p53-Dependent Apoptosis In Vivo: Impact of p53 Inactivation on Tumorigenesis
Holly Symonds, Leonard Krall, Lee Ann Remington, Maitane Robles, Tyler Jacks, Terry Van Dyke
Abstract
Holly Symonds, Leonard Krall, Lee Ann Remington, Maitane Robles, Tyler Jacks, Terry Van Dyke
Abstract
Loss of tumor suppressor function clearly contributes to the multistep process of tumorigenesis, as evidenced by the frequent mutation of these genes in human cancer (Marshall 1991; Hinds and Weinberg 1994). Investigation into the mechanisms by which inactivation of tumor suppressors contributes to tumorigenesis is therefore central to understanding cancer. The p53 gene is presently the most frequently mutated tumor suppressor gene in human cancers. Moreover, tumors of many different cell types harbor p53 mutations. Exactly how the disruption of p53 contributes to the genesis of these tumors and whether the contribution is the same or different in cancers of different cell types is not understood.
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Loss of tumor suppressor function clearly contributes to the multistep process of tumorigenesis, as evidenced by the frequent mutation of these genes in human cancer (Marshall 1991; Hinds and Weinberg 1994). Investigation into the mechanisms by which inactivation of tumor suppressors contributes to tumorigenesis is therefore central to understanding cancer. The p53 gene is presently the most frequently mutated tumor suppressor gene in human cancers. Moreover, tumors of many different cell types harbor p53 mutations. Exactly how the disruption of p53 contributes to the genesis of these tumors and whether the contribution is the same or different in cancers of different cell types is not understood.
Key concepts: Carcinogenesis, Suppressor, Tumor suppressor gene, Cancer research, Biology, Gene, Cancer, Mutation