Benard Anne, Zeestraten Eliane C M, Goossens-Beumer Inès J, Putter Hein, van de Velde Cornelis J H, Hoon Dave S B, Kuppen Peter J K
Department of Surgery, K6-R, Leiden University Medical Center, P.O. Box 9600, 2300 RC, Leiden, The Netherlands.
Apoptosis. 2014 Nov;19(11):1581-93. doi: 10.1007/s10495-014-1022-z.
Deregulation of the apoptotic pathway, one of the hallmarks of tumor growth and -progression, has been shown to have prognostic value for tumor recurrence in rectal cancer. In order to develop clinically relevant biomarkers, we studied the methylation status of promoter regions of key apoptosis genes in rectal cancer patients, using methylation-sensitive restriction enzymes. DNA was extracted from fresh-frozen tumor tissues of 49 stage I-III rectal cancer patients and 10 normal rectal tissues. The results of this pilot study were validated in 88 stage III tumor tissues and 18 normal rectal tissues. We found that methylation of the intrinsic apoptotic pathway genes Apaf1, Bcl2 and p53 correlated with the apoptotic status (M30) of the tumor. Combined survival analyses of these three genes, based on the number of genes showing high methylation (all low, 1 high, 2 high or all high), showed shorter patient survival and recurrence-free periods with an increasing number of methylated markers. Multivariate analyses showed significant differences for overall survival (p = 0.01; HR = 0.28 (0.09-0.83)), cancer-specific survival (p = 0.004; HR = 0.13 (0.03-0.67)) and distant recurrence-free survival (p = 0.001; HR = 0.22(0.05-0.94)). The shortest survival was observed for patients showing low methylation of all markers, which-as was expected-correlated with high apoptosis (M30), but also with high proliferation (Ki-67). The study of epigenetic regulation of apoptosis genes provides more insight in the tumorigenic process in rectal cancer and might be helpful in further refining treatment regimens for individual patients.
凋亡途径失调是肿瘤生长和进展的标志之一,已被证明对直肠癌的肿瘤复发具有预后价值。为了开发具有临床相关性的生物标志物,我们使用甲基化敏感限制酶研究了直肠癌患者关键凋亡基因启动子区域的甲基化状态。从49例I - III期直肠癌患者的新鲜冷冻肿瘤组织和10例正常直肠组织中提取DNA。这项初步研究的结果在88例III期肿瘤组织和18例正常直肠组织中得到验证。我们发现,内源性凋亡途径基因Apaf1、Bcl2和p53的甲基化与肿瘤的凋亡状态(M30)相关。基于显示高甲基化的基因数量(全部低、1个高、2个高或全部高)对这三个基因进行联合生存分析,结果显示随着甲基化标志物数量的增加,患者的生存期和无复发生存期缩短。多变量分析显示,总生存期(p = 0.01;HR = 0.28(0.09 - 0.83))、癌症特异性生存期(p = 0.004;HR = 0.13(0.03 - 0.67))和远处无复发生存期(p = 0.001;HR = 0.22(0.05 - 0.94))存在显著差异。所有标志物甲基化程度低的患者生存期最短,正如预期的那样,这与高凋亡(M30)相关,但也与高增殖(Ki - 67)相关。对凋亡基因的表观遗传调控研究为直肠癌的肿瘤发生过程提供了更多见解,可能有助于进一步优化个体患者的治疗方案。