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Analysis: Lung-cancer cause blows more smoke than facts
Wednesday, 18 October 2000 17:49 (ET)
By DAMARIS CHRISTENSEN, UPI Science News
WASHINGTON, Oct. 18 -- Although a duo of scientists has just
proposed the mechanism through which smoking causes cancer is different from
previous theory, experts in the field call the claim premature and overstated.
About two years ago, researchers showed a chemical in tobacco bound
to a cell's genetic material at the same places likely to be mutated in
The conclusion: that when the compound -- called benzopyrene diol
epoxide -- binds to DNA, it disrupts the normal process of copying DNA and
thus introduces errors into the cells. Eventually, such mutations can cause
cells to grow faster than normal, pile up on each other, and form cancerous
But Sergei Rodin of the Beckman Research Institute of the City of
Hope in Duarte, Calif., argues that instead of directly triggering those
mutations, smoking primarily causes cancer by promoting the growth of cells
whose genetic material was already damaged in other ways.
This selective pressure then ensures that cells with particular
mutations divide faster and can become tumors, he suggested in an article in
the Proceedings of the National Academy of Sciences, published online on Oct.
Rodin's claims, however, are debated by most scientists, who say
instead that smoking both triggers genetic damage and encourages the growth of
these damaged cells.
"The most important point is that, very clearly, this is not an
issue of whether cigarette smoke is responsible for cancer but simply a
question of how that happens," noted David Sidransky of the Johns Hopkins
Medical Institutions, Baltimore. "This is a very subtle distinction. At
the very least they are accentuating a controversy that is minimal, since most
scientists agree that not just genetic mutations but also selection pressure
(imposed by tobacco smoke) is important in causing cancer."
"The idea that cancer is more than just a mutation has been
around a long time," agreed Curtis Harris of the National Cancer
Institute in Bethesda, Md. "Are their arguments (that it is primarily due
to selection) compelling? The answer is no."
Rodin and his coauthor Andrew Rodin of the University of Texas-Health
Sciences Center in Houston looked at mutations in a gene known as p53, an
"emergency brake" that causes cells to undergo programmed cell death
when the cells are stressed by, for example, DNA damage. Mutations that
inactivate this gene are common in many cancers, including lung cancer.
Looking at a database of common mutations in this gene among a number
of cancers, Rodin and his son concluded that a particular kind of mutation
believed to be caused by benzopyrene was no more common in smokers than in
They also looked at cancers in areas of the body less directly
exposed to smoke than the lung or mouth, such as cancers of the skin, blood,
and colon, and reported that particular mutations were no more common in lung
cancers than in these tumors.
These findings led the two researchers to conclude the role of
benzopyrene in causing lung cancer was overstated.
Instead, they suggest other factors, such as physiologic stress
imposed on the lung from tobacco smoke, are really the culprit in
smoke-associated lung cancers.
To test the theory, Rodin looked at silent mutations -- mutations in the
DNA that don't affect the resulting protein and thus, essentially, have
no effect. Rodin reasoned that if silent mutations were due to carcinogenic
effects of benzopyrene, they should be should be more common in smokers than
non-smokers. However, he found they were equally likely.
However, such databases contain data that may be inaccurate or
misclassified, cautioned Sidransky. And since silent mutations are very rare,
it's difficult to prove a point based on this finding, he said.
"To a medical doctor, it doesn't matter what the mechanism is:
smoking is still bad for you," said Rodin's colleague Gerald Holmquist of
the Beckman Research Institute at the City of Hope.
Rodin's work "suggests that the mechanism by which [compounds in
smoke] are inducing mutations is different than previously believed,"
Holmquist told UPI. That's important, he added, because it means carcinogenic
compounds in isolation or in different situations might have different
Further, if Rodin's arguments were to be confirmed, it's possible
that ways of minimizing the risk of lung cancer might be developed.
"The problem is, we already know that the best way to prevent
lung cancer is to avoid smoking," Sidransky said. "There's no need
to change that message."
Copyright 2000 by United Press International.
All rights reserved.