Re: Challenging Conventional Wisdom on Cancer

From: David C Campbell <>
Date: Thu Aug 18 2005 - 15:47:49 EDT

Chromosome number varies naturally between species, yet clams with
hundreds of chromosomes are not especially prone to cancer. In fact, I
don't know of any reports of cancer from the ones with the highest
chromosome number, but I don't know that anyone has looked closely.

>Two well-publicized genes supposedly predispose women for breast
cancer, but in over 90 percent of cases these genes have shown no

The wording is not clear, but I think that this is claiming that over
90 percent of breast cancer cases are in people who do not have those
two mutations. But that would only prove that those two genes are not
the only causes of breast cancer. The relevant statistic would be the
proportion of people with either mutation who eventually develop cancer.

>Now, in the Washington Post article, we read that "researchers sifted
through 250 genes that had been identified as playing a role in breast
>So, up to 250 genes are "playing a role."<

As not all breast cancers are alike, and as gene products work
together in complicated ways, it should be expected that lots of
different genes can play a role in cancer. For example, suppose that
gene A, when mutated, directly causes cancer. Gene B's product
regulates gene A's product, helping keep it in line. A mutation in
gene B would thus also put one at higher risk. Gene C is involved in
DNA copying. If it is mutated, DNA copying can malfunction, making it
more likely that a mutant version of A will be produced. Many such
systems exist in cells. Consider, for example, the mutation that
produces lighter colored skin in many people of European ancestry.
This gene does not cause skin cancer. However, by decreasing the
amount of protective melanin, it makes people more vulnerable to skin
cancer if they get too much sun exposure.

One difficulty overlooked by the article is determining exactly what
the relevant genes do, which can be very difficult. Some
cancer-associated mutations are actually markers for cancer
suceptibility, rather than the cause of the cancer. I.e., it is a
harmless mutation in and of itself, but it happens to co-occur
frequently with cancer, probably because it is near a cancer-causing
mutation in the chromosome. An example comes from a Japanese study in
which differences in ear wax were linked to frequency of a particular
type of cancer. The gene affecting ear wax was not responsible for the
cancer; rather, it was near the cancer-causing gene and so tended to
travel together.

>As the cells of the body number perhaps trillions we would all have
cancer if a single hit was sufficient.<

By this reasoning, a single bullet can't kill you because many people
have survived a single hit. All mutations are not equal!

>Researchers have never been able to show that a mutated gene, taken
from a cancer cell, will transform normal cells in the petri dish. <

You can't just stick a gene in a petri dish and expect it to replace
the normal version in a group of cultured cells. Ensuring that the
mutant gene directly and totally replaces the normal version in the
experimental cells would be quite difficult. Another difficulty is
that cancer is a disease of multicellular organisms, not of petri
dishes. Does the petri dish adequately reflect the conditions in the
body that enable cancer cells to cause trouble?

Also, it might be a little more credible if changing chromosome numbers
in cells in petri dishes caused cancer. It's not too hard to cause
some types of chromosome number changes.

>There is even a genetically engineered strain of mice called OncoMouse.
 They have some of these oncogenes in every cell of their small bodies.
You would have thought they would die of cancer immediately. But they
leave the womb, gobble up food, and live long enough to reproduce and
pass on their deadly genes to the next generation.<

Most cancer takes a while to develop. How many people with cancer
survive long enough to reproduce? Also, earlier there was a passing
mention of the oncogenes being turned on by a carcinogen, rather than
directly causing cancer.

>The cell just keeps on dividing, its control mechanisms overridden by
the abundance of extra DNA in the cell. <

Many organisms have cells with lots and lots of DNA, without getting
cancer. It's the functioning of the genes on the extra DNA that may be
a problem. In other words, genes would still be causing the cancer
even if he were right about the role of aneuploidy. Another problem
with his argument is that a chromosome shortage is a problem, too.

Cancer is actually an excellent example of evolution. How can a mutant
cell survive and reproduce in the face of a body's many control
mechanisms? One thing that may work is to have a very high mutation
rate. Many of the mutants will die, but some may be successful. Some
of these mutants may have abnormal chromosome numbers. Not all cancer
cells do, however.

Additional lines of evidence for the role of genes in cancer come from
inheritance patterns. Propensity for cancer can be inherited. For
example, some types of eye cancer are found either as individual cases
in adults or as inherited versions. A child inheriting the
cancer-causing gene often gets cancer in both eyes early in life,
because the mutant gene is in all his eye cells. Adult onset versions,
which appear to represent mutations that occurred later in life,
generally only affect a single eye, because the mutation happened well
after the eyes had developed and was present in only one eye.

This is an attempt at promoting an ill-founded claim through charges of

Dr. David Campbell
425 Scientific Collections
University of Alabama, Box 870345
Tuscaloosa AL 35487
"James gave the huffle of a snail in
danger But no one heard him at all" A.
A. Milne
Received on Thu Aug 18 15:49:19 2005

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