Epigenetic alterations in intraductal papillary mucinous neoplasms of the pancreas.

Norihiro Sato, Michael Goggins
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引用次数: 50

Abstract

Intraductal papillary mucinous neoplasm (IPMN), an increasingly recognized cystic neoplasm of the pancreas with a broad spectrum of malignant potential, has been considered a precursor to infiltrating ductal adenocarcinoma. Because of its unique clinical, radiological, pathological, and molecular features, IPMN has attracted considerable interest among clinicians and researchers. Although some genetic alterations have been described in IPMNs, the molecular features that characterize the evolution and progression of these neoplasms are largely unknown. Recent studies have shown that aberrant methylation of the promoter cytosine-phospho-guanine (CpG) island is a common mechanism associated with the silencing of tumor-suppressor and cancer-related genes in IPMNs. Importantly, the prevalence of such methylation increases along with the grade of neoplasia, suggesting that these epigenetic events may contribute to the progression of IPMNs. Further studies of epigenetic alterations in IPMN will shed light on the molecular pathogenesis of this unique neoplasm and lead to the identification of epigenetic markers that can be applied in the clinical setting.

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胰腺导管内乳头状粘液瘤的表观遗传改变。
导管内乳头状黏液性肿瘤(IPMN)是一种越来越被认可的胰腺囊性肿瘤,具有广谱的恶性潜能,被认为是浸润性导管腺癌的前兆。由于其独特的临床、放射学、病理学和分子特征,IPMN引起了临床医生和研究人员的极大兴趣。虽然在IPMNs中已经描述了一些遗传改变,但表征这些肿瘤进化和进展的分子特征在很大程度上是未知的。最近的研究表明,启动子胞嘧啶-磷酸鸟嘌呤(CpG)岛的异常甲基化是ipmn中肿瘤抑制基因和癌症相关基因沉默的常见机制。重要的是,这种甲基化的发生率随着肿瘤的分级而增加,这表明这些表观遗传事件可能有助于IPMNs的进展。对IPMN表观遗传改变的进一步研究将揭示这种独特肿瘤的分子发病机制,并鉴定出可应用于临床的表观遗传标记。
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