<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(6)</volume><submitter>Dempke WCM</submitter><pubmed_abstract>Recently approved and highly specific small-molecule inhibitors of c-MET exon 14 skipping mutations (e.g., capmatinib, tepotinib) are a new and important therapeutic option for the treatment of non-small cell lung cancer (NSCLC) patients harbouring c-MET alterations. Several experimental studies have provided compelling evidence that c-MET is involved in the regulation of the immune response by up-regulating inhibitory molecules (e.g., PD-L1) and down-regulating of immune stimulators (e.g., CD137, CD252, CD70, etc.). In addition, c-MET was found to be implicated in the regulation of the inflamed tumour microenvironment (TME) and thereby contributing to an increased immune escape of tumour cells from T cell killing. Moreover, it is a major resistance mechanism following treatment of epiderm</pubmed_abstract><journal>Translational lung cancer research</journal><pagination>2667-2682</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8264346</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Has programmed cell death ligand-1 &lt;i>MET&lt;/i> an accomplice in non-small cell lung cancer?-a narrative review.</pubmed_title><pmcid>PMC8264346</pmcid><pubmed_authors>Fenchel K</pubmed_authors><pubmed_authors>Dempke WCM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Has programmed cell death ligand-1 &lt;i>MET&lt;/i> an accomplice in non-small cell lung cancer?-a narrative review.</name><description>Recently approved and highly specific small-molecule inhibitors of c-MET exon 14 skipping mutations (e.g., capmatinib, tepotinib) are a new and important therapeutic option for the treatment of non-small cell lung cancer (NSCLC) patients harbouring c-MET alterations. Several experimental studies have provided compelling evidence that c-MET is involved in the regulation of the immune response by up-regulating inhibitory molecules (e.g., PD-L1) and down-regulating of immune stimulators (e.g., CD137, CD252, CD70, etc.). In addition, c-MET was found to be implicated in the regulation of the inflamed tumour microenvironment (TME) and thereby contributing to an increased immune escape of tumour cells from T cell killing. Moreover, it is a major resistance mechanism following treatment of epiderm</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2025-04-04T09:37:43.005Z</modification><creation>2025-04-04T09:37:43.005Z</creation></dates><accession>S-EPMC8264346</accession><cross_references><pubmed>34295669</pubmed><doi>10.21037/tlcr-21-124</doi></cross_references></HashMap>