早期胃癌中低级别不典型上皮的起源。
The Origin of Epithelium with Low-Grade Atypia in Early Gastric Cancer.
机构信息
Department of Gastroenterology, Yokohama City University, Yokohama, Japan.
Division of Pathological Diagnosis, Yokohama City University Hospital, Yokohama, Japan.
出版信息
Digestion. 2022;103(3):217-223. doi: 10.1159/000521875. Epub 2022 Feb 16.
INTRODUCTION
Helicobacter 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.
METHODS
The 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.
RESULTS
The 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.
CONCLUSION
In most cases, ELA on the surfaces of GCs seems to have originated from normal gastric cells, not from cancer cells.
简介
幽门螺杆菌（HP）感染可导致胃黏膜的慢性炎症和萎缩，从而增加胃癌（GC）的风险。随着 HP 感染治疗的不断成功，根除后发生的 GC 数量也越来越多。多项研究表明，低级别异型增生（ELA）上皮是这些 GC 的常见特征，但这种情况的起源尚不清楚。在本研究中，我们比较了成功根除 HP 治疗后发生的 GC（根除组）和伴有 HP 感染的 GC（感染组）患者的 ELA 和癌组织的黏蛋白表型、细胞增殖和 p53 染色。
方法
研究人群包括 23 例成功根除 HP 治疗后发生的 GC（根除组）和 24 例伴有 HP 感染的 GC 患者（感染组）。通过苏木精和伊红染色确定 ELA 的发生率。通过免疫组织化学染色对 Muc5AC、Muc2、p53 和 Ki-67 进一步分析肿瘤组织和 ELA 样本。
结果
根除组的 ELA 覆盖率明显高于感染组。ELA 常表达胃型黏蛋白，ELA 和癌区的黏蛋白表型在 75%的病例中存在差异。ELA 的 Ki-67 标记指数始终低于癌性黏膜。21 例癌性病变中有 14 例（66.7%）为 p53 阳性，但只有 3 例 ELA 样本为阳性。
结论
在大多数情况下，GC 表面的 ELA 似乎起源于正常胃细胞，而不是癌细胞。
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