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- W2081570461 abstract "ABSTRACT Human cells are more resistant to both immortalization and malignant transformation than rodent cells. Recent studies have established the basic genetic requirements for the transformation of human cells, but much of this work relied on the expression of transforming proteins derived from DNA tumor viruses. We constructed an isogenic panel of human fibroblast cell lines using a combination of gene targeting and ectopic expression of dominantly acting mutants of cellular genes. Abolition of p21 Cip1/Waf1 and p16 Ink4a functions prevented oncogenically activated Ras from inducing growth arrest and was sufficient for limited anchorage-independent growth but not tumorigenesis. Deletion of the tumor suppressor p53 combined with abolition of p16 Ink4a function failed to mimic the introduction of simian virus 40 large T antigen, indicating that large T antigen may target additional cellular functions. Ha-Ras and Myc cooperated only to a limited extent, but in the absence of Ras, Myc cooperated strongly with the simian virus 40 small t antigen to elicit aggressive anchorage-independent growth. The experiments reported here further define specific components of human transformation pathways." @default.
- W2081570461 created "2016-06-24" @default.
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- W2081570461 creator A5063875415 @default.
- W2081570461 creator A5081797261 @default.
- W2081570461 date "2003-04-01" @default.
- W2081570461 modified "2023-10-18" @default.
- W2081570461 title "Abolition of Cyclin-Dependent Kinase Inhibitor p16<sup><i>Ink4a</i></sup> and p21<sup><i>Cip1/Waf1</i></sup> Functions Permits Ras-Induced Anchorage-Independent Growth in Telomerase-Immortalized Human Fibroblasts" @default.
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- W2081570461 doi "https://doi.org/10.1128/mcb.23.8.2859-2870.2003" @default.
- W2081570461 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/152557" @default.
- W2081570461 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12665584" @default.
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