Campo-Trapero Julian, Cano-Sánchez Jorge, Palacios-Sánchez Begoña, Llamas-Martínez Silvia, Lo Muzio Lorenzo, Bascones-Martínez Antonio
Department of Buccofacial Medicine and Surgery, School of Dentistry, Complutense University of Madrid, Spain.
Acta Oncol. 2008;47(8):1464-74. doi: 10.1080/02841860802183612.
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.
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.
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.
近期研究表明，人体具有通过使潜在致癌细胞失活来阻止其生长的能力。这种抗肿瘤机制被称为细胞衰老，它被定义为细胞转变为癌细胞过程中的一种应急防御系统。
对文献的综述表明，癌基因诱导的衰老可能是对致癌激活的一种反应，在癌前阶段作为肿瘤发生的天然屏障。因此，大量细胞在癌前病变中进入衰老状态，但在恶性肿瘤中则不然，这是由于衰老途径效应因子如p16(INK4a)或ARF-p53的缺失。口腔癌前病变中潜在的衰老标志物包括p21(WAF1)、p16(INK4a)、pRb、Maspin、RAR-β、G-肌动蛋白、p15(INK4b)、DCR2和DEC1，其中一些目前正在研究中。
短期内，对这一机制的研究可能会为口腔癌和癌前病变的管理提供有价值的数据，目前尚无有效的诊断或预后标志物。
