Tumor suppressor genetics

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Tumor suppressor genetics.

The observation that mutations in tumor suppressor genes can have haploinsufficient, as well as gain of function and dominant negative, phenotypes has caused a reevaluation of the 'two-hit' model of tumor suppressor inactivation. Here we examine the history of haploinsufficiency and tumor suppressors in order to understand the origin of the 'two-hit' dogma. The two-hit model of tumor suppressor...

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Population genetics of tumor suppressor genes.

Cancer emerges when a single cell receives multiple mutations. For example, the inactivation of both alleles of a tumor suppressor gene (TSG) can imply a net reproductive advantage of the cell and might lead to clonal expansion. In this paper, we calculate the probability as a function of time that a population of cells has generated at least one cell with two inactivated alleles of a TSG. Diff...

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Cancer genetics: Tumor suppressor meets oncogene

The adenomatous polyposis coli (APC) tumor suppressor protein is inactivated by mutations in the majority of colorectal cancers. A recent study has revealed that alterations in the APC signaling pathway can result in the transcriptional activation of the c-MYC gene.

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DNA methylation of tumor suppressor genes in hepatocellular carcinoma

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Loss-of-function genetics in mammalian cells: the p53 tumor suppressor model.

Using an improved system for the functional identification of active antisense fragments, we have isolated antisense fragments which inactivate the p53 tumour suppressor gene. These antisense fragments map in two small regions between nt 350 and 700 and nt 800 and 950 of the coding sequence. These antisense fragments appear to act by inhibition of p53 mRNA translation both in vivo and in vitro....

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ژورنال

عنوان ژورنال: Carcinogenesis

سال: 2005

ISSN: 1460-2180,0143-3334

DOI: 10.1093/carcin/bgi223