<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>Dama P</submitter><funding>Bristol-Myers Squibb</funding><pubmed_abstract>Immune checkpoint pathways active in Acute Myeloid Leukemia (AML) patients, especially during the course of remission induction chemotherapy, have not been well studied. Although dominant in mediating T cell dysfunction in cancer, it is now well-accepted that interruption of PD-1/PD-L1 axes alone does not always completely restore T cell function, indicating the involvement of additional negative regulatory pathways, such as TIM-3/Gal-9, in promoting T cell exhaustion.Here, we characterized these pathways in AML patients enrolled in a phase I dose escalation trial that combined Selinexor, a Selective Inhibitor of Nuclear Export (SINE), with high-dose cytarabine (HiDAC) and mitoxantrone (Mito) (NCT02573363) as induction therapy.To monitor changes in expression of immune checkpoint receptors</pubmed_abstract><journal>Journal for immunotherapy of cancer</journal><pagination>175</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6621946</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Gal9/Tim-3 expression level is higher in AML patients who fail chemotherapy.</pubmed_title><pmcid>PMC6621946</pmcid><pubmed_authors>Kline J</pubmed_authors><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Dama P</pubmed_authors><pubmed_authors>Tang M</pubmed_authors><pubmed_authors>Fulton N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Gal9/Tim-3 expression level is higher in AML patients who fail chemotherapy.</name><description>Immune checkpoint pathways active in Acute Myeloid Leukemia (AML) patients, especially during the course of remission induction chemotherapy, have not been well studied. Although dominant in mediating T cell dysfunction in cancer, it is now well-accepted that interruption of PD-1/PD-L1 axes alone does not always completely restore T cell function, indicating the involvement of additional negative regulatory pathways, such as TIM-3/Gal-9, in promoting T cell exhaustion.Here, we characterized these pathways in AML patients enrolled in a phase I dose escalation trial that combined Selinexor, a Selective Inhibitor of Nuclear Export (SINE), with high-dose cytarabine (HiDAC) and mitoxantrone (Mito) (NCT02573363) as induction therapy.To monitor changes in expression of immune checkpoint receptors</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jul</publication><modification>2026-04-30T15:09:24.908Z</modification><creation>2026-04-07T16:08:44.594Z</creation></dates><accession>S-EPMC6621946</accession><cross_references><pubmed>31291985</pubmed><doi>10.1186/s40425-019-0611-3</doi></cross_references></HashMap>