子宫内膜异位症:一种恶性指纹。

Christopher DeAngelo, Megan Burnett Tarasiewicz, Athena Strother, Heather Taggart, Caron Gray, Meaghan Shanahan, Christopher Glowacki, Jimmy Khandalavala, Erin Talaska, Andrea Kinnan, John Joseph Coté, Adrienne Perfilio Edwards, Gina Harper-Harrison, Murray Joseph Casey, Traci-Lynn Hirai, Sarah Schultz, Lynnea Stines, Roma Vora, Dominique Boudreau, Jennifer Burgart, Meredith Shama, Trevor Watson, Lisa Strasheim, Rachel Thompson, Rachel Lawlor, Kayleen Joyce, Claire M Magnuson, Jane Driano, Breanna Elger, Anne Lentino, Margaret Driscoll, Elise Tidwell, Apoorva Sharma, Sarah R Walker, Gretchen Jones, Poonam Sharma, Holly Stessman, Yanyuan Wu, Jay Vadgama, Dana Chase, Lesley Conrad, Srinivasa T Reddy, Robin Farias-Eisner
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引用次数: 4

摘要

背景:子宫内膜异位症是复杂的,但识别新的生物标志物、炎症分子和遗传联系是增强子宫内膜异位症和子宫内膜异位症相关恶性肿瘤的检测、预测和治疗的关键。在此,我们回顾了有关子宫内膜异位症中介导肿瘤发生的特定分子机制的文献。方法:确定指南(如Cochrane)和已发表的研究。通过PubMed采用系统评价方法筛选已发表的研究,并结合作者的主题知识进行筛选。我们对这些数据进行回顾,找出关键和相关的文章,以创建一篇全面的综述文章,探讨与子宫内膜异位症驱动的肿瘤发生相关的分子指纹。结果:C3aR1、PGR、ER1、SOX-17等相关基因表达谱与子宫内膜异位症驱动的肿瘤发生之间的关系是一个重要的焦点。进一步的研究还应关注CA-125与HE-4的联合使用,以及OVA1/MIA作为预测子宫内膜异位症驱动的肿瘤发生的临床相关诊断生物标志物的作用。结论:阐明子宫内膜异位症的分子指纹图谱,有助于了解驱动子宫内膜异位症相关恶性表型的分子机制。更好地了解这些基因的预测作用和生物标记蛋白的价值将允许推导独特的分子治疗算法,以更好地为我们的患者服务。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endometriosis: A Malignant Fingerprint.

Background: Endometriosis is complex, but identifying the novel biomarkers, inflammatory molecules, and genetic links holds the key to the enhanced detection, prediction and treatment of both endometriosis and endometriosis related malignant neoplasia. Here we review the literature relating to the specific molecular mechanism(s) mediating tumorigenesis arising within endometriosis.

Methods: Guidance (e.g. Cochrane) and published studies were identified. The Published studies were identified through PubMed using the systematic review methods filter, and the authors' topic knowledge. These data were reviewed to identify key and relevant articles to create a comprehensive review article to explore the molecular fingerprint associated with in endometriosis-driven tumorigenesis.

Results: An important focus is the link between C3aR1, PGR, ER1, SOX-17 and other relevant gene expression profiles and endometriosis-driven tumorigenesis. Further studies should also focus on the combined use of CA-125 with HE-4, and the role for OVA1/MIA as clinically relevant diagnostic biomarkers in the prediction of endometriosis-driven tumorigenesis.

Conclusions: Elucidating endometriosis' molecular fingerprint is to understand the molecular mechanisms that drive the endometriosis-associated malignant phenotype. A better understanding of the predictive roles of these genes and the value of the biomarker proteins will allow for the derivation of unique molecular treatment algorithms to better serve our patients.

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