<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Duan H</submitter><funding>Jie Zha</funding><funding>Bing Xu</funding><funding>Qian Lai</funding><funding>Li Zhang</funding><pagination>121</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11657277</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>A tyrosine kinase inhibitor (TKI) such as Imatinib (IM) is the preferred treatment for Chronic Myeloid Leukemia (CML). However, the emergence of IM resistance presents a significant challenge to disease management. A characteristic of cancer cells, including IM-resistant CMLs, are characterized by heightened uptake of glucose and aberrant glycolysis in the cytosol, which is known as the Warburg effect. In addition to its potential to modulate the Warburg effect, Chiglitazar (Chi), a compound that regulates glucose metabolism, has also been investigated for its implication in cancer treatment. This suggests that combining Chi with IM may be a therapeutic strategy for overcoming IM resistance in CML.&lt;h4>Methods&lt;/h4>Sensitive and IM-resistance CML cells were treated with Ch</pubmed_abstract><journal>Experimental hematology &amp; oncology</journal><pubmed_title>Chiglitazar diminishes the warburg effect through PPARγ/mTOR/PKM2 and increases the sensitivity of imatinib in chronic myeloid leukemia.</pubmed_title><pmcid>PMC11657277</pmcid><funding_grant_id>82400196</funding_grant_id><funding_grant_id>2023J06054</funding_grant_id><funding_grant_id>U22A2090</funding_grant_id><funding_grant_id>3502Z20227346</funding_grant_id><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Shan W</pubmed_authors><pubmed_authors>Yao J</pubmed_authors><pubmed_authors>Yang L</pubmed_authors><pubmed_authors>Xu B</pubmed_authors><pubmed_authors>Lai Q</pubmed_authors><pubmed_authors>Zha J</pubmed_authors><pubmed_authors>Deng M</pubmed_authors><pubmed_authors>Lin Z</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Duan H</pubmed_authors><pubmed_authors>Zhong M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Chiglitazar diminishes the warburg effect through PPARγ/mTOR/PKM2 and increases the sensitivity of imatinib in chronic myeloid leukemia.</name><description>&lt;h4>Background&lt;/h4>A tyrosine kinase inhibitor (TKI) such as Imatinib (IM) is the preferred treatment for Chronic Myeloid Leukemia (CML). However, the emergence of IM resistance presents a significant challenge to disease management. A characteristic of cancer cells, including IM-resistant CMLs, are characterized by heightened uptake of glucose and aberrant glycolysis in the cytosol, which is known as the Warburg effect. In addition to its potential to modulate the Warburg effect, Chiglitazar (Chi), a compound that regulates glucose metabolism, has also been investigated for its implication in cancer treatment. This suggests that combining Chi with IM may be a therapeutic strategy for overcoming IM resistance in CML.&lt;h4>Methods&lt;/h4>Sensitive and IM-resistance CML cells were treated with Ch</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-04T01:09:08.737Z</modification><creation>2025-04-04T01:09:08.737Z</creation></dates><accession>S-EPMC11657277</accession><cross_references><pubmed>39696470</pubmed><doi>10.1186/s40164-024-00589-1</doi></cross_references></HashMap>