Cancer: surviving on the edge.
Tumors arise from normal cells through the acquisition of multiple genetic alterations that endow cancer cells with the phenotypes associated with neoplasia. Although we still lack a complete understanding of the specific complement of mutations that together program the behavior of any particular cancer, several lines of evidence indicate that many of these alterations perturb regulatory networks critical for cell proliferation, growth, and survival. As such, cancer cells maintain a precarious balance among unfettered proliferation, genomic instability, cell cycle arrest, and apoptosis. This year's Beatson International Cancer Conference focused on recent advances in our understanding of the pathways that regulate senescence, apoptosis, and cancer.
Hahn
William C
WC
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA. william_hahn@dfci.harvard.edu
D017209:Apoptosis; D002455:Cell Division; D002470:Cell Survival; D002471:Cell Transformation, Neoplastic; D016922:Cellular Senescence; D043171:Chromosomal Instability; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D009369:Neoplasms / Q000235:genetics*; D013312:Stress, Physiological; D019098:Telomerase / Q000502:physiology; D016615:Telomere / Q000502:physiology
D019098:Telomerase