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Support for chromosomal theory of cancer found in cancers' development of drug resistance

Berkeley Thirty-six years into the war on cancer, scientists have not only failed to come up with a cure, but most of the newer drugs suffer from the same problems as those available in the pre-war days: serious toxicity, limited effectiveness and eventual resistance.

This is no surprise to University of California, Berkeley, genetics researcher Peter Duesberg, professor of molecular and cell biology. According to his novel yet controversial "chromosomal" theory of cancer, which is receiving increased attention among cancer researchers, each cancer is unique, and there is no magic bullet.

"The mutation theory of cancer says that a limited number of genes causes cancer, so cancers should all be more or less the same," Duesberg said. The chromosomal theory, which he laid out in an article in the May 2007 issue of Scientific American, implies instead that, "even if cancers are from the same tissue, and are generated with the same carcinogen, they are never the same. There is always a cytogenetic and a biochemical individuality in every cancer."

The most that can be expected from a drug, he said, is that it is less toxic to normal cells than cancer cells, and that as a result a cancer detected early can be knocked back by chemotherapy. His chromosomal theory offers hope of early detection, however, since it ascribes cancer to chromosomal disruption, called aneuploidy, that can be seen easily through a microscope.

"By screening for aneuploidy, you could detect the cancer early and also see what possible drugs to use and whether drugs would even help," Duesberg noted. "Then, you wouldn't have to give a cocktail of drugs that includes all the best poisons, but you could leave out those you could tell wouldn't work. If you could cut chemotherapy drug toxicity in half or two-thirds, and direct it better at cancer, that is some progress. But it is not a cure."

Duesberg and colleagues discuss the major problem of drug resis
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Contact: Robert Sanders
rsanders@berkeley.edu
510-643-6998
University of California - Berkeley
27-Jun-2007


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