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打破细胞致瘤网络的串扰：解决晚期非小细胞肺癌靶向治疗耐药性的假说

Breaking the crosstalk of the cellular tumorigenic network: Hypothesis for addressing resistances to targeted therapies in advanced NSCLC.

作者信息

Langhammer Stefan, Scheerer Joachim

机构信息

Life Science Consulting, Hirschweg, Burgwedel, Germany.

出版信息

Oncotarget. 2017 Jun 27;8(26):43555-43570. doi: 10.18632/oncotarget.16674.

DOI:10.18632/oncotarget.16674
PMID:28402937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5522169/
Abstract

In the light of current treatment developments for non-small cell lung cancer (NSCLC), the idea of a plastic cellular tumorigenic network bound by key paracrine signaling pathways mediating resistances to targeted therapies is brought forward. Based on a review of available preclinical and clinical data in NSCLC combinational approaches to address drivers of this network with marketed drugs are discussed. Five criteria for selecting drug combination regimens aiming at its disruption and thereby overcoming resistances are postulated.

摘要

鉴于非小细胞肺癌（NSCLC）当前的治疗进展，提出了一种由关键旁分泌信号通路绑定的可塑性细胞致瘤网络的概念，这些信号通路介导对靶向治疗的耐药性。基于对NSCLC现有临床前和临床数据的综述，讨论了使用上市药物解决该网络驱动因素的联合方法。提出了选择旨在破坏该网络从而克服耐药性的药物联合方案的五条标准。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1f/5522169/e9a28696af03/oncotarget-08-43555-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1f/5522169/e9a28696af03/oncotarget-08-43555-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1f/5522169/e9a28696af03/oncotarget-08-43555-g001.jpg

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