Boltin Doron, Gingold-Belfer Rachel, Dickman Ram, Halpern Marisa, Morgenstern Sara, Roth Miri, Layfer Olga, Vilkin Alex, Niv Yaron, Levi Zohar
Departments of aGastroenterology bPathology cGastroenterology Laboratory, Rabin Medical Center, Beilinson Campus dDepartment of Pathology, Rabin Medical Center, Hasharon Campus eThe Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Eur J Gastroenterol Hepatol. 2014 Jul;26(7):710-4. doi: 10.1097/MEG.0000000000000117.
There are currently no accepted clinical guidelines for the surveillance of first-degree relatives (FDRs) of gastric cancer patients. The existence of intestinal metaplasia, as well as altered mucin expression, might be associated with an increased risk for gastric cancer. In the present study we aimed to investigate the mucin phenotype of individuals with a family history of gastric cancer.
We included FDRs of gastric cancer patients. Individuals with functional chest pain served as controls. Upper endoscopy including extensive biopsy according to the Olga protocol was performed. Immunohistochemical staining for MUC1, MUC2, MUC5AC, and MUC6 was performed. Sera were assayed for pepsinogen I and II. Helicobacter status was determined through Giemsa staining and serological tests.
Forty FDRs and eight controls were included; the mean age was 46.7 ± 12.0 years. In both the study group and the control group there were no gross endoscopic findings and no histological evidence of intestinal metaplasia. Superficial MUC1 expression was significantly increased in the study group (47.5 vs. 0%; P=0.01). There was no difference in the expression of deep MUC1, MUC2, MUC5AC, or MUC6 between the groups, nor was there a difference in pepsinogen I/II levels or Helicobacter pylori exposure (35.0 vs. 25.0%; P=0.46).
Despite normal appearing mucosa and the absence of intestinal metaplasia according to histological analysis, FDRs of gastric cancer patients show increased expression of MUC1, which may serve as a predictor of future intestinal metaplasia, dysplasia, and cancer. Further studies are needed to verify these findings and their implications.
目前尚无被广泛接受的针对胃癌患者一级亲属(FDR)的监测临床指南。肠化生的存在以及黏蛋白表达的改变可能与胃癌风险增加有关。在本研究中,我们旨在调查有胃癌家族史个体的黏蛋白表型。
我们纳入了胃癌患者的FDR。有功能性胸痛的个体作为对照。根据Olga方案进行包括广泛活检的上消化道内镜检查。进行MUC1、MUC2、MUC5AC和MUC6的免疫组织化学染色。检测血清中的胃蛋白酶原I和II。通过吉姆萨染色和血清学检测确定幽门螺杆菌感染状况。
纳入了40名FDR和8名对照;平均年龄为46.7±12.0岁。研究组和对照组在内镜下均无明显异常发现,也无肠化生的组织学证据。研究组中浅表MUC1表达显著增加(47.5%对0%;P=0.01)。两组之间深层MUC1、MUC2、MUC5AC或MUC6的表达无差异,胃蛋白酶原I/II水平或幽门螺杆菌感染率也无差异(35.0%对25.0%;P=0.46)。
尽管根据组织学分析黏膜外观正常且无肠化生,但胃癌患者的FDR显示MUC1表达增加,这可能作为未来肠化生、发育异常和癌症的预测指标。需要进一步研究来验证这些发现及其意义。