作者: Stavroula Raptis , Bharati Bapat
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摘要: Genetic, or genomic, instability refers to a series of observed spontaneous genetic changes occurring at an accelerated rate in cell populations derived from the same ancestral precursor. This is far new finding, but one that has increasingly gained more attention last decade due its plausible role(s) tumorigenesis. The majority alterations contributing malignant transformation are seen growth regulatory genes, and genes involved cycle progression arrest. Genomic may present itself through length short repeat stretches coding non-coding DNA, resulting microsatellite instability. Tumors with such profiles referred as exhibiting mutator phenotype, which largely consequence inactivating mutations DNA damage repair genes. also, most commonly, results gross chromosomal changes, translocations amplifications, lead Telomere telomerase activity, important maintaining structure regulating normal cell’s lifespan, have been shown function both suppressing facilitating transformation. In addition direct sequence structural gene silencing hypermethylation promoter regions, increased expression hypomethylation together, form alternative, epigenetic mechanism leading Emerging evidence also suggests dietary environmental agents can further modulate contribution Currently, there still much debate over distinct classes genomic their specific roles initiation tumor formation, well progressive transition cancerous state. review examines various molecular mechanisms result this potential latter human carcinogenesis.