“What If Everything We Thought We Knew About Cancer Was Wrong?”

In this exclusive interview, Peter Duesberg, PhD, discusses his controversial cancer theory and why the scientific community and the mainstream media are forced to ignore it.

Question: Your recently proposed theory of cancer, based on the notion of abnormal numbers of chromosomes, runs contrary to currently accepted theory of genetic mutation. Can you give a brief overview of the theory for the uneducated reader?

Answer: Briefly, there are two very different mechanisms of mutation, gene mutation for minor adjustments within a species and chromosome number mutation for big dominant changes, good or bad.

All chromosome number mutations, such as the normal ones that determine sex and a new species and the abnormal ones that happen at conception or in rare cells after birth, change the phenotype dramatically, or dominantly as we say in "the business". The accidental chromosome number mutations that occur at conception and after birth all generate abnormal chromosome numbers, called aneuploidy, and abnormal phenotypes, such as Down syndrome and cancer.

For example a normal +/- of the Y chromosome = boy or girl, and a very, very rare addition of two extra chromosomes to your normal 46 and you or me are a gorilla!

An abnormal aneuploidy of + one extra #21 chromosome at conception means 'Down Syndrome'. And an abnormal aneuploidy of typically 20 additional and sometimes missing, otherwise normal chromosomes and you are looking at your favorite metastatic lung, colon, breast or liver cancer.

For those who are still a little fuzzy about the relationship between genes and chromosomes, here is a little analaogy that might help:

Assume the cell is a car factory (and that is a pretty good analogy). Then gene mutations are weak (negative) or strong (positive) assembly line workers. And chromosome number mutations (ie. aneuploidy or polyploidy) are extra assembly lines. If they are proportionally multiplied you get 2, 3 , etc. more normal cars, if they are randomly multiplied you get unpredictable monsters with 7 wheels, two steering wheels, no brakes, three engines, etc. While most of these would be lethal, some would be monstrous parasites (ie. cancer cells).

Q. What implications does your new theory have, if any, upon current cancer research efforts?

A. A whole new dimension, perhaps the right one!

Q. What implications does your new theory have, if any, upon current cancer cancer treatment practices (i.e., chemotherapy and radiation)?

A. Treatment of all mutations is as yet rather hopeless. But, if based on the aneuploidy hypothesis, cancer-suspect biopsies were tested and found to be aneuploid, early treatment could much improve cancer prevention.

Q. What implications does your new theory have, if any, upon current carcinogenic testing of various substances (i.e., drugs, environmental pollutants, drinking water chemicals, etc?

A. Again, if the very testable aneuploidy hypothesis were confirmed, we would test cancer-suspect substances for their ability to cause aneuploidy instead of gene mutation. That could revolutionize cancer prevention.

Q. Are there such things as cancer-specific genes?

A. Not one has been identified in about a century old search! There is but one exception, viral oncogenes - my old "claim to fame".

Q. Some women are being told that they are genetically more susceptible to breast cancer and as a result, many are deciding to have their healthy breasts removed (prophylactic mastectomy). What do you think of such practices?

A. Science at its worst! The genes that are identified may be (!) predisposition genes, rather than cancer causing genes. In other words, genes that facilitate the alteration/mutation that really causes cancer. Until this is settled, identifying disposition genes is speculative at best.

And prophylactic surgery is presumptuous, harmful and self-serving on the part of the presumptuous scientists with a licences to practice surgery. It is long known that blondes have a higher skin cancer risk than blacks. Should we start impregnating the skin of blondes with black dyes to reduce their skin cancer risks? Why not?

Q. Does your chromosome theory preclude cancer from being hereditary?

A. Yes, because aneuploidy is not heritable.

Q. How is it that cancer seems sometimes to run in families?

A. See above, "disposition" genes.

Q. You note that many carcinogens act without damaging genes, such as asbestos, hormones, arsenic, nickel, etc. How do these substances act then, according to your theory?

A. They cause aneuploidy, either by interfering with the spindle apparatus, or by breaking chromosomes (see our paper "Aneuploidy, the mutation that makes cancer a species of its own" Cell Motil & Cytoskel 2000; 47: 81-107). It describes that in detail.

Q. You state "cancer is by definition, a species of its own." This may surprise and confuse many lay people. Can you explain briefly?

A. The definition of a species includes a species-specific chromosome number, ie. 46 for humans. Once that number is changed all bets are off. You may be a monkey or a cancer or a Down Syndrome patient, depending directly on the degree of deviation from the normal human chromosome balance (and gene arrangement within chromosomes in different species).

Q. You also state that "It differs from authentic species in that it is parasitic, ie, it is unable to function independently." However, most parasites feed off of the host, but don't kill it, as that would be self-destructive. Therefore, the fact that cancer often kills would seem counterproductive.

A. Yes, cancer is self-destructive! It is not an exogenous parasite that has to make a living on its own. It is one of the many age-dependent diseases that are all also self-destructive. It is an inherent risk of all multicellular organisms.

Q. You note that the chromosome cancer theory was originally proposed over 100 years ago, but was abandoned. Can you explain briefly why this occurred?

A. The main reason was, that no cancer-specific aneuploidy, ie. aneuploid karyotype, was ever found. Even the cells of a given tumor have non-identical karyotypes. In view of this it was concluded that aneuploidy must be a consequence rather than the cause of cancer. The cause was/is thought to be a specific gene mutation, that has never been found.

Moreover, the enormous mutagenic range of aneuploidy is not part of the mind set of modern geneticists. They are all narrowly focused on genes. The word "aneuploidy" is not even in the index of the leading molecular biology text books, ie. Lewin, Lodish, Watson, Alberts etc.

Q. In a 1999 review of alternative cancer theories, the author states "From a view of philosophy of science such criticism is valuable and deserves careful evaluation." (Anticancer Res 1999 Nov-Dec;19(6A):4913-4) Do you think that your cancer theory is getting adequate attention and "careful evaluation", and is the scientific community actively engaging in a debate of it?

A. Not yet. Thirteen (13) grant applications to non-private funding agencies have all been turned down. Instead of welcoming alternative hypotheses, as for example our aneuploidy hypothesis, the proponents of the oncogene hypothesis use the quasi monopoly on American cancer research grants of the National Institutes of Health (NIH) to exclude alternative hypotheses from government grants.

The mechanism of exclusion takes advantage of the little known practice that the NIH "deputizes" its authority to distribute tax money to individual researchers to committees of "experts". These "experts" are cancer researchers who are distinguished for an outstanding contribution to the current orthodoxy. I used to be one of them, before I challenged the virus-AIDS hypothesis in 1987. Moreover, the experts are now even legally rewarded for their investments in the orthodoxy by income from commercial applications of their work via patents, shared with universities!

The only break for us so far was an article in the January issue of the Journal National Cancer Inst., "Webb T: When theories collide: Experts develop different models for carcinogenesis." (J Natl Cancer Inst 2001; 93: 92-94).

Q. What do you think of the lack of media attention to your recently published cancer papers (see bibliography list at end)?

A. The current mainstream "media" and the current mainstream scientists face the same dilemma: Both are highly specialized professionals that depend on the think collective (as Fleck and Kuhn used to call it) for support, recognition and survival! Take the AIDS/science writers Altman (New York Times) or Perlman (San Francisco Chronicle). Both are aware of the failures of the HIV-AIDS hypothesis to produce and to explain, but will they write about the basic flaws of HIV-AIDS? About Duesberg? Of course not.

If they did, it would probably be their last story on AIDS, if not on science, in the respective newspapers. Their weekly AIDS columns would no longer be wired in from the NIH press office, or from Nature or Science. Their phone calls to Fauci, Varmus, Baltimore, Gallo, Weinberg, etc., would no longer be answered. Their invitations and hotel reservations at the next AIDS or cancer meeting would no longer be offered.

Take Perlman's example: In 1992, when Nature editor Maddox almost came around to Duesberg for a while, Perlman had a story written about Duesberg and in no time, was twice in my lab, gave me his home number, email, etc. But then Nature reconsidered, in response to violent complaints from the AIDS establishment. And so did Perlman.

After consulting his "sources", Perlman now decided to make publication of his article dependent on an "agreement" between me and a leading AIDS researcher (J. Levy) from University of California San Fransisco (UCSF). Since our meeting did not generate the desired "agreement", Perlman never published his story and has been a faithful AIDS reporter ever since. Recently, he was decorated by UCSF with a medal for decades of faithful reporting of UCSF science breakthroughs, ie. without unnecessary questions by himself or other scientists.

Another recent case in point is a young reporter who called 2 months ago to write about my recent paper that the long investigated problem of drug-resistant cancer cells, could be explained by aneuploidy. Briefly, aneuploidy destabilizes chromosome segregation by unbalancing the spindle apparatus, and keeps regrouping the karyotype to generate ever new assortments of chromosomes, including those that confer resistance to chemotherapy.

But he was directed by his editor to write about my "discredited " AIDS views instead. In my office, he told me that several colleagues also told him not to write about Duesberg's aneuploidy-cancer hypothesis, in order not to "legitimize" him, and in order not to "isolate" himself.

Even Bob Sanders from the University of California - Berkely (the university where I work) press office was surprised about the unusual lack of responses, either positive or negative, to a press release which he had prepared on the my published paper in January.

Likewise my friend Russel Schoch, editor of the Cal Monthly magazine here at UCB is under a "Duesberg embargo" from the board of the journal's directors. Even if it is about cancer, Duesberg is not to be "legitimized".

So you can see that the "free" press that we enjoy in our country has limitations very similar to the free science, that our government sponsors so generously via "peer review".

Q. In a paper published last year in the Proceedings of the National Academy of Sciences (Proc Natl Acad Sci 2000 Mar 28;97:3236-41) you critically review the conclusions drawn from a previous study, which claimed to provide further evidence of the gene mutation theory of cancer. You analyzed the same exact data and cell samples yet came to completely different conclusions. How often do you think that stated conclusions in the published literature don't coincide with the actual data? How large of a problem is this? Is there any remedy for it?

A. The problem is very large in AIDS and in cancer, both areas of my expertise. The ONLY solution would be to free scientific spending from vested interests (i.e., the "expert" peer review). Science would have to be judged by "expert citizens" (i.e., those who can earn taxes, read and write and have common sense, just as those who serve because they are non-experts, ie.e, us, the people in the legal jury system). NOT by those who have exceedingly large vested interests like their professional egos, their grants, their summer salaries, their companies, their patents, their "Frequent Flier" benefits, and their awards on their minds.

Q. This essentially means that one needs to be very skeptical of conclusions drawn in ANY published study.

A. Think about the 200,000 plus healthy, HIV-positive fellow Americans who must take DNA chain-terminators in the name of the NIH's and CDC's HIV-AIDS hypothesis, that has yet to cure the first patient and has cost the US taxpayer to date over $93 billion since 1981!

Q. You note that the gene mutation hypothesis doesn't make sense in light of the very long "latent" periods between carcinogen exposure and cancer, which can be as long as several decades. With this being the case, how is it possible to introduce new chemicals (e.g., drugs, etc.) and declare them "safe" after very short duration testing?

A. Because the current scientific dogma, endorsed by the National Cancer Institute (see their web site - www.nci.nih.gov), holds that carcinogens are mutagens. Thus if a cancer-suspect substance does not react in an over-night bacterial mutagenesis test (the Ames test) it is generally assumed to be safe, ie. non-carcinogenic.

Q. What is your opinion of the cachexia or malnutrition cancer theory promoted by Gershom Zajicek M.D., of Hebrew University in Jerusalem, which states that the malnutrition often seen with cancer comes first and is actually the cause of the tumor, which develops to produce a substance that the body lacks?

A. I suspect that this hypothesis is flawed on the grounds that malnutrition does not cause cancer. On the contrary, malnourished people have a lower cancer-risk than their overfed counterparts. For example, there was much less breast, colon and stomach cancer in war time and postwar Germany than there is now.

Q. You did a lot of cancer research earlier in your career, before becoming probably the leading "dissident" AIDS scientist in the world. What has brought you back into the cancer field?

A. All my experimental work has been on viral or non-viral cancer ever since I became a professor at UC Berkeley in 1968. My AIDS work was all theoretical, based on my 25 years of experience working with retroviruses. Since I have lost all my non-private grants and students and academic perks as a result of my questions about the HIV-AIDS hypothesis, I had time to think, particularly about the even bigger challenge, cancer.

It was a result of this, that I concluded that cancer is caused by nature's biggest and most consequential mutation (ie., aneuploidy) rather than by the recessive genes, that are now called dominant oncogenes. Indeed, nearly all oncogenes have been introduced into transgenic mice, without causing cancer.

I hoped that the fronts in cancer research were not as entrenched, and above all, not as US-controlled as in AIDS, and that I would have a chance to make a major contribution to cancer, since I was not accepted as a sincere contributor to AIDS.

Peter Duesberg can be reached at duesberg@uclink4.berkeley.edu and has a website www.duesberg.com. You can also snail mail him at:

UC Berkeley
Department of Molecular and Cell Biology
Stanley Hall
Berkeley, CA 94720

Selected Bibiography of the Chromosome or "Aneuploidy" Cancer Theory (In reverse chronological order):

Duesberg P, Rasnick D. Aneuploidy, the somatic mutation that makes cancer a species of its own. Cell Motil & Cytoskel 2000; 47: 81-107 (Abstract)

Duesberg P, Li R, Rasnick D, Rausch C, Willer A, Kraemer A, Yerganian G, Hehlmann R. Aneuploidy precedes and segregates with chemical carcinogenesis. Cancer Genet Cytogenet 2000 Jun;119(2):83-93 (Abstract)

Li R, Sonik A, Stindl R, Rasnick D, Duesberg P. Aneuploidy vs. gene mutation hypothesis of cancer: recent study claims mutation but is found to support aneuploidy. Proc Natl Acad Sci U S A. 2000 Mar 28;97:3236-41. (Abstract)

Duesberg P, Rasnick D, Li R, Winters L, Rausch C, Hehlmann R. How aneuploidy may cause cancer and genetic instability. Anticancer Res. 1999 Nov-Dec;19:4887-906. (Abstract)

Duesberg P, Stindl R, Hehlmann R. Explaining the high mutation rates of cancer cells to drug and multidrug resistance by chromosome reassortments that are catalyzed by aneuploidy. Proc Natl Acad Sci U S A. 2000 Dec 19;97:14295-300. (Abstract)

Duesberg P. Are centrosomes or aneuploidy the key to cancer? Science. 1999 Jun 25;284:2091-2.

Rasnick D, Duesberg PH. How aneuploidy affects metabolic control and causes cancer. Biochem J. 1999 Jun 15;340 (Pt 3):621-30. (Abstract)

Duesberg P, Rausch C, Rasnick D, Hehlmann R. Genetic instability of cancer cells is proportional to their degree of aneuploidy. Proc Natl Acad Sci U S A. 1998 Nov 10;95(23):13692-7. (Abstract)

Li R, Yerganian G, Duesberg P, Kraemer A, Willer A, Rausch C, Hehlmann R. Aneuploidy correlated 100% with chemical transformation of Chinese hamster cells. Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14506-11. (Abstract)

Dr. Mercola's Comments:

Cancer is not one of my areas of expertise, as I don't treat a lot of cancer patients. Also, I am not a molecular biologist. However, Peter Duesberg seems like a very intelligent and certainly incorruptible scientist, so I believe that his theory should definitely not be dismissed out of hand.

Probably the most disturbing facts presented above are that the scientific community seems unwilling to engage in open debate on many subjects and is likely being manipulated by the almighty dollar. In addition, the mainstream media continue to demonstrate that they are very negligent in their obligation to inform the public about issues that have any controversy surrounding them. Again, this is likely due to financial conflicts of interest.

Posted by: Dr. Mercola