Inactivating mutations of proapoptotic Bad gene in human colon cancers

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Inactivating mutations of proapoptotic Bad gene in human colon cancers.

Evidence exists that deregulation of apoptosis is involved in the mechanisms of cancer development, and the somatic mutations of apoptosis-related genes have been reported in human cancers. Bcl-XL/Bcl-2-associated death promoter (Bad), a proapoptotic member of Bcl-2 family, plays an important role in the intrinsic apoptosis pathway. To explore the possibility that the genetic alterations of Bad...

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Inactivating germ-line and somatic mutations in polypeptide N-acetylgalactosaminyltransferase 12 in human colon cancers.

Aberrant glycosylation is a pathological alteration that is widespread in colon cancer, and usually accompanies the onset and progression of the disease. To date, the molecular mechanisms underlying aberrant glycosylation remain largely unknown. In this study, we identify somatic and germ-line mutations in the gene encoding for polypeptide N-acetylgalactosaminyltransferase 12 (GALNT12) in indiv...

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Proapoptotic Bad and Bid protein expression predict survival in stages II and III colon cancers.

PURPOSE Proapoptotic BH3-only proteins Bad and Bid initiate apoptosis by binding to regulatory sites on prosurvival Bcl-2 proteins to directly neutralize their function. We determined if expression of these proteins in colon cancers may account for differences in patient survival. EXPERIMENTAL DESIGN Tumor-node-metastasis stages II and III primary colon carcinomas from patients treated in 5-f...

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Mutations of p53 Gene in Skin Cancers: a Case Control Study

Background: The most frequently mutated tumor suppressor gene found in human cancer is p53. In a normal situation, p53 is activated upon the induction of DNA damage to either arrest the cell cycle or to induce apoptosis. However, when mutated, p53 is no longer able to properly accomplish these functions. The aim of this study was to investigate the expression of p53 gene in cases of skin cancer...

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Much excitement has recently been generated by the discovery of the Smad genes, encoding proteins that transduce signals from the transforming growth factor beta family of cytokines. Here, we report the completion of cloning of the six known human Smads, providing novel sequences for Smad5 and Smad6. Previously, Smad4 and Smad2 were shown to be mutated in human cancers. However, analysis of the...

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ژورنال

عنوان ژورنال: Carcinogenesis

سال: 2004

ISSN: 1460-2180,0143-3334

DOI: 10.1093/carcin/bgh145