PATHOLOGY & ONCOLOGY RESEARCHVol. 1 No. 1, 1995

 Review

Recessive oncogenes: current status

Xiang GAO1, Kenneth V HONN2

1Division of Cancer Biology, Department of Radiation Oncology, Wayne State University, School of Medicine, Detroit, USA
2Gershenson Radiation Oncology Center, Harper Hospital, Detroit Medical Center, Detroit, USA
3Department of Pathology, Wayne State University, School of Medicine, Detroit, USA
4Department of Chemistry, Wayne State University, School of Medicine, Detroit, USA

 

Cell growth is under the control of a variety of positive and negative signals. An imbalance of such signals results in deregulation of cell behavior. Recessive oncogenes or tumor suppressor genes, opposite to dominant oncogenes, encode important cellular proteins which could function as negative regulators of the cell cycle, i.e., cell cycle brakes. Inactivation of recessive oncogenes, by allelic deletion, loss of expression, mutation, or functional inactivation by interacting with oncogene products of DNA tumor viruses or with amplified cellular binding proteins, will lead to uncontrolled cell growth or tumor formation. Besides the classic suppressor genes such as the p53 and RB, a growing number of novel tumor suppressor genes have been identified in recent years. While some tumor suppressor genes have been found to be important for the development of a large number of human malignancies (e.g., the p53 gene), others are more tumor type-specific (e.g., the NF-1 gene). Many human cancer types showed abnormalities of multiple tumor suppressor genes, offering strong support to the concept that tumorigenesis and progression result from an accumulation of multiple genetic alterations. In this review, we will begin with an overview (gene, transcript, protein and mechanisms of action) of the tumor suppressor genes (the RB, p53, DCC, APC, MCC, WT1, VHL, MST1, and BRCA1 genes) identified to date and then discuss the specific involvement of tumor suppressor genes in human malignancies including prostate cancer. Various chromosomal regions which potentially may contain tumor suppressor genes also will be reviewed. Pathology & Oncology Research, Vol 1, Nr 1, 7-22, 1995

Key words: oncogenes; cell cycle; heterozygosity; mutation


Received: Mar 20, 1995; accepted: May 13, 1995
Correspondence: Kenneth V HONN, Division of Cancer Biology, Department of Radiation Oncology, Wayne State University, School of Medicine, 432 Chemistry Building Detroit MI48202, USA; Tel: (313)577-1018, Fax: (313)577-0798

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