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Oncogene. 1996 Aug 1;13(3):655-9.

Induction of p53 and increased sensitivity to cisplatin in ataxia-telangiectasia cells.

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Queensland Cancer Fund Research Unit, Queensland Institute of Medical Research, Brisbane, Australia.


Several reports have demonstrated a defective p53 response to ionizing radiation exposure in ataxia-telangiectasia (A-T) cells. On the other hand, p53 induction was normal after u.v. irradiation, an agent to which A-T cells are not hypersensitive. We show here that A-T cells are more sensitive than normal lymphoblastoid cells to cisplatin treatment but the rate of induction of p53 by cisplatin is similar in both cell types. In addition, the half-life of p53, both in the induced and uninduced forms, is the same in A-T and normal lymphoblastoid cells. The use of a reporter assay to determine the functional status of p53 confirmed the results obtained in the induction experiments with cisplatin. These results demonstrate that p53 induction status in A-T cells does not correlate with sensitivity to the inducting agent and there is no inherent defect in the turn-over of p53 in the induced or uninduced states in A-T.

[Indexed for MEDLINE]

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