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胰腺癌发病机制的分子驱动因素:向内审视以向前迈进。

Molecular Drivers of Pancreatic Cancer Pathogenesis: Looking Inward to Move Forward.

作者信息

Khan Mohammad Aslam Aslam, Azim Shafquat, Zubair Haseeb, Bhardwaj Arun, Patel Girijesh Kumar, Khushman Moh'd, Singh Seema, Singh Ajay Pratap

机构信息

Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.

Departments of Interdisciplinary Clinical Oncology, Mitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.

出版信息

Int J Mol Sci. 2017 Apr 6;18(4):779. doi: 10.3390/ijms18040779.

DOI:10.3390/ijms18040779
PMID:28383487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5412363/
Abstract

Pancreatic cancer (PC) continues to rank among the most lethal cancers. The consistent increase in incidence and mortality has made it the seventh leading cause of cancer-associated deaths globally and the third in the United States. The biggest challenge in combating PC is our insufficient understanding of the molecular mechanism(s) underlying its complex biology. Studies during the last several years have helped identify several putative factors and events, both genetic and epigenetic, as well as some deregulated signaling pathways, with implications in PC onset and progression. In this review article, we make an effort to summarize our current understanding of molecular and cellular events involved in the pathogenesis of pancreatic malignancy. Specifically, we provide up-to-date information on the genetic and epigenetic changes that occur during the initiation and progression of PC and their functional involvement in the pathogenic processes. We also discuss the impact of the tumor microenvironment on the molecular landscape of PC and its role in aggressive disease progression. It is envisioned that a better understanding of these molecular factors and the mechanisms of their actions can help unravel novel diagnostic and prognostic biomarkers and can also be exploited for future targeted therapies.

摘要

胰腺癌(PC)仍然是最致命的癌症之一。其发病率和死亡率持续上升,已使其成为全球癌症相关死亡的第七大主要原因,在美国则位列第三。对抗胰腺癌的最大挑战在于我们对其复杂生物学背后分子机制的了解不足。过去几年的研究已帮助识别出几个假定的因素和事件,包括遗传和表观遗传方面的,以及一些失调的信号通路,这些都与胰腺癌的发生和发展有关。在这篇综述文章中,我们努力总结目前对胰腺恶性肿瘤发病机制中涉及的分子和细胞事件的理解。具体而言,我们提供了有关胰腺癌起始和进展过程中发生的遗传和表观遗传变化及其在致病过程中的功能参与的最新信息。我们还讨论了肿瘤微环境对胰腺癌分子格局的影响及其在侵袭性疾病进展中的作用。可以预见,更好地理解这些分子因素及其作用机制有助于揭示新的诊断和预后生物标志物,也可用于未来的靶向治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ae/5412363/dff0fb28c1a5/ijms-18-00779-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ae/5412363/dff0fb28c1a5/ijms-18-00779-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ae/5412363/dff0fb28c1a5/ijms-18-00779-g001.jpg

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本文引用的文献

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Non-coding RNA/microRNA-modulatory dietary factors and natural products for improved cancer therapy and prevention: Alkaloids, organosulfur compounds, aliphatic carboxylic acids and water-soluble vitamins.用于改善癌症治疗与预防的非编码RNA/微小RNA调节性饮食因子及天然产物:生物碱、有机硫化合物、脂肪族羧酸和水溶性维生素。
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Non-coding RNAs: A tale of junk turning into treasure.
B7 同源物 3 在胰腺癌中的作用。
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LRG1 in pancreatic cancer cells promotes inflammatory factor synthesis and the angiogenesis of HUVECs by activating VEGFR signaling.胰腺癌细胞中的LRG1通过激活VEGFR信号促进炎症因子合成及人脐静脉内皮细胞的血管生成。
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Highlights on the Role of Mutations in Reshaping the Microenvironment of Pancreatic Adenocarcinoma.亮点在于基因突变重塑胰腺腺癌微环境的作用。
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Oncol Lett. 2021 Nov;22(5):809. doi: 10.3892/ol.2021.13070. Epub 2021 Sep 27.
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Cyclin Dependent Kinase-1 (CDK-1) Inhibition as a Novel Therapeutic Strategy against Pancreatic Ductal Adenocarcinoma (PDAC).细胞周期蛋白依赖性激酶-1(CDK-1)抑制作为一种针对胰腺导管腺癌(PDAC)的新型治疗策略。
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