New strategies for targeting drug combinations to overcome mutation-driven drug resistance. (February 2017)

• Record Type: Journal Article
• Authors: Wang, Linyan; Wang, Haiyun; Song, Dongli; Xu, Menglin; Liebmen, Michael
• Is Part Of: Seminars in cancer biology. Volume 42(2017)
• Page Start: 44
• Page End: 51
• Publication Date: 2017-02
• Subjects: EGFR Epidermal growth factor receptor -- TP53 Tumor protein p53 -- KRAS Kirsten rat carcoma viral oncogene -- ALK Anaplastic lymphoma kinase -- RTK Protein receptor tyrosine kinase -- TKI Tyrosine kinase inhibitor -- PI3K Phosphatidylinositol 3-kinase -- NSCLC Non-small cell lung cancer -- EMT Epithelial-mesenchymal transition -- PXN Paxillin -- PTEN Phosphatase and tensin homolog on chromosome 10 -- NF1 Neurofibromatosis type 1 -- FOXO3a Forkhead box O3 -- MAGE-A Melanoma-associated antigens family A -- CTLA-4 CTL antigen 4 -- PD-L1 Programmed cell death protein ligand -- MAPK Mitogen-activated protein kinases -- STAT3 Signal transducer and activator of transcription 3 -- GAS6 Growth arrest-specific 6 -- TGF-beta Transforming growth factor beta -- SCLC Small cell lung cancer -- FGFR Fibroblast growth factor receptor -- IGF-1R Insulin-like growth factor-1 receptor -- DDR1 Discoidin domain receptor 1 -- KIT Proto-oncogene receptor tyrosine kinase -- CDC25A Cell division cycle 25A -- CCLE Cancer Cell Line Encyclopedia -- CNV DNA copy number variation -- CGP Cancer Genome Project; Drug resistance -- Lung cancer -- Precision medicine -- Pharmacogenomics profile -- CRISPR-Cas9 screening -- Pathway-centric therapy; Cancer -- Periodicals; Neoplasms -- Periodicals; Review Literature; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.semcancer.2016.11.002
• Languages: English
• ISSNs: 1044-579X

Abstract

Abstract: Targeted therapies are suggested as an effective alternative for patients with cancer that harbor mutations, but treatment outcomes are frequently limited by primary or acquired drug resistance. The present review describes potential mechanisms of primary or acquired drug resistances to provide a resource for considering how to be overcome. We focus on strategies of targeted drug combinations to minimize the development of drug resistance within the context how resistance develops. Strategies benefit from the combined use of "omics" technologies, i.e., high-throughput functional genomics data, pharmacogenomics, or genome-wide CRISPR-Cas9 screening, to analyze and design targeted drug combinations for mutation-driven drug resistance. We also introduce new insights towards pathway-centric combined therapies as an alternative to overcome the heterogeneity and benefit patient prognoses.