings, both pro and con. After gaining fame in 1970 as the virologist who first identified a cancer-causing gene, in the 1980s he became the leading scientific torchbearer for the so-called AIDS dissidents who dispute that HIV causes the immunodeficiency disorder. To the dissidents, Duesberg is Galileo, oppressed for proclaiming scientific truth against biomedical dogma. A far larger number of AIDS activists, physicians and researchers, however, think Duesberg has become a crank who refuses to accept abundant proof that he is wrong. To them, he is at best a nuisance and at worst a source of dangerous disinformation on public health.

Readers may therefore be shocked to see Duesberg as an author in this month’s issue. He is not here because we have misgivings about the HIV-AIDS link. Rather Duesberg has also developed a novel theory about the origins of cancer, one that supposes a derangement of the chromosomes, rather than of individual genes, is the spark that ignites malignant changes in cells. That concept is still on the fringe of cancer research, but laboratories are investigating it seriously. Thus, as wrong as Duesberg surely is about HIV, there is at least a chance that he is significantly right about cancer. We consider the case worthy of bringing to your attention, with the article beginning on page 52.

Thousands of scientific papers appear in technical journals every month; why do some rate more fame and journalistic attention? It helps for science news to have dramatic relevance to human affairs: Is there strong new hope for curing a disease, transforming the economy, building a better mousetrap? Alternatively, reporters and editors may gravitate toward new science that easily inspires the public’s sense of wonder, as so many astronomy stories do. And reports that appear in certain major scientific journals tend to get more play because those
publications have a self-fulfilling reputation for releasing the most noteworthy papers. (It doesn’t hurt that those journals have particularly strong public relations departments, too.)

When we look at submitted manuscripts from scientists, we consider it a reassuring sign when the authors forthrightly acknowledge both their collaborators and their competitors and note potential conflicts of interest before we ask. If we see that they are describing the science of their rivals fairly, we can have more confidence that they are being similarly candid about their own work. (Still, the old nuclear disarmament treaty maxim applies: trust, but verify.) We typically steer away from controversial ideas too new to have much supporting evidence. Those that have lasted for years and accumulated some substantiation have earned consideration. Our judgments are imperfect, but they tend to mirror those of the scientific community.

Blots on a researcher’s history often should bear on regard for his or her new work. Scientists who have intentionally published fraudulent papers, as the stem cell researcher Woo Suk Hwang so notoriously did two years ago, may be irredeemably tainted. But to dismiss a scientist solely for holding some wrong or controversial views risks sweeping away valuable nuggets of truth. We respect the opinions of any readers who may criticize our choice to publish Duesberg in this case but hope they will nonetheless evaluate his ideas about cancer on their own merits.

http://www.sciam.com/print_version.cfm?articleID=E6AE9A0B-E7F2-99DF-3C6C9B72962EE534

Scientific American: When Pariahs Have Good Ideas
© 1996-2007 Scientific American, Inc.

On the whole a wretched document, demonstrating how editorial torchbearers of the truth have to mollify the mob by joining in the nonsense about Duesberg failing to grasp the reality of HIV∫AIDS while, despite the vindictive and fearful withdrawal of NIH support, he triumphs over a far more complex subject by establishing world leadership in a new avenue of research.


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