ReviewBlood2024
Escape from T-cell-targeting immunotherapies in acute myeloid leukemia.
Review in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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
52 citing papers in PubMed, 58 citations in OpenAlex.
- FGF18 mediates fibroblast-leukemia cross talk to promote acute myeloid leukemia progression.Blood · 2026Article
- Tet2 deficiency drives age-related heterogeneous progression of myeloid neoplasms through epigenetic-immune microenvironment imbalance.Journal of translational medicine · 2026Article
- SIX1 drives acute myeloid leukemia progression by reprogramming glycolytic metabolism and impairing CD8⁺ T-cell effector function.Immunologic research · 2026Article
- TP53 deficiency in AML induces resistance to T-cell engagers through an immunosuppressive secretome.Leukemia · 2026Article
- Cholesterol Reprogramming in Acute Myeloid Leukemia: Integrating Tumor-Intrinsic Metabolism and Immune Crosstalk.Diseases (Basel, Switzerland) · 2026Review
- TIM-3 in AML: a janus-faced orchestrator of immune exhaustion and leukemic self-renewal.Cancer cell international · 2026Review
- Targeting immunoglobulin superfamily member 9 (IGSF9) to overcome acute myeloid leukemia resistance to CAR-T therapy.Journal of experimental & clinical cancer research : CR · 2026Article
- Combined PD-1 and TIGIT blockade via siRNA enhances anti-leukemic T-cell function and promotes AML cell apoptosis.Scientific reports · 2026Article
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- Integrated multi-target pharmacology of ginseng in acute myeloid leukemia through single-cell sequencing, molecular docking, network pharmacology, and in vitro experiments.Discover oncology · 2026Article
- Advanced Drug Delivery Strategies for Overcoming Biological Barriers: Tumor Microenvironment and Blood-Brain Barrier.Drugs in R&D · 2026Review
- HSCs/MPPs as cells of origin with altered differentiation hierarchy impairing immunomicroenvironment inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- From monoclonals to bispecific T cell engagers: the evolving antibody-based therapy landscape in acute myeloid leukemia.Frontiers in immunology · 2026Review
- Immunological barriers and engineering strategies for CAR-T cell therapy in acute myeloid leukemia.Frontiers in immunology · 2026Review
- HERV-K TM Subunit Elicits CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Delineation of molecular subtypes based on pathway activation signatures reveals intrinsic tumor heterogeneity and pan-cancer shared features.Frontiers in oncology · 2026Article
- Advances in protein ubiquitination modification and immune evasion of breast cancer.Frontiers in cell and developmental biology · 2026Review
- Article
- FUBP3 mediates MXI1 stability to silence RRAS and hinder MAPK signaling in acute megakaryoblastic leukemia progression.Cancer immunology, immunotherapy : CII · 2025Article
- International consensus guidelines for the conduct and reporting of CAR T-cell clinical trials in AML.Blood advances · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractSingle-cell and spatial multimodal technologies have propelled discoveries of the solid tumor microenvironment (TME) molecular features and their correlation with clinical response and resistance to immunotherapy. Computational tools are incessantly being developed to characterize tumor-infiltrating immune cells and to model tumor immune escape. These advances have led to substantial research into T-cell hypofunctional states in the TME and their reinvigoration with T-cell-targeting approaches, including checkpoint inhibitors (CPIs). Until recently, we lacked a high-dimensional picture of the acute myeloid leukemia (AML) TME, including compositional and functional differences in immune cells between disease onset and postchemotherapy or posttransplantation relapse, and the dynamic interplay between immune cells and AML blasts at various maturation stages. AML subgroups with heightened interferon gamma (IFN-γ) signaling were shown to derive clinical benefit from CD123×CD3-bispecific dual-affinity retargeting molecules and CPIs, while being less likely to respond to standard-of-care cytotoxic chemotherapy. In this review, we first highlight recent progress into deciphering immune effector states in AML (including T-cell exhaustion and senescence), oncogenic signaling mechanisms that could reduce the susceptibility of AML cells to T-cell-mediated killing, and the dichotomous roles of type I and II IFN in antitumor immunity. In the second part, we discuss how this knowledge could be translated into opportunities to manipulate the AML TME with the aim to overcome resistance to CPIs and other T-cell immunotherapies, building on recent success stories in the solid tumor field, and we provide an outlook for the future.
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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.