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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)
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