Keller G, Rudelius M, Vogelsang H, Grimm V, Wilhelm M G, Mueller J, Siewert J R, Höfler H
Institute of Pathology, Technische Universität München, Germany.
Am J Pathol. 1998 May;152(5):1281-9.
We compared 29 gastric carcinomas from patients with a variably strong family history for gastric cancer (group 1) with 36 gastric carcinomas from patients without a family history of this disease (group 2) for microsatellite instability (MSI) and loss of heterozygosity (LOH) with 12 microsatellite markers. Both study groups had similar proportions of histological types and tumor locations. Widespread MSI (alterations at > or = 6 loci) was seen in 5 of 29 (17%) of the tumors belonging to group 1 and in 4 of 36 (11%) group 2 tumors. MSI at a low level (alterations at 1 to 3 loci) was observed in 12 of 29 (41%) of tumors in group 1 and in 10 of 36 (28%) of tumors in group 2, differences that were not statistically significant. A significant difference with respect to low level MSI was observed between the two groups when considering the overall mutation rate of microsatellites. Seventeen of 281 (6%) analyzed microsatellite loci showed alterations in group 1 and 11 of 381 (2.9%) in group 2 (P = 0.046). Comparison of both types of MSI to the clinicopathological parameters in both groups revealed a significant association of low level MSI with advanced tumor stages (P = 0.046) in the group 2, whereas no such association was observed in group 1. In respect to LOH, a significant difference between the two groups was observed at chromosome 17p12, as 13 of 22 (59%) informative cases of group 1 showed LOH in comparison with 7 of 26 (27%) (P = 0.024) in group 2. No correlation of LOH at chromosome 17p12 to the pathological or clinical data was observed either in the two groups or in the study as a whole. Our data show that gastric carcinomas of patients with a positive family history of gastric cancer in group 1 are characterized by a higher mutation rate in respect to low level MSI, particularly at dinucleotide repeats, and by a higher frequency of LOH at chromosome 17p12, indicating that different genetic pathways are involved in the pathogenesis of gastric carcinomas arising in patients with and without a familial background of this disease.
我们采用12个微卫星标记,比较了29例有不同程度胃癌家族史患者的胃癌(第1组)和36例无胃癌家族史患者的胃癌(第2组)的微卫星不稳定性(MSI)及杂合性缺失(LOH)情况。两个研究组的组织学类型和肿瘤位置比例相似。第1组29例肿瘤中有5例(17%)出现广泛MSI(≥6个位点改变),第2组36例肿瘤中有4例(11%)出现。第1组29例肿瘤中有12例(41%)出现低水平MSI(1至3个位点改变),第2组36例肿瘤中有10例(28%)出现,差异无统计学意义。在考虑微卫星的总体突变率时,两组之间观察到低水平MSI存在显著差异。第1组281个分析的微卫星位点中有17个(6%)显示改变,第2组381个中有11个(2.9%)显示改变(P = 0.046)。将两组中两种类型的MSI与临床病理参数进行比较,发现第2组中低水平MSI与肿瘤晚期显著相关(P = 0.046),而第1组未观察到这种相关性。关于LOH,在17号染色体p12区域两组之间观察到显著差异,第1组22例信息充分的病例中有13例(59%)显示LOH,而第2组26例中有7例(27%)显示(P = 0.024)。在两组或整个研究中均未观察到17号染色体p12区域的LOH与病理或临床数据之间存在相关性。我们的数据表明,第1组有胃癌家族史患者的胃癌具有以下特征:低水平MSI的突变率较高,尤其是二核苷酸重复序列,以及17号染色体p12区域的LOH频率较高,这表明有和无该疾病家族背景的患者发生的胃癌在发病机制中涉及不同的遗传途径。