ANDREAS STRASSER

Key discoveries have been that abnormalities in cell death can cause cancer or autoimmune disease; that BCL-2 antagonises multiple pathways to cell death; that activation of the BCL-2 regulated apoptotic pathway is critical for the response of malignant cells to anti-cancer therapeutics; that BCL-2 inhibits the death of lymphocytes that fail to receive a signal through cytokine or antigen receptors; that BCL-2 and death receptors regulate distinct pathways to apoptosis; that DNA damage can induce apoptosis in lymphocytes via a pathway that is independent of p53 but can be blocked by BCL-2; the discovery of pro-apoptotic BH3-only proteins BIM and BMF; that BH3-only proteins are essential for initiation of programmed cell death and stress-induced apoptosis; that BIM is required for negative selection of autoreactive T and B lymphoid cells; that the BH3-only proteins PUMA and NOXA are essential for DNA damage-induced apoptosis mediated by the tumour suppressor p53 or its relative p63; that coordination of DNA repair is critical for p53-mediated tumour suppression.