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THE MOSS REPORTS Newsletter (07/26/03)

 

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Ralph W. Moss, Ph.D. Weekly CancerDecisions.com

Newsletter #92 07/26/03

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HIGH PRAISE

 

 

 

For the last 9 years, we at the Moss Reports have tried

to be helpful and approachable to all people who are

grappling with the difficult problem of cancer.

Recently, we received a letter about one of our

employees, Dr. Louise Kehoe, that I wanted to share

with you. A client wrote: " I am very moved by the work

that Louise put into her report to us. Please thank

her, on behalf of myself, my father, sister, and

brother-in-law. If nothing else it opens the heart to

know that there are people out there you don't know who

will go to bat for you in this way " (Howard R.) It is

comments like this that keep us going and make us so

proud of our entire staff. If we can be of help to you

in your struggle, just let us know.

 

 

Incidentally, our summer sale on our comprehensive Moss

Reports on specific cancer diagnoses continues. You can

still save $50 off the normal cost of $297 if you order

now. Just call Anne or Diane at 800-980-1234

(814-238-3367 if calling from abroad) and they will be

happy to help you.

 

 

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WHAT CAUSES CANCER? PART ONE

 

 

 

" Funny thing, cancer. " He lit a cigarette, and

considered the spent match. A crop duster flew

overhead, and he waved his arms in greeting. " Yes, sir,

it's a real mystery. "

-David Sedaris, Naked (1997), p. 164.

 

 

 

What causes cancer? Most people would say that it is

caused by cigarette smoke, pesticide residues, grilled

meats, or some other well-publicized carcinogen.

However, although there are statistical associations

between such exposures and cancer rates, none of them

can be considered the root cause of the disease. A

cause, by definition, must lead invariably to its

effects…or else it is simply a risk factor. For

example, many people in this barbeque season will eat

their fill of grilled meat, yet few will succumb to

dangerous tumors as a result. I once paid a memorable

visit to the Canadian town of Asbestos, and watched in

incredulity as the miners added insult to injury,

sitting around smoking unfiltered cigarettes and

tossing back beer after beer. Yet dangerous as their

life style might be, we know that many such individuals

never succumb to mesothelioma or lung cancer.

 

 

So what is the ultimate cause of cancer, or even of any

particular kind of cancer? For the last 25 years there

has been a consensus among cancer scientists that has

driven the field forward and has led to tremendous

optimism. Geneticists repeatedly assured us that they

were homing in on a final answer. Cancer, they agreed,

was in large measure a genetic disease. With the

deciphering of the human genome, we were told, sterling

new cures were close at hand.

 

 

Soon after the discovery of the two alleged " breast

cancer genes " (abbreviated BRCA-1 and BRCA-2), I

attended a meeting at Columbia University, at which a

jubilant scientist claimed that within just a few years

he and his colleagues would be able to " drop a bit of

tumor in one end of a machine and extract a

prescription at the other end. " Cancer patients in the

audience literally cheered. Cancer, scientists assured

us, was " the result of cumulative mutations that alter

specific locations on a cell's DNA and thus change the

particular proteins encoded by cancer-related genes at

those spots. "

 

 

These mutations could supposedly affect two opposite

kinds of genes. The first were tumor suppressor genes,

which produce proteins that normally restrain a cell's

tendency to divide in an uncontrolled manner. The

second were oncogenes - literally " cancer genes " - which

stimulate cell division and growth. An oncogene is

defined as a gene that, when activated or expressed at

higher than normal levels, can precipitate uncontrolled

cell growth and multiplication. If the brakes of tumor

suppression failed, the argument went, then the " gas

pedal " of the oncogenes would accelerate towards

cancerous growth.

 

 

Now, however, this conventional explanation of cancer

is coming unraveled, leaving room for some less

dogmatic theories. If you want to understand where

things stand on this crucial question I suggest that

you read " Untangling the Roots of Cancer, " in the July

2003 Scientific American. This article, by senior

writer W. Wayt Gibbs, provides an excellent overview of

the current controversy and reveals why the cancer

research establishment suddenly finds itself bereft of

a cogent theory to explain the overall phenomenon of

malignant growth.

 

 

The notion that cancer results from the interplay of

oncogenes and tumor suppressor genes is what Mr. Gibbs

aptly characterizes as the " standard dogma " of cancer's

causation. Drs. J. Michael Bishop and Harold Varmus

(now president of Memorial Sloan-Kettering Cancer

Center) shared the 1989 Nobel Prize in Physiology or

Medicine for their discovery of " the cellular origin of

retroviral oncogenes. " As of this morning, there were

86,885 scientific articles in PubMed, the National

Library of Medicine database, that discuss oncogenes,

and another 25,000 about tumor suppressor genes. That's

a lot of scientific ink spilled on a single theory.

 

 

" Some researchers still take it as axiomatic, " Gibbs

said, " that such growth-promoting changes to a small

number of cancer genes are the initial event and root

cause of every human cancer. " But now the link between

these genetic changes and the causation of most cancers

is in doubt.

 

 

It is startling (but also somewhat liberating) to

realize that in recent months, the standard dogma has

been severely battered on several fronts. For instance,

it has become apparent that five or six separate

regulatory systems -not a single oncogene - would have

to be disrupted in order for cancer to occur. The

dominant paradigm, says Gibbs, predicted that tumors

would grow " in spurts of mutation and expansion. "

Damage to a cell supposedly disables a tumor suppressor

gene (such as RB, p53 or APC) and thereby disrupts the

orderly assembly of proteins that would normally ensure

not only the integrity of that cell's genes but also

the whole process of cell division. Conversely, a

mutation supposedly increases the activity of a

dangerous cancer-precipitating oncogene, whose products

are then thought to stimulate a cell to reproduce until

eventually a tumor results.

 

 

The theory also predicts that all cancer cells in a

tumor should share an identical flaw that causes

malignant behavior. " If mutations, which are copied

from a cell to its progeny, give tumor cells their

powers, " ask Gibbs, " then shouldn't all clones in the

army be equally powerful? " They should. But they're

not. In fact tumors are anything but homogeneous masses

of identical clones, instead, they reveal an amazing

genetic diversity. Some are almost normal while others

are so different from normal that they might be thought

of as a new species. The supposed causes of cancer are

almost infinite in nature and are all over the genetic

map.

 

 

While a few genes (such as p53) are indeed mutated in

many cancers, others are sprinkled at random among

hundreds of different tumor types, millions of cases,

and billions of individual cancer cells. It is a

pattern of such mind-boggling complexity that no one is

likely to make sense out of it any time soon.

Scientists at Johns Hopkins, for instance, tested the

DNA from 476 tumors. The oncogene BRAF was altered in

two-thirds of the papillary thyroid cancers, but not in

any of several other kinds of thyroid cancer. And that

is just thyroid cancer; there are over a hundred other

kinds of cancer, each of which has its own unique

cellular and molecular intricacies.

 

 

To confuse matters further, oncogenes (as the name

implies) are supposed to cause or promote cancer. But

now it turns out that some oncogenes are more active in

normal cells than they are in cancerous ones!

Conversely, so-called " tumor suppressor " genes may not

suppress tumors at all, but may actually aid their

growth. For example, a suppressor gene called RB is not

disabled, but actually hyperactive in some colon

cancers. Perversely, says Gibbs, RB seems to protect

those tumors from their autodestruct mechanisms.

" Searching for the mere presence or absence of a gene's

protein is too simplistic, " Gibbs concludes. But that

search is precisely what has preoccupied many orthodox

cancer researchers for the last 25 years, and more than

a few glorious careers have been based on this

widespread and tenacious illusion.

 

 

To be concluded next week.

 

 

 

--Ralph W. Moss, PhD

 

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IMPORTANT DISCLAIMER

 

 

The news and other items in this newsletter are

intended for informational purposes only. Nothing in

this newsletter is intended to be a substitute for

professional medical advice.

 

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