The Origin of Epithelium with Low-Grade Atypia in Early Gastric Cancer
The Origin of Epithelium with Low-Grade Atypia in Early Gastric Cancer
复制标题
早期胃癌低度异型性上皮的起源
作者：
Yamada Hiroaki;Kaneko Hiroaki;Kuwashima Hirofumi;Sugimori Makoto;Tsuyuki Sho;Sanga Katsuyuki;Irie Kuniyasu;Sasaki Tomohiko;Kondo Masaaki;Miyake Akio;Maeda Shin
幽门螺杆菌（Helicobacter pylori，HP）感染可引起胃粘膜慢性炎症和萎缩，是胃癌（gastric cancer，GC）的高危因素。随着HP感染治疗的日益成功，可以评估根除后发生的大量GC。几项研究表明，上皮细胞与低级别的上皮细胞（ELA）是这些GC的常见特征，但这种情况的起源是未知的。在这项研究中，我们比较了粘蛋白的表型，细胞增殖，和p53染色ELA和癌组织中获得的患者与GC与HP根除和不根除。MethodsThe研究人群包括23例胃癌患者成功HP根除治疗后发展（根除组）和24例胃癌和HP感染（感染组）。ELA的患病率通过苏木精-伊红染色确定。免疫组化检测Muc 5AC、Muc 2、p53、Ki-67的表达。结果根除组ELA覆盖率明显高于感染组。ELA常表达胃型粘蛋白，75%的病例ELA和癌区的粘蛋白表型不同。Ki-67标记指数在ELA中始终低于癌性粘膜。14 21（66.7%）的癌病变，但只有3 ELA样品，p53-conclusionIn大多数情况下，ELA上的GC表面似乎起源于正常胃细胞，而不是从癌细胞。
IntroductionHelicobacter pylori (HP) infection causes chronic inflammation and atrophy of the gastric mucosa and thus a high risk of gastric cancer (GC). With the increasing success of HP infection treatment, a larger number of GCs that develop after eradication can be assessed. Several studies have shown that epithelium with low-grade atypia (ELA) is a frequent characteristic of these GCs, but the origin of this condition is unknown. In this study, we compared the mucin phenotype, cellular proliferation, and p53 staining in ELA and cancerous tissues obtained from patients with GC with and without HP eradication.MethodsThe study population consisted of 23 patients with GC that developed after successful HP eradication therapy (eradicated group) and 24 patients with GC and HP infection (infected group). The prevalence of ELA was determined by hematoxylin and eosin staining. Tumor tissue and ELA samples were further analyzed by immunohistochemical staining for Muc5AC, Muc2, p53, and Ki-67.ResultsThe ELA coverage rate was significantly higher in the eradicated group than in the infected group. Gastric-type mucin was frequently expressed by the ELA, and the mucin phenotypes of ELA and cancerous areas differed in 75% of cases. The Ki-67 labeling index was consistently lower in ELA than in the cancerous mucosa. Fourteen of 21 (66.7%) cancerous lesions, but only 3 ELA samples, were p53-positive.ConclusionIn most cases, ELA on the surfaces of GCs seems to have originated from normal gastric cells, not from cancer cells.