“…The finding that bci-2 provides a survival advantage for the cells [4043] by preventing the onset of apoptosis [44,45] suggests that, in some cells, programmed death may bc negatively modulated by other genes. hcl-2 has been shown to be involved in prevention of apoptosis in T cells [46], thymocytes [47], germinal center 6 ceils and Burkitt lymphoma cells [48], and in pre-B leukemia lines [49]. Recent evidence suggests that high levels of bcl-2 enhances cell survival under conditions of repressed c-rrt~+c expression, probably by mobilisation of Ca" from mitochondria to cytoplasm.…”