ArticleJournal for immunotherapy of cancer2019
Gal9/Tim-3 expression level is higher in AML patients who fail chemotherapy.
Article in Journal for immunotherapy of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02573363 (Phase I Investigator Sponsored Study to Assess the Tolerability and Efficacy of Selinexor in Combination With High Dose Cytarabine), which is not on this map. Cited by 71 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phase I Investigator Sponsored Study to Assess the Tolerability and Efficacy of Selinexor in Combination With High Dose Cytarabine (HiDAC) and Mitoxantrone Chemotherapy for Remission Induction in Acute Myelogenous Leukemia (AML)
Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Bibliometric analysis of knowledge maps and future trends of TIM-3 in cancer.Frontiers in oncology · 2026Pooled it
- Immune Checkpoints in Leukaemia as Gatekeepers of Immuno-Modulation.Immunology · 2026Review
- TIM3-targeted delivery of venetoclax overcomes drug resistance and reinvigorates NK cell activity in acute myeloid leukemia.Nature cancer · 2026Article
- OT-55 reshapes tolerogenic BH3-mimetic-induced apoptosis toward immunogenic cell death in acute myeloid leukemia, potentiating PD-1/Tim-3 blockade.Cell death & disease · 2026Article
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- CD28 and ICOS in immune regulation: Structural insights and therapeutic targeting.Bioorganic & medicinal chemistry letters · 2025Review
- IGSF9-targeted therapy inhibits the progression of acute myeloid leukemia.Blood advances · 2025Article
- Galectin-9-An Emerging Glyco-Immune Checkpoint Target for Cancer Therapy.International journal of molecular sciences · 2025Review
- One step further in targeting acute leukemia by combining antibody-based immunotherapies and small molecule inhibitors.Cancer cell international · 2025Review
- Surface downmodulation of TIM3 safeguards healthy cells but not acute myeloid leukemia from CAR T-cell therapy.HemaSphere · 2025Article
- The expression patterns and prognostic significance of PD-1 and TIM-3 on T cells and the differentiated subsets in acute myeloid leukemia.Annals of hematology · 2025Article
- "Galectin-9: A double-edged sword in Acute Myeloid Leukemia".Annals of hematology · 2025Review
- LAG3 as a marker of immune activation in esophageal squamous carcinoma treated with concurrent chemoradiotherapy.Cancer immunology, immunotherapy : CII · 2025Article
- Immune Escape of Acute Myeloid Leukemia after Transplantation.Blood cancer discovery · 2025Review
- CD200 in acute myeloid leukemia: marked upregulation in CEBPA biallelic mutated cases.Diagnostic pathology · 2025Article
- Galectin-9 induces IL-1β production as a key inflammatory cytokine in the acute myeloid leukemia cell line (U937).Research in pharmaceutical sciences · 2025Article
- Genome-wide CRISPR screen identifies IRF1 and TFAP4 as transcriptional regulators of Galectin-9 in T cell acute lymphoblastic leukemia.Science advances · 2025Article
- XPO1/Exportin-1 in Acute Myelogenous Leukemia; Biology and Therapeutic Targeting.Biomolecules · 2025Review
- Bone marrow immune cells and drug resistance in acute myeloid leukemia.Experimental biology and medicine (Maywood, N.J.) · 2025Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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, multi-parameter flow cytometry was performed on peripheral blood and bone marrow biopsy specimens at diagnosis and following induction therapy in 26 AML patients. Expression of CD47, PD-L1, PD-L2 and Gal9 was assessed on CD34
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.