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

tance in cancer and how it supports the chromosomal theory of cancer in a paper appearing in the current issue of the journal Drug Resistance Updates (Vol. 10, issue 2).

Duesberg proposed in 2000 that the assumption underlying most cancer research today is wrong. That assumption, that cancer results from a handful of genetic mutations that drive a cell into uncontrolled growth, has failed to explain many aspects of cancer, he said, and has led researchers down the wrong path.

His alternative theory is that cancer results from aneuploidy - that is, duplication or sometimes loss of one or more of our 46 chromosomes, which throws thousands of genes out of whack. This condition, generated by a defect in the mechanism that duplicates chromosomes during cell growth, leads to more and more chromosomal disorder as the cells divide and proliferate, disrupting even more genes and providing ample opportunity for the development of resistance to drugs being used to control the cancer.

"In this new study and in one published in 2005, we have proved that only chromosomal rearrangements, rather than mutations, can explain the high rates and wide ranges of drug resistance in cancer cells," he said.

Duesberg even argues that the anti-leukemia drug imatinib (Gleevec), the poster child for rational drug design once hailed as a therapy that would make drug resistance a thing of the past, has been rendered less useful because the aneuploid nature of leukemia has led to resistance. In fact, he said, this resistance suggests that imatinib is not a highly targeted drug, as advertised, but just another cell "poison" that happens to kill more leukemia cells than normal cells.

Development of drug resistance in cancer is one of the strongest arguments for the aneuploidy, or chromosomal, theory of cancer, Duesberg said, and is one aspect of cancer that can be studied experimentally. Normal cancers typically take decades to develop, making it har
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Contact: Robert Sanders
rsanders@berkeley.edu
510-643-6998
University of California - Berkeley
27-Jun-2007


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