<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bollig-Fischer A</submitter><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><pagination>26</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8607376</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2(1)</volume><pubmed_abstract>The development of targeted therapies that inhibit cancer-driving oncogenes has improved outcomes of patients diagnosed with lung adenocarcinoma (LUAD). In contrast, patients diagnosed with lung squamous cell carcinoma (LUSC) suffer worse survival outcomes and lack effective targeted treatment options. Identification of molecular drivers of LUSC to support development of targeted treatments is urgently needed. Addressing this need, the current report introduces the novel cancer gene SLIT- and NTRK-like family member 3 (SLITRK3) and its role in activating the neurotrophic receptor tyrosine kinase 3 (NTRK3) in LUSC cells. Multiple genome-wide data sets from patient samples were produced by us or downloaded from public databases to analyze tumor gene copy number aberrations, mRNA expression a</pubmed_abstract><journal>Molecular biomedicine</journal><pubmed_title>Role of novel cancer gene SLITRK3 to activate NTRK3 in squamous cell lung cancer.</pubmed_title><pmcid>PMC8607376</pmcid><funding_grant_id>P30 CA022453</funding_grant_id><funding_grant_id>P30CA022453</funding_grant_id><pubmed_authors>Bepler G</pubmed_authors><pubmed_authors>Mittal S</pubmed_authors><pubmed_authors>Michelhaugh SK</pubmed_authors><pubmed_authors>Mamdani H</pubmed_authors><pubmed_authors>Bollig-Fischer A</pubmed_authors><pubmed_authors>Bao B</pubmed_authors><pubmed_authors>Manning M</pubmed_authors><pubmed_authors>Dyson G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of novel cancer gene SLITRK3 to activate NTRK3 in squamous cell lung cancer.</name><description>The development of targeted therapies that inhibit cancer-driving oncogenes has improved outcomes of patients diagnosed with lung adenocarcinoma (LUAD). In contrast, patients diagnosed with lung squamous cell carcinoma (LUSC) suffer worse survival outcomes and lack effective targeted treatment options. Identification of molecular drivers of LUSC to support development of targeted treatments is urgently needed. Addressing this need, the current report introduces the novel cancer gene SLIT- and NTRK-like family member 3 (SLITRK3) and its role in activating the neurotrophic receptor tyrosine kinase 3 (NTRK3) in LUSC cells. Multiple genome-wide data sets from patient samples were produced by us or downloaded from public databases to analyze tumor gene copy number aberrations, mRNA expression a</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2026-05-08T16:38:36.765Z</modification><creation>2022-02-11T15:13:15.887Z</creation></dates><accession>S-EPMC8607376</accession><cross_references><pubmed>35006496</pubmed><doi>10.1186/s43556-021-00051-2</doi></cross_references></HashMap>