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胰腺导管内乳头状黏液性肿瘤的分子发病机制。

Molecular pathogenesis of intraductal papillary mucinous neoplasms of the pancreas.

机构信息

Department of Internal Medicine, The University of Texas Health Science Center at Houston, TX, USA.

出版信息

Pancreas. 2010 Nov;39(8):1129-33. doi: 10.1097/MPA.0b013e3181f66cdf.

Abstract

Over the last 3 decades, there have been substantial improvements in diagnostic imaging and sampling techniques to evaluate pancreatic diseases. The modern technology has helped us to recognize premalignant conditions of pancreas including mucinous cystic neoplasms and intraductal papillary mucinous neoplasms (IPMNs). Differentiation between benign and malignant lesions and early detection of any malignant transformation in premalignant lesion are extremely important for further management decisions. Diagnostic cytology has limited sensitivity to further differentiate between benign, premalignant, and malignant lesions of the pancreas. There is limited information about the epidemiological risk factors and molecular mechanisms leading to development and further progression to malignancy of IPMNs. Several studies have shown that pancreatic juice and pancreatic tissue from the lesion can be tested for molecular markers including K-ras, p53, and p16 to differentiate between cancer and chronic inflammatory process. We review cellular signaling pathways that contribute to pathogenesis of IPMNs of the pancreas to further identify potential biomarkers and molecular targets.

摘要

在过去的 30 年中,用于评估胰腺疾病的诊断成像和采样技术取得了实质性的进步。现代技术帮助我们认识到了胰腺的癌前状态,包括黏液性囊腺瘤和胰管内乳头状黏液性肿瘤(IPMN)。区分良性和恶性病变,以及早期发现癌前病变中的任何恶性转化,对于进一步的管理决策非常重要。诊断细胞学对进一步区分胰腺的良性、癌前和恶性病变的敏感性有限。关于导致 IPMN 发生和进一步发展为恶性的流行病学风险因素和分子机制的信息有限。几项研究表明,可以测试胰腺分泌物和病变组织中的分子标志物,包括 K-ras、p53 和 p16,以区分癌症和慢性炎症过程。我们综述了导致胰腺 IPMN 发病机制的细胞信号通路,以进一步确定潜在的生物标志物和分子靶点。

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