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VIRUS TAKES ADVANTAGE OF CANCER
A virus that exploits a gene defect common to cancer cells and selectively kills them may offer a new avenue for therapy, suggest researchers in this week’s Nature (Vol. 412, No. 6850, 30 Aug 2001).
The gene p53 is mutated in about half of all human cancers (an event directly implicated in tumour progression) so a way of killing such cells offers the attractive possibility of treating multiple cancer types with one drug. The human adeno-associated virus (AAV) selectively induces cell death in p53-defective cells, Peter Beard and his colleagues of the Swiss Institute for Cancer Research (ISREC) in Epalinges, Switzerland, have now discovered. Cells retaining their copy of p53 instead halt cell division.
Even AAVs engineered to lack all genes and containing only hairpin-looped DNA ends cause cell death, suggesting that the viral DNA structure mimics DNA damage in the cell. Cells have very sensitive sensors for DNA damage that can activate repair mechanisms or drive them to suicide to prevent mutation accumulation and hence potential oncogenic transformation. Tumours in mice were also reduced by injection of the virus, the team found. Continued research into strategies to exploit p53 should eventually lead to one that bears fruit — "each of which has the potential to benefit millions," say Bert Vogelstein and Kenneth Kinzler at the Howard Hughes Medical Institute and Johns Hopkins Oncology Center in Baltimore, Maryland, in an accompanying News and Views article. CONTACT: Peter Beard
tel +41 21 692 5921
e-mail peter.beard@isrec.unil.ch Bert Vogelstein
tel +1 410 955 8877
e-mail vogelbe@welch.jhu.edu Kenneth Kinzler
tel +1 410 955 2928
e-mail kinzlke@welchlink.welch.jhu.edu (C) Nature press release.
Message posted by: Trevor M. D'Souza
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