<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10</volume><submitter>Correa S</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Although chronic myeloid leukemia (CML) treatment has improved since the introduction of imatinib mesylate (IM), cases of resistance have been reported. This resistance has been associated with the emergence of multidrug resistance (MDR) phenotype, as a BCR-ABL independent mechanism. The classic pathway studied in MDR promotion is ATP-binding cassette (ABC) family transporters expression, but other mechanisms that drive drug resistance are largely unknown. To better understand IM therapy relapse due to the rise of MDR, we compared the proteomic profiles of K562 and Lucena (K562/VCR) cells.&lt;h4>Results&lt;/h4>The use of 2-DE coupled with a MS approach resulted in the identification of 36 differentially expressed proteins. Differential mRNA levels of leucine-rich PPR motif-con</pubmed_abstract><journal>Proteome science</journal><pagination>23</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3361502</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A comparative proteomic study identified LRPPRC and MCM7 as putative actors in imatinib mesylate cross-resistance in Lucena cell line.</pubmed_title><pmcid>PMC3361502</pmcid><pubmed_authors>Pizzatti L</pubmed_authors><pubmed_authors>Pinto D</pubmed_authors><pubmed_authors>Correa S</pubmed_authors><pubmed_authors>Du Rocher B</pubmed_authors><pubmed_authors>Mencalha A</pubmed_authors><pubmed_authors>Abdelhay E</pubmed_authors></additional><is_claimable>false</is_claimable><name>A comparative proteomic study identified LRPPRC and MCM7 as putative actors in imatinib mesylate cross-resistance in Lucena cell line.</name><description>&lt;h4>Background&lt;/h4>Although chronic myeloid leukemia (CML) treatment has improved since the introduction of imatinib mesylate (IM), cases of resistance have been reported. This resistance has been associated with the emergence of multidrug resistance (MDR) phenotype, as a BCR-ABL independent mechanism. The classic pathway studied in MDR promotion is ATP-binding cassette (ABC) family transporters expression, but other mechanisms that drive drug resistance are largely unknown. To better understand IM therapy relapse due to the rise of MDR, we compared the proteomic profiles of K562 and Lucena (K562/VCR) cells.&lt;h4>Results&lt;/h4>The use of 2-DE coupled with a MS approach resulted in the identification of 36 differentially expressed proteins. Differential mRNA levels of leucine-rich PPR motif-con</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Mar</publication><modification>2026-05-03T04:31:22.352Z</modification><creation>2025-07-06T03:04:41.021Z</creation></dates><accession>S-EPMC3361502</accession><cross_references><pubmed>22458888</pubmed><doi>10.1186/1477-5956-10-23</doi></cross_references></HashMap>