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Download Prostate Cancer: Biology, Genetics, and the New Therapeutics by Leland W. K. Chung, William B. Isaacs, Jonathan W. Simons PDF

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

Major melanoma biologists and medical researchers comprehensively assessment the newest simple learn and its translational value for the molecular biology and genetics of prostate melanoma and its program in constructing novel therapeutics. Highlights of modern molecular genetics examine contain new mild on inactivated tumor suppressor genes, HPC households, the position of the androgen receptor, the development of prostate melanoma, and promising effects from transcriptome profiling and proteomics. learn into the fundamental biology and regulatory mechanisms controlling prostate melanoma progress and development has printed many new percentages for healing intervention, together with cellphone adhesion molecules, the androgen receptor, use of the nuclear matrix, Caveolin-1, and the prostate-specific membrane antigen. accomplished and state of the art, Prostate melanoma: Biology, Genetics, and the recent Therapeutics synthesizes all of the significant contemporary paintings that's not merely swiftly unraveling the mysteries of prostate melanoma, but additionally dramatically enhancing modern healing methods.

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

Sample text

ASSOCIATION STUDIES Association studies are generally case-controlled studies based on a comparison of the frequency of an allele in unrelated cases and normal controls. A significant difference in the allele frequency between cases and controls can be expected if the allele sequence itself is causal, or if the allele is in linkage disequilibrium (LD) with a disease-causing mutation. Since LD can only be observed when two markers are closely linked, a significant finding of LD can pinpoint the location of the disease gene.

Although association studies for fine mapping have been performed successfully in many simple Mendelian diseases, this approach presents some difficulty in complex diseases, particularly in genetically heterogeneous populations. Association studies are susceptible to etiological heterogeneity (genetic or environmental), inheritance (dominant, recessive, or X-linked), and locus heterogeneity, as well as allelic (same gene but different mutations) and founder (same mutation exists in different genetic background) heterogeneity.

1995. S. blacks and whites with a family history of cancer. Int. J. Cancer 60: 361–364. 34. Hsieh, C. , I. Oakley-Girvan, R. Gallagher, A. Wu, L. Kolonel, C. Teh, et al. 1997. Prostate cancer susceptibility locus on chromosome 1q: a confirmatory study (letter; comment). J. Natl. Cancer Inst. 89: 1893,1894. 35. Ingles, S. , R. Ross, M. Yu, R. Irvine, G. La Pera, R. Haile, et al. 1997. Association of prostate cancer risk with genetic polymorphisms in vitamin D receptor and androgen receptor (see comments).

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