Inactivation of E2f1 enhances tumorigenesis in a Myc transgenic model.

Abstract	Previous studies have demonstrated both oncogenic and tumor suppressive properties for the E2F1 transcription factor. In this study, E2f1-null mice were crossed with transgenic mice expressing Myc under the control of an epithelial-specific keratin 5 promoter to determine whether the absence of E2F1 would modulate the oncogenic activity of Myc. Inactivation of E2f1 was found to significantly accelerate tumor development in keratin 5 Myc transgenic mice. Acceleration of tumorigenesis occurred despite the fact that apoptosis levels were increased in transgenic tissue and tumors null for E2f1, whereas Myc-induced proliferation was unaffected by the status of E2f1. These findings provide new insight into the tumor suppressive activity of E2F1 and identify for the first time a specific oncogenic alteration that cooperates with the loss of E2F1 in tumorigenesis.
Authors	Robert J Rounbehler, Pamela M Rogers, Claudio J Conti, David G Johnson
Journal	Cancer research (Cancer Res) Vol. 62 Issue 11 Pg. 3276-81 (Jun 01 2002) ISSN: 0008-5472 [Print] United States
PMID	12036945 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References	Cell Cycle Proteins DNA-Binding Proteins E2F Transcription Factors E2F1 Transcription Factor E2f1 protein, mouse Proto-Oncogene Proteins c-myc Transcription Factors Tumor Suppressor Protein p53
Topics	Animals Apoptosis (genetics) Cell Cycle Proteins Cell Division (genetics) DNA-Binding Proteins E2F Transcription Factors E2F1 Transcription Factor Gene Silencing Genes, Tumor Suppressor Genes, myc (physiology) Genetic Predisposition to Disease Head and Neck Neoplasms (genetics, metabolism, pathology) Mice Mice, Knockout Mice, Transgenic Proto-Oncogene Proteins c-myc (biosynthesis, genetics, physiology) Skin Neoplasms (genetics, metabolism, pathology) Transcription Factors (biosynthesis, genetics, physiology) Tumor Suppressor Protein p53 (biosynthesis, genetics, physiology)

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