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Download Oncogenes and Tumor Suppressor Genes in Human Malignancies by Edison Liu, Bernard Weissman (auth.), Christopher C. Benz, PDF

By Edison Liu, Bernard Weissman (auth.), Christopher C. Benz, Edison T. Liu (eds.)

The first version of Oncogenes (1989) thinking about numerous of the higher recognized remodeling mechanisms and surveyed a spectrum of good tumors and hematologic malignancies. a number of of the approximately 50 identified oncogenes such a lot correct to human illness have been tested. by contrast, this quantity provides a truly assorted profile and stability of material that displays the speedily altering box of molecular oncology and its newly rising recommendations. one of the most vital discoveries of the prior four years are the id of approximately a dozen varied tumor suppressor genes and the discovering of a wholly new category of cancer-causing gene (bcl-2) that acts by means of inhibiting mobile dying instead of stimulating mobile proliferation. This variation starts through reviewing chosen malignancies within which our past look for clinically suitable oncogenes has ended in extra concentrated reviews on gain-of-function and loss-of-function genetic abnormalities, in addition to autocrine and paracrine progress issue loops recognized to control tumor body structure and malignant telephone habit. interestingly, a lot of those genetic and useful abnormalities are shared via numerous varied tumor varieties and aren't uniformly found in all tumors of an analogous sort. This remark brings up molecular questions on the tissue-specific determinants that underlie person cancers and in addition provides extra impetus to the recommendation that molecular abnormalities (referred to as tumor markers) be incorporated one of the histopathologic positive factors used for medical prognosis and deal with­ ment.

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In contrast, these 26 mutations are frequently found in carcinogen-induced rodent mammary carcinomas, and activated ras oncogenes readily produce mammary cancers in transgenic mouse models. N-nitroso-N-methylurea (NMU) will consistently induce estrogendependent mammary cancers in female rats after a 6 to 12-month delay. Over 80% of these mammary tumors contain a GGA to GAA mutation in codon 12 of the c-Ha-ras gene, in keeping with the ability of NMU to methylate the N7 and 0 6 positions, thus causing G to A mutations [181].

Overexpression of p21 ras has been observed in 21-83% of cases [170,187,191,193-202], with the wide variation in this observed incidence probably due to different antibodies, techniques, and threshholds for positivity used by the different investigators. Most studies have shown that p21 ras is overexpressed in both malignant and benign breast neoplasms but not in normal breast tissue. , however, found no significant difference in p21 ras staining between breast cancers, benign breast tumors, or the normal breast tissue adjacent to tumors using the same antibody [203].

Both amplification and overexpression of c-erbB-2 have since been shown to correlate with reduced survival in patients with other adenocarcinomas, particularly ovarian cancer [247,248]. Overexpression of c-erbB-2 in the absence of gene amplification has been associated with worse prognosis for patients with lung adenocarcinomas [249]. Since the first clinical reports on c-erbB-2, numerous retrospective studies have been performed using archival tumor tissues and patient follow-up data in attempts to determine the actual incidence and clinical significance of c-erbB-2 amplification and overexpression in human breast cancers (Table 2).

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