“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
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
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
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?
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"
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
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
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
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
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 firstname.lastname@example.org
and has a website www.duesberg.com. You can also snail mail him at:
Department of Molecular and Cell Biology
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
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.
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
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