Abstract
Carcinogenesis is a multistep process during which normal cells undergo a series of genetic and phenotypic changes that lead to immortalization, transformation, acquisition of tumorigenic properties, and eventually to metastatic propensity. Carcinogenesis involves the inactivation or inhibition of genes that function as tumor suppressors and the activation of genes that function as oncogenes (1). Changes in the expression and function of a variety of genes result from deletions, mutations, or epigenetic activation or silencing of transcription, and the changes in protein levels that follow or result from post-transcriptional modifications can lead to altered growth, differentiation, and apoptosis rates. Identification of the molecules and mechanisms involved in carcinogenesis holds promise for improved diagnosis and prognosis and for targeted approaches to cancer prevention and therapy.

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