{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Dama P"],"funding":["Bristol-Myers Squibb"],"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"],"journal":["Journal for immunotherapy of cancer"],"pagination":["175"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6621946"],"repository":["biostudies-literature"],"pubmed_title":["Gal9/Tim-3 expression level is higher in AML patients who fail chemotherapy."],"pmcid":["PMC6621946"],"pubmed_authors":["Kline J","Liu H","Dama P","Tang M","Fulton N"],"additional_accession":[]},"is_claimable":false,"name":"Gal9/Tim-3 expression level is higher in AML patients who fail chemotherapy.","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","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jul","modification":"2026-04-30T15:09:24.908Z","creation":"2026-04-07T16:08:44.594Z"},"accession":"S-EPMC6621946","cross_references":{"pubmed":["31291985"],"doi":["10.1186/s40425-019-0611-3"]}}