How cancers escape their oncogene habit.
Many recent reports demonstrate that at least initially, the inactivation of an oncogene can induce sustained regression of even a highly invasive and genetically complex cancer. However, upon prolonged oncogene inactivation, some cancers ultimately relapse, becoming independent of the very oncogene that initiated the process of tumorigenesis. Understanding the specific mechanisms by which cancers can escape dependence upon a particular oncogene will be critical to anticipate mechanisms by which human cancers will evade therapies that target individual oncogenes. Thereby, more effective strategies will be developed to clinically treat cancer.
Giuriato
Sylvie
S
Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California 94305-5151, USA.
Felsher
Dean W
DW
D000818:Animals; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D006801:Humans; D051379:Mice; D023421:Models, Animal; D009369:Neoplasms / Q000378:metabolism*; D009374:Neoplasms, Experimental / Q000235:genetics / Q000378:metabolism; D009857:Oncogenes / Q000502:physiology*; D013629:Tamoxifen / Q000031:analogs & derivatives* / Q000494:pharmacology; D013752:Tetracycline / Q000494:pharmacology
D013629:Tamoxifen; C016601:afimoxifene; D013752:Tetracycline