Rosin Miriam P, Lam Wan L, Poh Catherine, Le Nhu D, Li Robert Jinze, Zeng Tao, Priddy Robert, Zhang Lewei
British Columbia Cancer Research Centre, Vancouver, British Columbia, V5Z 1L3, Canada.
Cancer Res. 2002 Nov 15;62(22):6447-50.
Treatment induces reactive changes that often resemble low-grade dysplasia at former oral cancer sites, complicating histopathological assessment. We tested a set of microsatellite markers shown previously to be predictive of progression for oral premalignant lesions for the ability to predict development of second oral malignancy (SOM). Sixty-eight oral leukoplakia at former cancer sites (with known outcome, 36 progressed to SOM) were evaluated for loss of heterozygosity at 19 loci on seven chromosome arms. 3p and/or 9p loss in these posttreatment leukoplakia was associated with a 26.3-fold increase in risk of developing SOM compared with those that retained both of these arms (P < 0.001), with 60% of cases with loss of heterozygosity developing SOM in 2 years. In contrast, histological diagnosis (moderate or severe dysplasia versus hyperplasia or mild dysplasia) had only a 1.7-fold increase in risk (P = 0.11). The identification of 3p and 9p loss in posttreatment lesions could serve as a simple and direct test for stratifying risk of SOM development.
治疗会引发一些反应性变化，这些变化在既往口腔癌部位常类似于低度发育异常，从而使组织病理学评估变得复杂。我们测试了一组先前已证明可预测口腔癌前病变进展的微卫星标记物，以评估其预测第二原发性口腔恶性肿瘤（SOM）发生的能力。对68例位于既往癌症部位的口腔白斑（已知转归情况，36例进展为SOM）进行了评估，检测其7条染色体臂上19个位点的杂合性缺失情况。与保留这两条染色体臂的患者相比，这些治疗后白斑中3p和/或9p缺失与发生SOM的风险增加26.3倍相关（P < 0.001），60%杂合性缺失的病例在2年内发生了SOM。相比之下，组织学诊断（中度或重度发育异常与增生或轻度发育异常）的风险仅增加1.7倍（P = 0.11）。识别治疗后病变中的3p和9p缺失可作为一种简单直接的检测方法，用于对SOM发生风险进行分层。
