Nuclear overexpression of the E2F3 transcription factor in human lung cancer

Cooper, Colin S ORCID: https://orcid.org/0000-0003-2013-8042, Nicholson, Andrew G, Foster, Christopher, Dodson, Andrew, Edwards, Sandra, Fletcher, Anne, Roe, Toby, Clark, Jeremy, Joshi, Anupam, Norman, Andrew, Feber, Andrew, Lin, Dongmei, Gao, Yanning, Shipley, Janet and Cheng, Shu-Jun (2006) Nuclear overexpression of the E2F3 transcription factor in human lung cancer. Lung Cancer, 54 (2). pp. 155-62. ISSN 0169-5002

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Abstract

The E2F3 transcription factor has an established role in controlling cell cycle progression. In previous studies we have provided evidence that nuclear E2F3 overexpression represents a mechanism that drives the development of human bladder cancer and that determines aggressiveness in human prostate cancer. We have proposed a model in which E2F3 overexpression co-operates with removal of the E2F inhibitor pRB to facilitate cancer development. Since small cell lung cancers (SCLC) have one of the highest reported frequencies of functional abnormalities in the pRB protein (90%) of any human cancer, we wish to assess to what extent E2F3 would be overexpressed in this and other classes of human lung cancer.

Item Type: Article
Uncontrolled Keywords: adenocarcinoma,carcinoid tumor,carcinoma, neuroendocrine,carcinoma, small cell,carcinoma, squamous cell,cell nucleus,e2f3 transcription factor,gene expression regulation, neoplastic,genes, retinoblastoma,humans,immunohistochemistry,lung neoplasms,oligonucleotide array sequence analysis,sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
Faculty of Science > School of Biological Sciences
UEA Research Groups: Faculty of Medicine and Health Sciences > Research Groups > Cancer Studies
Depositing User: Pure Connector
Date Deposited: 20 Jan 2014 16:00
Last Modified: 24 Oct 2022 05:32
URI: https://ueaeprints.uea.ac.uk/id/eprint/46154
DOI: 10.1016/j.lungcan.2006.07.005

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