胃癌旁粘膜的胃肠化生很少与非整倍体相关,而非整倍体是胃发育不良或胃癌的特征。

Ruth Zhang, Peter S Rabinovitch, Aras N Mattis, Gregory Y Lauwers, Won-Tak Choi
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引用次数: 0

摘要

大多数胃癌(GCs)被认为是通过胃肠道化生(GIM)-发育不良-癌途径发展的。据报道,广泛和/或不完全GIM患者发生GC的风险更高。GIM也可表现为局限于胃窝底部而不累及表面的发育不良样细胞结构异型性。然而,只有一小部分GIM患者会发生胃瘤变,GIM是否是直接的前体尚存疑问。我们对82例胃癌合并GIM患者行胃切除术进行了分析。对82例GCs相邻粘膜的109例GIM样本(包括88例主要完整GIM和21例主要不完整GIM)进行了DNA流式细胞术检测。109例GIM样本中只有2例(2%)显示非整倍体,均来自2例少数民族患者(亚洲和西班牙),具有有限和完全的GIM,没有细胞结构异型性。其余107例GIM样本显示轻度至局部中度基底腺(化生)异型性,仅限于胃窝基部,但无论解剖位置、组织学GIM亚型或不同程度的基底腺异型性如何,它们都显示出正常的DNA含量。总之,绝大多数GIM样本(98%)缺乏非整倍体,而非整倍体是胃发育不良或胃癌的特征。这表明非整倍体通常发生在胃发育不良之后,而不是在GIM阶段。该发现还表明,仅存在GIM可能不足以表明胃癌风险增加,其他高风险特征(即广泛的GIM、发育不良、少数种族和/或一级亲属中有GC家族史)和/或非整倍体应该在选择需要内镜监测的GIM患者时发挥作用。最后,在大多数情况下,伴有轻度至局部中度基底腺异型性的GIM可能代表化生异型性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gastric Intestinal Metaplasia in Mucosa Adjacent to Gastric Cancers Is Rarely Associated With the Aneuploidy That Is Characteristic of Gastric Dysplasia or Cancer.
Most gastric cancers (GCs) are thought to develop via gastric intestinal metaplasia (GIM)-dysplasia-carcinoma pathway. Patients with extensive and/or incomplete GIM have been reported to have a higher risk of GC. GIM can also display dysplasia-like cytoarchitectural atypia limited to the bases of gastric pits without surface involvement. However, only a small proportion of GIM patients will develop gastric neoplasia, and it remains questionable if GIM is a direct precursor. A cohort of 82 GC patients with GIM who underwent gastrectomy were analyzed. DNA flow cytometry was performed on 109 GIM samples (including 88 predominantly complete GIM and 21 predominantly incomplete GIM subclassified based on morphology) obtained from adjacent mucosa of the 82 GCs. Only 2 (2%) of the 109 GIM samples demonstrated aneuploidy, both from 2 minority patients (Asian and Hispanic) with limited and complete GIM and no cytoarchitectural atypia. The remaining 107 GIM samples showed mild to focally moderate basal gland (metaplastic) atypia limited to the bases of gastric pits, but they all demonstrated normal DNA content regardless of anatomic location, histologic GIM subtype, or varying degrees of basal gland atypia. In conclusion, the vast majority of the GIM samples (98%) lack the aneuploidy that is characteristic of gastric dysplasia or cancer. This indicates that aneuploidy usually occurs after the development of gastric dysplasia rather than at the stage of GIM. The finding also suggests that the presence of GIM alone may not be sufficient to suggest an increased risk for GC and that the inclusion of other high-risk features (ie, extensive GIM, dysplasia, racial minorities, and/or family history of GC in a first-degree relative) and/or aneuploidy ought to play a role in the selection of GIM patients who may warrant endoscopic surveillance. Finally, GIM with mild to focally moderate basal gland atypia is likely to represent metaplastic atypia in most cases.
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