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Forces Comité van Aanbeveling

Analysis: Lung-cancer cause blows more smoke than facts

Wednesday, 18 October 2000 17:49 (ET)


 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 lung-cancer cells.

 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 tumors.

 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. 17 ().

 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 nonsmokers.

 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 effects.

 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.

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