在突变 Kras 驱动的胰腺癌模型中，敲除芳基烃受体可加速 PanIN 的形成和纤维炎症。

IF 1.7 4区医学 Q3 GASTROENTEROLOGY & HEPATOLOGY

Pancreas Pub Date : 2024-05-01 DOI:10.1097/mpa.0000000000002357

Morgan T Walcheck, Patrick B Schwartz, Noah D Carrillo, Kristina A Matkowsky, Manabu Nukaya, Christopher A Bradfield, Sean M Ronnekleiv-Kelly

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引用次数: 0

摘要

人们对胰腺癌（PDAC）的发病机制仍然知之甚少，这阻碍了开发更有效的胰腺癌治疗方法的努力。最近的发现表明，芳基烃受体（AHR）在多种癌症的发展过程中起着至关重要的作用，可以作为治疗效果的靶点。然而，它在 PDAC 发病机制中的参与情况仍不清楚。为了填补这一空白，我们评估了 AHR 在体内 PDAC 癌前病变发展过程中的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Aryl hydrocarbon receptor knockout accelerates PanIN formation and fibro-inflammation in a mutant Kras-driven pancreatic cancer model.

The pathogenesis of pancreas cancer (PDAC) remains poorly understood, hindering efforts to develop a more effective therapy for PDAC. Recent discoveries show the aryl hydrocarbon receptor (AHR) plays a crucial role in the development of several cancers, and can be targeted for therapeutic effect. However, its involvement in the pathogenesis of PDAC remains unclear. To address this gap, we evaluated the role of AHR in the development of PDAC pre-cancerous lesions in vivo.

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来源期刊

Pancreas 医学-胃肠肝病学

CiteScore

4.70

自引率

3.40%

发文量

289

审稿时长

1 months

期刊介绍： Pancreas provides a central forum for communication of original works involving both basic and clinical research on the exocrine and endocrine pancreas and their interrelationships and consequences in disease states. This multidisciplinary, international journal covers the whole spectrum of basic sciences, etiology, prevention, pathophysiology, diagnosis, and surgical and medical management of pancreatic diseases, including cancer.