Cellular senescence in oral cancer and precancer and treatment implications: A review
Open Access
- 1 January 2008
- journal article
- review article
- Published by Taylor & Francis Ltd in Acta Oncologica
- Vol. 47 (8), 1464-1474
- https://doi.org/10.1080/02841860802183612
Abstract
Introduction. Recent studies have demonstrated the capacity of the human organism to prevent the growth of potentially carcinogenic cells by paralyzing them. This antitumor mechanism is known as cellular senescence and is defined as an emergency defence system for cells on the way to becoming cancerous. Results. This review of the literature suggests that oncogene-induced senescence may be a response to oncogenic activation, acting as a natural barrier against tumorigenesis at a premalignant stage. Thus, a large number of cells enter senescence in premalignant lesions but none do so in malignant tumors, due to the loss of senescent pathway effectors such as p16INK4a or ARF-p53. Potential senescence markers in oral precancerous lesions include p21WAF1, p16INK4a, pRb, Maspin, RAR-β, G-actin, p15INK4b, DCR2, and DEC1, some of which are currently under study. Conclusion. In the short term, the study of this mechanism may yield valuable data for the management of oral cancer and precancer, for which no effective diagnostic or prognostic markers are yet available.Keywords
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