By J. Martin Brown PhD, Bradly G. Wouters PhD (auth.), John A. Hickman, Caroline Dive (eds.)
The prior few years have witnessed an brilliant foreign attempt that validated the function of a few 20 new molecules in apoptosis and extra activation or suppression of apoptosis to the authorised organic services of an outstanding many others already usual in melanoma biology. a few of these molecules are receptors, transducing cytokine-mediated signs; others seem to accentuate or shrink the danger compro mised cellphone will hearth its apoptosis effector mechanism. All are of curiosity as power objectives for tumor remedy, and a few might end up to be keep watch over issues prompted within the pathogenesis of melanoma and different ailments as various as viral an infection, neurodegenerative issues, and stroke. occasionally, in the course of those advancements, a type of euphoria ap pears to have gripped the learn group, with the expectancy that apoptosis will manage to pay for causes to many unsolved questions in cellu lar law. This publication, in a sequence of considerate and provocative ar ticles--some from validated leaders within the box, and others from more youthful scientists--seeks to redress the balance.
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Hence, the outcome of p53 activation in tumors does not simply reflect tissue of origin, but also may be determined by the cumulative impact of the oncogenic mutations in each tumor cell. These issues, in tum, may have a substantial impact on p53's relationship to chemosensitivity. Chapter 2 I p53, Apoptosis, and Chemosensitivity 29 THERAPEUTIC STRATEGIES An improved understanding of the relationship between p53 and chemosensitivity may lay the groundwork for new cancer therapies. In tumors that retain p53 function, it may be possible to superactivate p53 to promote apoptosis in combination with standard chemotherapy.
Upon activation, p53 regulates a series of target genes, including the p21 CIPIIWAFI cyclin-dependent kinase inhibitor and Bax. p53 also associates with a series of cellular or viral proteins that modulate its activity, including Mdm2, HPV E6, p33 ING , and p19 ARF (1,2,56-,57-). Extragenic mutations that affect p53 function occur in human cancer; for example, HPV E6 in cervical carcinomas; Mdm-2 in a variety of tumors, and Bax in heredity nonpolyposis colorectal Chapter 2 I p53, Apoptosis, and Chemosensitivity 27 cancer-type colon cancer (1,2,58").
Radiation apoptosis of serous acinar cells of salivary and lacrimal glands. Cancer 1991; 67: 1539-1543 . 51. Kastan MB, Onyekwere 0, Sidransky D, Vogelstein B, Craig RW. Participation of p53 protein in the cellular response to DNA damage. Cancer Res 1991; 51: 6304-6311. Seminal paper established the paradigm that the G I arrest following ionizing radiation is mediated by wild-type p53. Chapter 1 I Apoptosis and Cell Sensitivity 19 052. Brown JM. NCI's anticancer drug screening program may not be selecting for clinically active compounds.