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从系统角度看细胞因子在非小细胞肺癌联合免疫治疗中的作用。

Role of cytokines in combinatorial immunotherapeutics of non-small cell lung cancer through systems perspective.

机构信息

National Centre for Cell Science, SP Pune University Campus, Pune, India.

出版信息

Cancer Med. 2019 May;8(5):1976-1995. doi: 10.1002/cam4.2112. Epub 2019 Apr 17.

DOI:10.1002/cam4.2112
PMID:30997737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6536974/
Abstract

Lung cancer is the leading cause of deaths related to cancer and accounts for more than a million deaths per year. Various new strategies have been developed and adapted for treatment; still the survival for 5 years is just 16% in patients with non-small cell lung cancer (NSCLC). Most of these strategies to combat NSCLC whether it is a drug molecule or immunotherapy/vaccine candidate require a big cost and time. Integration of computational modeling with systems biology has opened new avenues for understanding complex cancer biology. Resolving the complex interactions of various pathways and their crosstalk leading to oncogenic changes could identify new therapeutic targets with lesser cost and time. Herein, this review provides an overview of various aspects of NSCLC along with available strategies for its cure concluding with our insight into how systems approach could serve as a therapeutic intervention dissecting the immunologic parameters and cross talk between various pathways involved.

摘要

肺癌是癌症相关死亡的主要原因,每年导致超过 100 万人死亡。已经开发并采用了各种新策略来进行治疗;然而,患有非小细胞肺癌(NSCLC)的患者 5 年生存率仅为 16%。这些对抗 NSCLC 的策略,无论是药物分子还是免疫疗法/疫苗候选物,都需要大量的成本和时间。将计算建模与系统生物学相结合,为理解复杂的癌症生物学开辟了新的途径。解决导致致癌变化的各种途径及其串扰的复杂相互作用,可以确定成本和时间较低的新治疗靶点。本文综述了 NSCLC 的各个方面以及其治疗的现有策略,并总结了我们对系统方法如何作为一种治疗干预的见解,以剖析涉及的各种途径之间的免疫参数和串扰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e867/6536974/efc7a92fa69d/CAM4-8-1976-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e867/6536974/5ba8090a0741/CAM4-8-1976-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e867/6536974/efc7a92fa69d/CAM4-8-1976-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e867/6536974/5ba8090a0741/CAM4-8-1976-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e867/6536974/efc7a92fa69d/CAM4-8-1976-g002.jpg

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ITCH facilitates proteasomal degradation of TXNIP in hypoxia- induced lung cancer cells.ITCH 促进低氧诱导的肺癌细胞中 TXNIP 的蛋白酶体降解。
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