Harden Susan V, Tokumaru Yutaka, Westra William H, Goodman Steven, Ahrendt Steven A, Yang Stephen C, Sidransky David
Department of Otolaryngology-Head and Neck Surgery, Division of Head and Neck Cancer Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21206-2198, USA.
Clin Cancer Res. 2003 Apr;9(4):1370-5.
Promoter hypermethylation is an important pathway for repression of gene transcription in cancer cells and a promising marker for cancer detection. We tested five gene promoters [CDKN2A (p16), O(6)-methylguanine-DNA-methyltransferase, glutathione S-transferase P1 (GSTP1), adenomatous polyposis coli (APC), and death-associated protein kinase (DAPK)] by real-time methylation-specific PCR in primary tumors from 90 stage I lung cancer patients for aberrant DNA methylation. We then used the presence of tumor methylation as a marker to investigate the presence of occult metastasis in corresponding histologically negative lymph nodes. Of the primary tumors, 73 of 90 (81%) displayed promoter hypermethylation in at least one of the genes studied: 17% (15 of 90) at p16 (CDKN2A); 16% (14 of 90) at O(6)-methylguanine-DNA-methyltransferase; 8% (7 of 90) at GSTP1; 72% (65 of 90) at APC; and 17% (15 of 90) at DAPK. Squamous histology was predictive of worse overall survival (P = 0.074, log-rank test). APC methylation and GSTP1 methylation in the primary tumor were both correlated with nonsquamous histology (P = 0.02 and P = 0.01 likelihood ratio respectively). The presence of both APC methylation and DAPK methylation in the primary tumor predicted a worse outcome, with 7 of 13 (54%) deaths in this group compared with 21 of 77 (27%) deaths in cases without both genes methylated (P = 0.229, log-rank test). The same methylation pattern was detected in DNA from at least one of the corresponding lymph nodes in 11 of 73 (15%) cases. Five of 11 (45%) patients with occult metastasis detected by methylation analysis have died compared with 17 of 62 (27%) patients with negative lymph nodes, although survival analysis did not reach statistical significance (P = 0.632, log-rank test). Promoter hypermethylation is common in lung cancer and represents a promising marker for the molecular staging of lung cancer patients. Although this study showed important trends, a larger prospective study is required to better understand the value of methylation analysis in detecting occult metastasis.
启动子高甲基化是癌细胞中基因转录抑制的重要途径,也是癌症检测中一个有前景的标志物。我们通过实时甲基化特异性PCR检测了90例I期肺癌患者原发肿瘤中五个基因启动子[细胞周期蛋白依赖性激酶抑制剂2A(p16)、O(6)-甲基鸟嘌呤-DNA甲基转移酶、谷胱甘肽S-转移酶P1(GSTP1)、腺瘤性息肉病 coli(APC)和死亡相关蛋白激酶(DAPK)]的异常DNA甲基化情况。然后,我们以肿瘤甲基化的存在作为标志物,研究相应组织学检查阴性的淋巴结中隐匿转移的存在情况。在原发肿瘤中,90例中有73例(81%)在至少一个研究基因中显示启动子高甲基化:p16(CDKN2A)为17%(90例中的15例);O(6)-甲基鸟嘌呤-DNA甲基转移酶为16%(90例中的14例);GSTP1为8%(90例中的7例);APC为72%(90例中的65例);DAPK为17%(90例中的15例)。鳞状组织学预示总体生存率较差(P = 0.074,对数秩检验)。原发肿瘤中的APC甲基化和GSTP1甲基化均与非鳞状组织学相关(分别为P = 0.02和P = 0.01,似然比)。原发肿瘤中同时存在APC甲基化和DAPK甲基化预示预后较差,该组13例中有7例(54%)死亡,而两个基因均未甲基化的病例中77例中有21例(27%)死亡(P = 0.229,对数秩检验)。在通过甲基化分析检测到隐匿转移的73例中的11例(15%)的相应淋巴结的DNA中检测到相同的甲基化模式。甲基化分析检测到隐匿转移的11例患者中有5例(45%)死亡,而淋巴结阴性的62例患者中有17例(27%)死亡,尽管生存分析未达到统计学意义(P = 0.632,对数秩检验)。启动子高甲基化在肺癌中很常见,是肺癌患者分子分期的一个有前景的标志物。尽管本研究显示了重要趋势,但需要更大规模的前瞻性研究来更好地了解甲基化分析在检测隐匿转移中的价值。