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Breast cancers caused by mutations in BRCA1 and BRCA2 genes might be halted via a novel and targeted therapeutic strategy: interfering with the process of DNA repair
BRCA1 and BRCA2 are important for the repair of DNA damage by homologous recombination, a process in which the faulty section of DNA is swapped for a matching, healthy one. Groups led by Alan Ashworth and Thomas Helleday now show Nature (14 April 2005, Vol. 434, No. 7035, pp. 917-921 & 913-917), that another enzyme involved in DNA repair, called poly(ADP-ribose) polymerase (PARP), becomes essential in cells that lack a working form of BRCA1 or BRCA2. Blocking PARP activity appears to leave breaks in DNA, which cause damage that cannot be repaired by recombination when BRCA1 or BRCA2 is absent. The groups show that blocking PARP slows the growth of BRCA2-deficient tumours in mice. This same approach might be used to treat human breast cancer, because only the tumour cells in which BRCA1 or BRCA2 have stopped working would be killed. CONTACT Alan Ashworth (The Institute of Cancer Research, London, UK) Paper [1]
E-mail: alan.ashworth@icr.ac.uk Thomas Helleday (Currently at: Stockholm University, Sweden) Paper [2]
E-mail: t.helleday@sheffield.ac.uk (C) Nature press release.
Message posted by: Trevor M. D'Souza
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