Molecular mechanisms of therapy resistance in solid tumors: chasing “moving” targets
- 10 March 2017
- journal article
- review article
- Published by Springer Science and Business Media LLC in Virchows Archiv A Pathological Anatomy and Histopathology
- Vol. 471 (2), 155-164
- https://doi.org/10.1007/s00428-017-2101-7
Abstract
The goal of personalized cancer therapy is to treat tumors based on genomic aberrations that drive their survival and progression. Most patients who receive targeted therapies typically develop resistance and disease progression within a year’s time. This review focuses on the heterogeneous mechanisms of therapy resistance to tyrosine kinase inhibitors, endocrine/hormone therapy and checkpoint blockade using non-small cell lung cancer, breast and castration-resistant prostate cancer, and melanoma as classical examples, respectively. In addition, testing for resistance mechanisms and therapeutic approaches to overcoming resistance is addressed.Keywords
This publication has 86 references indexed in Scilit:
- Crizotinib-Resistant ROS1 Mutations Reveal a Predictive Kinase Inhibitor Sensitivity Model for ROS1- and ALK-Rearranged Lung CancersClinical Cancer Research, 2016
- MED15 overexpression in prostate cancer arises during androgen deprivation therapy via PI3K/mTOR signalingOncotarget, 2016
- Molecular Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors inALK-Rearranged Lung CancerCancer Discovery, 2016
- Emergence of resistance to tyrosine kinase inhibitors in non-small-cell lung cancer can be delayed by an upfront combination with the HSP90 inhibitor onalespibBritish Journal of Cancer, 2016
- Inherited DNA-Repair Gene Mutations in Men with Metastatic Prostate CancerThe New England Journal of Medicine, 2016
- Prospective Validation of Rapid Plasma Genotyping for the Detection ofEGFRandKRASMutations in Advanced Lung CancerJAMA Oncology, 2016
- Heterogeneity of resistance mutations detectable by next-generation sequencing in TKI-treated lung adenocarcinomaOncotarget, 2016
- NOTCH, ASCL1, p53 and RB alterations define an alternative pathway driving neuroendocrine and small cell lung carcinomasInternational Journal of Cancer, 2015
- Acquired resistance mechanisms to tyrosine kinase inhibitors in lung cancer with activating epidermal growth factor receptor mutation—diversity, ductility, and destinyCancer and Metastasis Reviews, 2012
- Clinical Definition of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small-Cell Lung CancerJournal of Clinical Oncology, 2010