ReviewCancer science2021
TIM-3 in normal and malignant hematopoiesis: Structure, function, and signaling pathways.
Review in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Cell-type specificity of Tim-3 in respiratory diseases: from mechanisms to clinical translation.Frontiers in immunology · 2026Pooled it
- Review
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- From monoclonals to bispecific T cell engagers: the evolving antibody-based therapy landscape in acute myeloid leukemia.Frontiers in immunology · 2026Review
- The TIM-3/Gal-9 Pathway: A Promising Therapeutic Target for Regulation of Immune Checkpoint in Rheumatoid Arthritis.Current rheumatology reviews · 2026Review
- Emerging strategies and novel therapeutic targets in acute myeloid leukemia: current advances and future directions.Biomarker research · 2025Review
- Surface downmodulation of TIM3 safeguards healthy cells but not acute myeloid leukemia from CAR T-cell therapy.HemaSphere · 2025Article
- Unraveling the immunomodulatory role of TIM-3 in head and neck squamous cell carcinoma: implications for targeted therapy.Discover oncology · 2025Review
- Unravelling T cell exhaustion through co-inhibitory receptors and its transformative role in cancer immunotherapy.Clinical and translational medicine · 2025Review
- Effect of FLT3 ligand on the gene expression of TIM-3, HIF1-α, and TNF-α in an acute myeloid leukemia cell line.Molecular biology reports · 2025Article
- TIM-3 marks measurable residual leukemic stem cells responsible for relapse after allogeneic stem cell transplantation.Cancer science · 2025Article
- Beyond monotherapy: multimodal strategies integrating immune checkpoint inhibitors in lymphoma management.Frontiers in immunology · 2025Review
- Article
- Association of TIM-3 checkpoint receptor expression on T cells with treatment-free remission in chronic myeloid leukemia.Blood advances · 2023Article
- TIM-3 signaling hijacks the canonical Wnt/β-catenin pathway to maintain cancer stemness in acute myeloid leukemia.Blood advances · 2023Article
- TIM-3/Gal-9 interaction affects glucose and lipid metabolism in acute myeloid leukemia cell lines.Frontiers in immunology · 2023Article
- A novel anti-galectin-9 immunotherapy limits the early progression of pancreatic neoplastic lesions in transgenic mice.Frontiers in immunology · 2023Article
- Clinical roles of TIM-3 in myeloid malignancies and its importance in cellular therapy.Blood cell therapy · 2022Article
- Therapeutic Advances in Immunotherapies for Hematological Malignancies.International journal of molecular sciences · 2022Review
- Immune Checkpoint Receptors Signaling in T Cells.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is hierarchically organized by self-renewing leukemic stem cells (LSCs). LSCs originate from hematopoietic stem cells (HSCs) by acquiring multistep leukemogenic events. To specifically eradicate LSCs, while keeping normal HSCs intact, the discrimination of LSCs from HSCs is important. We have identified T-cell immunoglobulin and mucin-domain containing-3 (TIM-3) as an LSC-specific surface molecule in human myeloid malignancies and demonstrated its essential function in maintaining the self-renewal ability of LSCs. TIM-3 has been intensively investigated as a "coinhibitory" or "immune checkpoint" molecule of T cells. However, little is known about its distinct function in T cells and myeloid malignancies. In this review, we discuss the structure of TIM-3 and its function in normal blood cells and LSCs, emphasizing the specific signaling pathways involved, as well as the therapeutic applications of TIM-3 molecules in human myeloid malignancies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.