作者: Philip J Coates , Sally A Lorimore , Eric G Wright
DOI: 10.1002/PATH.1701
关键词:
摘要: Cancers arise as a consequence of the accumulation multiple genetic mutations in susceptible cell, resulting perturbation regulatory networks that control proliferation, survival, and cellular function. Here, sources stress can cause oncogenic responses cells to DNA damage are reviewed. The role different repair pathways potential for cell- tissue-specific reliance on individual mechanisms discussed. Evidence activation p53-mediated growth arrest apoptosis after exposure an genotoxin is assessed some mediators these provided. These particular forms likely be key determinants tumour susceptibility, there good evidence variations responses. genotoxic agents play altering microenvironment produce indirect effects tumourigenesis through altered production free radicals cytokines characteristic inflammatory-type processes also evaluated. Changes direct or involved both initiation progression may even prerequisite tumourigenesis. Therefore, susceptibility endogenous exogenous represents balance between cell-intrinsic target changes microenvironment. A fuller understanding responses, alterations microenvironment, modifiers could lead novel prevention therapeutic strategies common human malignancy.