Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8361971 | Seminars in Cancer Biology | 2017 | 8 Pages |
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.
Keywords
Cdc25aFOXO3aNF1DDR1IGF-1REGFRTP53TKIRTKFGFRCCLEMAGE-ADNA copy number variationCTLA-4cell division cycle 25AGrowth arrest-specific 6Cancer Cell Line Encyclopediaphosphatase and tensin homolog on chromosome 10PI3KCNVPD-L1KRASCGPSTAT3PaxillinMAPKTGF-betaPXNALKSCLCTransforming Growth Factor Betatumor protein p53EMTforkhead box O3Lung cancerNSCLCSmall cell lung cancerNon-small cell lung cancerPhosphatidylinositol 3-kinaseAnaplastic lymphoma kinasesignal transducer and activator of transcription 3Drug resistanceTyrosine kinase inhibitorneurofibromatosis type 1Precision medicinePtenKitmitogen-activated protein kinasesGas6Epithelial-mesenchymal transitiondiscoidin domain receptor 1Insulin-like growth factor-1 receptorEpidermal growth factor receptorfibroblast growth factor receptor
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Authors
Linyan Wang, Haiyun Wang, Dongli Song, Menglin Xu, Michael Liebmen,