Retention of γH2AX foci as an indication of lethal DNA damage.

Abstract

The application of biological responses of tumours to predict clinical responses to treatment represents a challenging goal with the potential to inform treatment decisions and improve outcome. If tumour cell death is the result of the inability of a cell to repair complex DNA damage, and if γH2AX foci mark sites of unrepaired double-strand breaks, then it may be possible to use residual γH2AX foci to identify treatment-resistant tumour cells early in the course of therapy. This review will highlight some of the evidence that supports the idea that residual γH2AX foci, within certain limitations, may be useful as an early indicator of tumour response to radiotherapy in situ, either alone or in combination with chemotherapy.