<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Leung AW</submitter><funding>Canadian Institutes of Health Research</funding><pagination>e0150675</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4777418</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(3)</volume><pubmed_abstract>Platinum-based combination chemotherapy is the standard treatment for advanced non-small cell lung cancer (NSCLC). While cisplatin is effective, its use is not curative and resistance often emerges. As a consequence of microenvironmental heterogeneity, many tumour cells are exposed to sub-lethal doses of cisplatin. Further, genomic heterogeneity and unique tumor cell sub-populations with reduced sensitivities to cisplatin play a role in its effectiveness within a site of tumor growth. Being exposed to sub-lethal doses will induce changes in gene expression that contribute to the tumour cell's ability to survive and eventually contribute to the selective pressures leading to cisplatin resistance. Such changes in gene expression, therefore, may contribute to cytoprotective mechanisms. Here, </pubmed_abstract><journal>PloS one</journal><pubmed_title>Combined Use of Gene Expression Modeling and siRNA Screening Identifies Genes and Pathways Which Enhance the Activity of Cisplatin When Added at No Effect Levels to Non-Small Cell Lung Cancer Cells In Vitro.</pubmed_title><pmcid>PMC4777418</pmcid><funding_grant_id>MOP 136982</funding_grant_id><funding_grant_id>MOP89948</funding_grant_id><pubmed_authors>Poon S</pubmed_authors><pubmed_authors>Segovia R</pubmed_authors><pubmed_authors>Bally MB</pubmed_authors><pubmed_authors>Backstrom I</pubmed_authors><pubmed_authors>Ricaurte D</pubmed_authors><pubmed_authors>Qadir MA</pubmed_authors><pubmed_authors>Aparicio S</pubmed_authors><pubmed_authors>Leung AW</pubmed_authors><pubmed_authors>Rawji J</pubmed_authors><pubmed_authors>Steidl C</pubmed_authors><pubmed_authors>Kwok B</pubmed_authors><pubmed_authors>McKinney S</pubmed_authors><pubmed_authors>Stirling PC</pubmed_authors><pubmed_authors>Hung SS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Combined Use of Gene Expression Modeling and siRNA Screening Identifies Genes and Pathways Which Enhance the Activity of Cisplatin When Added at No Effect Levels to Non-Small Cell Lung Cancer Cells In Vitro.</name><description>Platinum-based combination chemotherapy is the standard treatment for advanced non-small cell lung cancer (NSCLC). While cisplatin is effective, its use is not curative and resistance often emerges. As a consequence of microenvironmental heterogeneity, many tumour cells are exposed to sub-lethal doses of cisplatin. Further, genomic heterogeneity and unique tumor cell sub-populations with reduced sensitivities to cisplatin play a role in its effectiveness within a site of tumor growth. Being exposed to sub-lethal doses will induce changes in gene expression that contribute to the tumour cell's ability to survive and eventually contribute to the selective pressures leading to cisplatin resistance. Such changes in gene expression, therefore, may contribute to cytoprotective mechanisms. Here, </description><dates><release>2016-01-01T00:00:00Z</release><publication>2016</publication><modification>2025-04-26T09:18:35.289Z</modification><creation>2019-03-26T22:53:30Z</creation></dates><accession>S-EPMC4777418</accession><cross_references><pubmed>26938915</pubmed><doi>10.1371/journal.pone.0150675</doi></cross_references></HashMap>