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

Stefan Langhammer; Joachim Scheerer

doi:10.18632/oncotarget.16674

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

Stefan Langhammer _ and Joachim Scheerer

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Oncotarget. 2017; 8:43555-43570. https://doi.org/10.18632/oncotarget.16674

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Abstract

Stefan Langhammer1 and Joachim Scheerer1

1 Life Science Consulting, Hirschweg, Burgwedel, Germany

Correspondence to:

Stefan Langhammer, email:

Keywords: NSCLC, targeted therapy, EGFR, angiogenesis

Received: December 16, 2016 Accepted: March 13, 2017 Published: March 29, 2017

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.

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PII: 16674

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

Abstract