J. Cano-Sánchez

Cellular senescence in oral cancer and precancer and treatment implications: a review.

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.

No differences in caspase-3 and Bax expression in atrophic-erosive vs. reticular oral lichen planus

Background  Caspase‐3 (CPP32) and Bax expression levels in oral lichen planus (OLP) lesions are considered reliable markers of apoptosis. The malignant transformation of OLP remains a very controversial matter. The objective of this study was to compare histological and apoptotic phenomena between atrophic‐erosive and reticular forms of OLP.