ArticleBlood cancer journal2021
Activated naïve γδ T cells accelerate deep molecular response to BCR-ABL inhibitors in patients with chronic myeloid leukemia.
Article in Blood cancer journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Dasatinib boosts γδ T cell expansion and memory phenotypes with enhanced antitumor immunity.Cancer immunology, immunotherapy : CII · 2026Article
- TIGIT Blockade Potentiates the Anti-Leukemic Activity of Exercise-Mobilized Donor Lymphocytes and Expanded γδ T-Cells.Cancers · 2026Article
- Targeting MDSCs in cancer: emerging immunotherapeutic and metabolic strategies.Frontiers in immunology · 2026Review
- Innate CD8 T-cells as a potential predictive biomarker for deep molecular response in chronic myeloid leukemia patients.Cancer immunology, immunotherapy : CII · 2025Article
- Balancing Tumor Immunotherapy and Immune-Related Adverse Events: Unveiling the Key Regulators.International journal of molecular sciences · 2024Review
- γδ T Lymphocytes as a Double-Edged Sword-State of the Art in Gynecological Diseases.International journal of molecular sciences · 2022Review
- The prognostic value and therapeutic targeting of myeloid-derived suppressor cells in hematological cancers.Frontiers in immunology · 2022Review
- Identification of the immunosuppressive effect of γδ T cells correlated to bone morphogenetic protein 2 in acute myeloid leukemia.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase inhibitors (TKIs) that target BCR-ABL are the frontline treatments in chronic myeloid leukemia (CML). Growing evidence has shown that TKIs also enhance immunity. Since gamma-delta T (γδT) cells possess the potent anticancer capability, here we investigated the potential involvement of γδT cells in TKI treatments for CML. We characterized γδT cells isolated from chronic-phase CML patients before and during TKI treatments. γδT expression increased significantly in CML patients who achieved major molecular response (MMR) and deep molecular response (DMR). Their Vδ2 subset of γδT also expanded, and increased expression of activating molecules, namely IFN-γ, perforin, and CD107a, as well as γδT cytotoxicity. Mechanistically, TKIs augmented the efflux of isopentenyl pyrophosphate (IPP) from CML cells, which stimulated IFN-γ production and γδT expansion. Notably, the size of the IFN-γ
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Registered trials
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