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首页> 外文期刊>Oncology: International Journal of Cancer Research and Treatment >Difference in the Role of Loss of Heterozygosity at 10p15 (KLF6 Locus) in Colorectal Carcinogenesis between Sporadic and Familial Adenomatous Polyposis and Hereditary Nonpolyposis Colorectal Cancer Patients
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Difference in the Role of Loss of Heterozygosity at 10p15 (KLF6 Locus) in Colorectal Carcinogenesis between Sporadic and Familial Adenomatous Polyposis and Hereditary Nonpolyposis Colorectal Cancer Patients

机译：散发性和家族性腺瘤性息肉病与遗传性非息肉病大肠癌患者在10p15杂合性丧失（KLF6位点）在大肠癌发生中的作用差异

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Objectives: To clarify the role of the KLF6 (Kruppel-like factor 6) locus in multistep colorectal carcinogenesis, we analyzed loss of heterozygosity (LOH) at 10p15 (KLF6 locus) and mutations of the KLF6 gene in 298 colorectal tumors at various pathological stages of sporadic and familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC) patients. Methods: 10pl5 LOH was analyzed using KLF6M1 and KLF6m~2, and KLF6 gene mutation was analyzed using PCR-SSCP and sequencing. Results: It was found that the frequencies of LOH (sum of M1 and m~2) were 4% in adenomas, 0% in intramucosal carcinomas, 35% in invasive carcinomas, and 33% in liver metastases in sporadic cases. Invasive carcinomas from FAP patients showed only 6% LOH, and invasive carcinomas from HNPCC patients exhibited 0% LOH. Mutation analysis of the KLF6 gene in 298 colorectal tumors detected no somatic mutations. Conclusions: The present data suggest that LOH of the KLF6 locus at chromosome 10p15 contributes to theinvasion step from an intramucosal carcinoma to an invasive carcinoma specifically in sporadic colorectal carcinogenesis, but is rarely in- volved in the carcinogenesis of FAP and HNPCC cases. Moreover, the absence of somatic mutations suggests the uncertainty of the KLF6 gene as a classical tumor suppressor gene at the lost 10p15 region in colorectal carcinogenesis.
机译：目的：为阐明KLF6（Kruppel样因子6）基因座在多步结直肠癌发生中的作用，我们分析了298个不同病理阶段的298个大肠肿瘤在10p15（KLF6基因座）的杂合性缺失（LOH）和KLF6基因突变。和家族性腺瘤性息肉病（FAP）和遗传性非息肉病性大肠癌（HNPCC）患者的治疗。方法：用KLF6M1和KLF6m〜2分析10pl5 LOH，并用PCR-SSCP和测序法分析KLF6基因突变。结果：散发病例中，腺瘤的LOH频率（M1和m〜2之和）为4％，粘膜内癌为0％，浸润癌为35％，肝转移为33％。来自FAP患者的浸润癌仅显示6％的LOH，来自HNPCC患者的浸润癌仅显示0％的LOH。在298例大肠肿瘤中KLF6基因的突变分析未发现体细胞突变。结论：目前的数据表明，第10p15号染色体上的KLF6基因座的LOH参与了从粘膜内癌到浸润性癌的侵袭步骤，特别是在散发性结直肠癌的发生中，但很少涉及FAP和HNPCC病例的癌变。此外，体细胞突变的缺乏表明在大肠癌发生过程中丢失的10p15区，KLF6基因作为经典抑癌基因的不确定性。

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