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Cancer, human somatic mutations

Greenman C, Stephens P, Smith R, et al (2007) Patterns of somatic mutation in human cancer genomes. Nature 446 153-158... [Pg.1012]

Human exposures to RF radiation arise from military use, industrial use, broadcasting, and cellular phone use. These exposures have been linked to increased numbers of spontaneous abortion, neurological effects, altered red and white blood cell counts, increased somatic mutation rates in lymphocytes, cardiovascular effects, increased cancer risk, and increased childhood cancers/28 311 Other studies.however, have refuted these findings) 27,32 As stated in the introduction, only a relatively few studies addressed the combined effects of toxic chemical and RF exposure. A thorough search of the literature shows that such studies have not been refuted. The following are illustrative examples of these mixture studies. [Pg.252]

Pleasance ED, Cheetham RK, Stephens PJ, McBride DJ, Humphray SJ, Greenman CD et al (2010) A comprehensive catalogue of somatic mutations from a human cancer genome. Nature 463 191-1964... [Pg.64]

Erickson RP (2010) Somatic gene mutation and human disease other than cancer an update. Mutat Res 705 96-106... [Pg.326]

Miyamoto H, Kubota Y, Fujinami K, et al. Infrequent somatic mutations of the pl6 and pl5 genes in human bladder cancer pl6 mutations occur only in low-grade and superficial bladder cancers. Oncol Res. 1995 7 327. [Pg.656]

Sevenet N, Lellouch-Tubiana A, Schofield D, et al. Spectrum of hSNF5/INIl somatic mutations in human cancer and genotype-phenotype correlations. Hum Mol Genet. 1999 8 2359-2368. [Pg.688]

The first hint of a link between Wnt signaling and cancer was observed when ectopic expression of Wnt-1 was found to promote the formation of mouse mammary tumors (Nusse and Varmus, 1982). However, subsequent research has not been able to establish a direct link between Wnt signaling and human breast cancer. During recent years, much attention has focused on the molecular events contributing to the transformation of colon epithelial cells following loss of function of the tumor suppressor protein APC. The vast majority of germline and somatic mutations in APC result in the for-... [Pg.17]

As in cancer predisposing syndromes, these genetic alterations are sometimes carried in the germline. Among human tumours, heritable mutations are an exception. Most alterations are acquired in somatic life in the form of chromosomal translocations, deletions, inversions, amplifications or point mutations. Certain oncogenic viruses play important roles in a few human tumours. Examples are human papilloma-virus in cervical cancer and skin tumours, Ep-stein-Barr virus in nasopharyngeal carcinoma and Burkitt s lymphoma, and human T-cell leukaemia viruses (e.g. HTLV-I, HTLV-II) in T-cell leukaemia. [Pg.200]

BRCAl and BRCA2 are frequently mutated in a variety of human cancers. Breast cancer is the most common malignancy in women. A total of more than a million women will be diagnosed with breast cancer worldwide with more than 400,000 deaths annually. The germ line mutations of BRCAl/2 are associated with hereditary breast cancer which account for 5-7% of all breast cancer cases (12, 13). Ovarian cancer is the leading cause of death from gynecological cancer with more than 140,000 deaths annually worldwide. The germ line and somatic BRCAl/2 mutations have been reported to occur in approximately 10% of ovarian cancer patients (14, 15). BRCAl/2 mutations have also been shown to occur frequently in Ashkenazi Jewish families with pancreatic cancer (16). [Pg.127]


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See also in sourсe #XX -- [ Pg.539 ]




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