Ribeiro Ulysses, Jorge Uana M, Safatle-Ribeiro Adriana V, Yagi Osmar K, Scapulatempo Cristovam, Perez Rodrigo O, Corbett Carlos E P, Alves Venâncio A F, Zilberstein Bruno, Gama-Rodrigues Joaquim
Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, São Paulo, 01327-002, Brazil.
J Gastrointest Surg. 2007 Mar;11(3):233-9. doi: 10.1007/s11605-007-0101-7.
The aim of this investigation was to evaluate clinicopathologic and immunohistochemical characteristics of synchronous primary gastric adenocarcinomas. Immunohistochemistry for p53 (suppressor pathway) and for hMLH1, hMSH2, and hMSH6 (mutator pathway) was performed using ABC-technique amplification by biotinylated tyramide. Synchronous primary gastric adenocarcinomas were detected in 19/553 (3.43%) of the patients. The tumors were localized in distal stomach in 22, body in 14, and proximal in five. There was a predominance of intestinal type in the group of synchronic tumors compared to the solitary lesions, 73.2 vs 37.3%, p = 0.001. Synchronous neoplasias were diagnosed in earlier stage than solitary neoplasias, T1-T2 = 60.9% vs T1-T2 = 28.4%, p = 0.0001; and N0 = 68.4% vs N0 = 26.2%, p = 0.001. p53 was detected in 52.6% of the patients with synchronous tumors. Altered hMLH1 immunoexpression occurred in 26.3% of the patients and hMSH6 in 5.3%. hMSH2 immunoreactivity was positive in all tumors. p53 was solely detected in 17 tumors, while hMLH1 was altered in 10/24 negative p53 tumors, p = 0.01. Synchronous gastric adenocarcinomas presented higher frequency of intestinal type and early gastric cancer in comparison to solitary gastric cancer. Two routes of carcinogenesis, mutator, and suppressor appear to be involved independently in the development of synchronous tumors.
本研究的目的是评估同时性原发性胃腺癌的临床病理及免疫组化特征。采用生物素化酪胺ABC技术扩增法对p53(抑制途径)、hMLH1、hMSH2和hMSH6(错配途径)进行免疫组化检测。在553例患者中有19例(3.43%)检测到同时性原发性胃腺癌。肿瘤位于胃远端者22例,胃体部14例,胃近端5例。与单发肿瘤相比,同时性肿瘤组肠型占优势,分别为73.2%和37.3%,p = 0.001。同时性肿瘤的诊断分期早于单发肿瘤,T1-T2期分别为60.9%和28.4%,p = 0.0001;N0期分别为68.4%和26.2%,p = 0.001。52.6%的同时性肿瘤患者检测到p53。26.3%的患者hMLH1免疫表达改变,5.3%的患者hMSH6免疫表达改变。所有肿瘤的hMSH2免疫反应均为阳性。仅在17个肿瘤中检测到p53,而在24个p53阴性肿瘤中有10个hMLH1改变,p = 0.01。与单发胃癌相比,同时性胃腺癌肠型和早期胃癌的发生率更高。错配和抑制这两条致癌途径似乎独立参与了同时性肿瘤的发生发展。