Abstract
Resistance to molecularly targeted therapies can result from genomic alterations in the tumor cells that reactivate oncogenic signaling. Less is known of tumor cell-extrinsic mechanisms of resistance to targeted therapies. Two recent studies have identified HGF as a soluble factor capable of mediating resistance to BRAF and HER2 inhibitors in a paracrine manner. These new findings suggest an important role for the tumor microenvironment in mediating resistance to molecularly targeted therapies.
MeSH terms
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Cell Line, Tumor
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Cell Survival / drug effects
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Drug Resistance, Neoplasm
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Hepatocyte Growth Factor / metabolism
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Humans
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Neoplasms / drug therapy
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Neoplasms / metabolism
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Neoplasms / pathology
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Protein Kinase Inhibitors / pharmacology
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Protein Kinase Inhibitors / therapeutic use
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Proto-Oncogene Proteins B-raf / antagonists & inhibitors
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Proto-Oncogene Proteins B-raf / metabolism
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Receptor, ErbB-2 / antagonists & inhibitors
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Receptor, ErbB-2 / metabolism
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Signal Transduction / drug effects
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Tumor Microenvironment*
Substances
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Antineoplastic Agents
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Protein Kinase Inhibitors
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Hepatocyte Growth Factor
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Receptor, ErbB-2
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BRAF protein, human
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Proto-Oncogene Proteins B-raf