The accumulation of multiple genetic changes underlies the process of tumorigenesis, and both dominantly acting oncogenes and inactivated tumor suppressor genes co-exist in the same tumor. Individual mutations are thought to independently contribute to the kaleidoscopic transformed phenotype. Several examples have now been found of mutations in genes that, through different mechanisms, act on central control points either to ensure genome stability or to regulate the common pathways that signal cell proliferation, survival and differentiation. Mutations at these loci may have multiple, and apparently unrelated, phenotypic consequences.
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