By Leland W. K. Chung, William B. Isaacs, Jonathan W. Simons

ISBN-10: 0585439648

ISBN-13: 9780585439648

ISBN-10: 0896038688

ISBN-13: 9780896038684

ISBN-10: 1588296962

ISBN-13: 9781588296962

Prime melanoma biologists and medical researchers comprehensively overview the most recent uncomplicated study and its translational importance for the molecular biology and genetics of prostate melanoma and its software in constructing novel therapeutics. Highlights of contemporary molecular genetics learn comprise new mild on inactivated tumor suppressor genes, HPC households, the function of the androgen receptor, the development of prostate melanoma, and promising effects from transcriptome profiling and proteomics. study into the fundamental biology and regulatory mechanisms controlling prostate melanoma development and development has published many new probabilities for healing intervention, together with mobilephone adhesion molecules, the androgen receptor, use of the nuclear matrix, Caveolin-1, and the prostate-specific membrane antigen. entire and state of the art, Prostate melanoma: Biology, Genetics, and the hot Therapeutics synthesizes the entire significant contemporary paintings that's not in basic terms swiftly unraveling the mysteries of prostate melanoma, but additionally dramatically bettering trendy healing techniques.

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Extra info for Prostate Cancer: Biology, Genetics, and the New Therapeutics (Contemporary Cancer Research)

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B. Henderson, M. Yu, C. Shi, M. Pike, R. Ross, et al. 1997. Genetic variation of 3 beta-hydroxysteroid dehydrogenase type II in three racial/ethnic groups: implications for prostate cancer risk. Prostate 33: 9–12. 15. Durrin, L. , R. Haile, S. Ingles, and G. Coetzee. 1999. Vitamin D receptor 3′-untranslated region polymorphisms: lack of effect on mRNA stability. Biochim. Biophys. Acta 1453: 311–320. 16. , H. Hammond, L. Jin, C. Caskey, and R. Chakraborty. 1992. Genetic variation at five trimeric and tetrameric tandem repeat loci in four human population groups.

Cox proportional hazards analysis in the case relatives revealed that risk was particularly increased to relatives of younger probands (<55 yr). These studies suggest a familial clustering in risk to prostate cancer, but do not directly address the underlying etiologic mechanism. Indeed, familial clustering can reflect either a shared environmental risk factor or a genetic mechanism. Two approaches which can be used to distinguish these possibilities are twin studies and complex segregation analysis.

Interestingly, a region on chromosome X was implicated in the genome-wide scan for linkage described by Smith et al. (76). In a follow-up study, this region was analyzed in a combined study population of 360 prostate cancer families collected at four different sites in North America, Finland, and Sweden. Evidence of linkage to Xq27-28 was observed at the locus termed HPCX (86). 85 between DXS1120 and DXS297. Significant evidence for locus heterogeneity was observed, with 16% of the families in the combined study population estimated to be linked to HPCX, and a similar proportion in each separate family collection.

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Prostate Cancer: Biology, Genetics, and the New Therapeutics (Contemporary Cancer Research) by Leland W. K. Chung, William B. Isaacs, Jonathan W. Simons

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