Wild-typeK-rashas a tumour suppressor effect on carcinogen-induced murine colorectal adenoma formation

Author:

Luo Feijun1,Poulogiannis George12,Ye Hongtao13,Hamoudi Rifat1,Dong Gehong1,Zhang Wenyan1,Ibrahim Ashraf E. K.1,Arends Mark J.14

Affiliation:

1. Department of Pathology; University of Cambridge; Addenbrooke's Hospital; Cambridge UK

2. Division of Signal Transduction; Beth Israel Deaconess Medical Center and Department of Systems Biology; Harvard Medical School; Boston MA USA

3. Department of Histopathology; Institute of Orthopaedics and Musculoskeletal Science; Royal National Orthopaedic Hospital NHS Trust; University College London; Stanmore Middlesex UK

4. Division of Pathology; University of Edinburgh; Institute of Genetics & Molecular Medicine; Western General Hospital; Edinburgh UK

Funder

Cancer Research UK

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Pathology and Forensic Medicine

Reference35 articles.

1. Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability;Arends;Br. J. Cancer,1993

2. Apoptosis is inversely related to necrosis and determines net growth in tumours bearing constitutively expressed myc, ras, and HPV oncogenes;Arends;Am. J. Pathol.,1994

3. Frequent deletion of chromosome 12p12.3 in children with acute lymphoblastic leukaemia;Baccichet;Br. J. Haematol.,1997

4. Increasing complexity of Ras signaling;Campbell;Oncogene,1998

5. Combinatorial roles for pRB, p107, and p130 in E2F-mediated cell cycle control;Classon;Proc. Natl Acad. Sci. USA,2000

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