title: Antitumor mechanisms when pRb and p53 are genetically inactivated.
abstract: pRb and p53 are the two major tumor suppressors. Their inactivation is frequent when cancers develop and their reactivation is rationale of most cancer therapeutics. When pRb and p53 are genetically inactivated, cells irreparably lose the antitumor mechanisms afforded by them. Cancer genome studies document recurrent genetic inactivation of RB1 and TP53, and the inactivation becomes more frequent in more advanced cancers. These findings may explain why more advanced cancers are more likely to resist current therapies. Finding successful treatments for more advanced and multi-therapy-resistant cancers will depend on finding antitumor mechanisms that remain effective when pRb and p53 are genetically inactivated. Here, we review studies that have begun to make progress in this direction.
authors.affiliation: Department of Developmental and Molecular Biology, and Ophthalmology and Visual Sciences, and Medicine, The Albert Einstein Comprehensive Cancer Center and Liver Research Center, Albert Einstein College of Medicine, Bronx, NY, USA.
authors.forename: L
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Developmental and Molecular Biology, and Ophthalmology and Visual Sciences, and Medicine, The Albert Einstein Comprehensive Cancer Center and Liver Research Center, Albert Einstein College of Medicine, Bronx, NY, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Lu
authors.affiliation: Department of Developmental and Molecular Biology, and Ophthalmology and Visual Sciences, and Medicine, The Albert Einstein Comprehensive Cancer Center and Liver Research Center, Albert Einstein College of Medicine, Bronx, NY, USA.
authors.forename: H
authors.initials: H
authors.lastname: Zhao
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000235:genetics*; D049109:Cell Proliferation; D019008:Drug Resistance, Neoplasm; D020022:Genetic Predisposition to Disease; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D016160:Retinoblastoma Protein / Q000235:genetics* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
chemical_list: D016160:Retinoblastoma Protein; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53