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In the 14 April 2005 issue of Nature (Vol. 434, No. 7035), two papers (pp. 864-870, 907-913) offer insights into how cells can fight off the earliest stages of cancer.
Biologists have wondered why human cancer is not more frequent, given the trillions of susceptible cells and the countless mutations that could potentially trigger uncontrolled cell proliferation. One intensely debated idea is that cells usually recognize and stop abnormal division. Teams led by Jiri Bartek and Thanos Halazonetis now show that cells in very early stage human cancers from different tissues (including bladder, breast, colon and lung) activate a series of events involved in recognizing and repairing DNA damage. These include activation of the tumour suppressor protein p53. They suggest that aberrant cell division at the earliest stages of carcinogenesis triggers DNA damage - and that the cell responds by activating a programme of DNA repair that arrests cell division and can trigger cell death. The authors suggest that uncontrolled cell division somehow upsets the DNA replication process so that mistakes are introduced. Their results suggest why mutations that disable the DNA repair process, such as p53 mutations, are commonly associated with cancer and help it to progress. CONTACT Jiri Bartek (Institute of Cancer Biology, Copenhagen, Denmark)
E-mail: jb@cancer.dk Thanos Halazonetis (The Wistar Institute, Philadelphia, PA, USA)
E-mail: halazonetis@wistar.upenn.edu Ashok R. Venkitaraman (University of Cambridge, UK)
E-mail; arv22@cam.ac.uk (C) Nature press release.
Message posted by: Trevor M. D'Souza
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