title: Two Faces of SIVA.
abstract: In non-small cell lung cancer cells that contain a mutated KRAS gene, SIVA, a p53 target gene that is critical for apoptosis, is overexpressed in a p53-independent manner and promotes tumorigenesis through the stimulation of mTOR signaling. The ablation of Siva in conditional knockout mice results in an inhibition of tumor development that makes SIVA an interesting new candidate therapeutic target for the treatment of a carcinoma with few therapeutic options.
authors.affiliation: Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
authors.forename: Lois
authors.initials: L
authors.lastname: Resnick-Silverman
authors.affiliation: Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York. james.manfredi@mssm.edu.
authors.forename: James J
authors.initials: JJ
authors.lastname: Manfredi
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D051017:Apoptosis Regulatory Proteins; C106549:SIVA1 protein, human; D016159:Tumor Suppressor Protein p53