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The role of oncogenes, tumour suppressor genes and growth factors in oral squamous cell carcinoma: a case of apoptosis versus proliferation
Author(s) -
Sugerman PB,
Joseph BK,
Savage NW
Publication year - 1995
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.1995.tb00181.x
Subject(s) - cell growth , apoptosis , suppressor , cancer research , basal cell , gene , tumor suppressor gene , biology , medicine , pathology , carcinogenesis , genetics
Mutation, deactivation and disregulated expression of oncogenes and tumour‐suppressor genes may be involved in the pathogenesis of oral squamous cell carcinoma (SCC). Deactivation of the p53 tumour‐suppressor gene allows cell proliferation and blocks apoptosis of malignant oral keratinocytes. Mutation in the ras oncog‐ene results in persistent mitogenic signalling. Upregul‐ated c‐Myc expression, in the presence of growth factors, provides an additional proliferative signal. Loss of retino‐blastoma tumour‐suppressor gene (Rb) function may contribute to oral keratinocyte hyperproliferation and recent evidence suggests that simultaneous deactivation of both p53 and Rb is required for tumourigenesis. Enhanced Bcl‐2 and reduced Fas expression inhibit tumour cell apoptosis and may convey resistance to cyto‐toxic drugs and T cell‐mediated cytotoxicity, respectively. Exogenous mutagens such as tobacco, alcohol and viral oncogenes may cause altered expression of oncogenes and tumour‐suppressor genes in some cases of oral SCC. The impact of these mechanisms on future therapies for oral SCC is highlighted.