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BH3-only proteins in cell death initiation, malignant disease and anticancer therapy Labi V; Erlacher M; Kiessling S; Villunger ACell Death Differ 2006[Aug]; 13 (8): 1325-38Induction of apoptosis in tumour cells, either by direct activation of the death receptor pathway using agonistic antibodies or recombinant ligands, or direct triggering of the Bcl-2-regulated intrinsic apoptosis pathway by small molecule drugs, carries high hopes to overcome the shortcomings of current anticancer therapies. The latter therapy concept builds on a more detailed understanding of how Bcl-2-like molecules maintain mitochondrial integrity and how BH3-only proteins and Bax/Bak-like molecules can undermine it. Means to unleash the apoptotic potential of BH3-only proteins in tumour cells, or bypass the need for BH3-only proteins by blocking possible interactions of Bcl-2-like prosurvival molecules with Bax and/or Bak allowing their direct activation, constitute interesting options for the design of novel anticancer therapies.|Animals[MESH]|Cell Death[MESH]|Cell Transformation, Neoplastic[MESH]|Humans[MESH]|Neoplasms/genetics/*metabolism/*pathology/therapy[MESH]|Proto-Oncogene Proteins c-bcl-2/classification/genetics/*metabolism[MESH]|Tumor Suppressor Protein p53/metabolism[MESH] |
