Peter Duesberg, professor of molecular and cell biology at the University of California, Berkeley, considers 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 and has led researchers down the wrong path.
His alternative theory, which is receiving increased attention among cancer researchers, 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.
Professor Duesberg suggests 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.
Development of drug resistance in cancer is one of the strongest arguments for the aneuploidy, or chromosomal theory of cancer according to professor Duesberg. The major problem of drug resistance in cancer and how it supports the chromosomal theory of cancer is discussed in a paper appearing in the current issue of the journal Drug Resistance Updates
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