Mutation of BCL-2 Family Proteins in Cancer.
Apoptosis is a genetically controlled cell death process that is required for normal development and tissue homeostasis. Suppression of apoptosis can confer a growth advantage to cells and contribute to cancer; many cancers are relatively resistant to apoptosis, including that induced by radiation or chemotherapeutics. Mutations which inactivate pro-apoptotic or activate anti-apoptotic proteins in cancer cells are therefore likely to be responsible for some of these differences. BCL-2 family proteins are key regulators of apoptosis and there is evidence supporting a role for mutation of BCL-2 family proteins in cancer. This includes well established events such as activation of BCL-2 via translocations in follicular lymphoma, as well as more recent observations implicating activation of Bcl-X(L) expression and frameshift and missense mutations of BAX and BCL-2 in cancer.
Packham
G
G
Ludwig Institute for Cancer Research and Virology and Cell Biology, Department of Medical Microbiology, Imperial College School of Medicine at St Mary's, Norfolk Place, London, W2 1PG, UK. g.packham@ic.ac.uk