Molecular biology of pancreatic carcinoma.

摘要: Although the genetic basis of cancer has been speculated upon for almost a century, proof causal relationship between mutation and human came within last 20 years. Since early discovery oncogenic virus cancer-causing mutagenic compounds, research uncovered many families genes that are, in some way, related to tumorigenic pathway. The malignant phenotype represents end result not one alteration but cascade events accumulate through successive stages tumor initiation progression. In somatic cells, spontaneous mutations occur at an approximate rate 10-6/cell generation, this figure could account certain incidence without invoking effects induced mutations. It estimated common cancers require average 4 6 rate-limiting steps achieve their full potential. Thus, by time clinical presentation, most solid tumors would have acquired complex set eventually dictates biologic behavior type.