Cellular senescence in oral cancer and precancer and treatment implications: a review.
BACKGROUND
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 p16(INK4a) or ARF-p53. Potential senescence markers in oral precancerous lesions include p21(WAF1), p16(INK4a), pRb, Maspin, RAR-beta, G-actin, p15(INK4b), DCR2, and DEC1, some of which are currently under study.


CONCLUSIONS
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.
Campo-Trapero
Julian
J
Department of Buccofacial Medicine and Surgery, School of Dentistry, Complutense University of Madrid, Spain. jcampo@odon.ucm.es
Cano-Sánchez
Jorge
J
Palacios-Sánchez
Begoña
B
Llamas-Martínez
Silvia
S
Lo Muzio
Lorenzo
L
Bascones-Martínez
Antonio
A
D000818:Animals; D016922:Cellular Senescence; D006801:Humans; D009062:Mouth Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D011230:Precancerous Conditions / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D025521:Tumor Suppressor Proteins / Q000378:metabolism
D025521:Tumor Suppressor Proteins