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是时候放弃胃肠道神经内分泌肿瘤的传统管理方法了。

Time to give up traditional methods for the management of gastrointestinal neuroendocrine tumours.

作者信息

Yozgat Ahmet, Kekilli Murat, Altay Mustafa

机构信息

Department of Gastroenterology, Ufuk University, Ankara, 06510, Turkey.

Department of Gastroenterology, Gazi University, Ankara 06560, Turkey.

出版信息

World J Clin Cases. 2021 Oct 16;9(29):8627-8646. doi: 10.12998/wjcc.v9.i29.8627.

Abstract

Neuroendocrine tumors (NETs) are a rare and heterogeneous disease group and constitute 0.5% of all malignancies. The annual incidence of NETs is increasing worldwide. The reason for the increase in the incidence of NETs is the detection of benign lesions, incidental detection due to the highest use of endoscopic and imaging procedures, and higher recognition rates of pathologists. There have been exciting developments regarding NET biology in recent years. Among these, first of all, somatostatin receptors and downstream pathways in neuroendocrine cells have been found to be important regulatory mechanisms for protein synthesis, hormone secretion, and proliferation. Subsequently, activation of the mammalian target of rapamycin pathway was found to be an important mechanism in angiogenesis and tumor survival and cell metabolism. Finally, the importance of proangiogenic factors (platelet-derived growth factor, vascular endothelial growth factor, fibroblastic growth factor, angiopoietin, and semaphorins) in the progression of NET has been determined. Using the combination of biomarkers and imaging methods allows early evaluation of the appropriateness of treatment and response to treatment.

摘要

神经内分泌肿瘤(NETs)是一种罕见且异质性的疾病组,占所有恶性肿瘤的0.5%。全球范围内,NETs的年发病率正在上升。NETs发病率上升的原因包括良性病变的检出、内镜检查和影像学检查的高使用率导致的偶然发现以及病理学家更高的识别率。近年来,NET生物学方面有了令人兴奋的进展。其中,首先,神经内分泌细胞中的生长抑素受体和下游途径已被发现是蛋白质合成、激素分泌和增殖的重要调节机制。随后,发现雷帕霉素哺乳动物靶标途径的激活是血管生成、肿瘤存活和细胞代谢中的重要机制。最后,已确定促血管生成因子(血小板衍生生长因子、血管内皮生长因子、成纤维细胞生长因子、血管生成素和信号素)在NET进展中的重要性。结合使用生物标志物和影像学方法可对治疗的适宜性和治疗反应进行早期评估。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b301/8546836/3a8f390272f0/WJCC-9-8627-g001.jpg

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