ArticleJournal of hematology & oncology2025
Directly reprogrammed NK cells driven by BCL11B depletion enhance targeted immunotherapy against pancreatic ductal adenocarcinoma.
Article in Journal of hematology & oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Microfluidic perspectives on chimeric antigen receptor T-cell migration in solid tumours: highlighting physical confinement as a key barrier.Molecular systems design & engineering · 2026Review
- Targeting the MICA/B-NKG2D axis in cancer: from molecular structure to immunotherapeutic strategies-a narrative review.Translational cancer research · 2026Review
- Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1.Scientific reports · 2026Article
- Targeting PKMYT1 enhances antitumor immune responses to PD-L1 blockade in castration-resistant prostate cancer.Journal for immunotherapy of cancer · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy characterized by desmoplastic stroma, immunosuppressive tumor microenvironment (TME), and resistance to standard therapies. Natural killer (NK) cell-based immunotherapies have shown limited efficacy due to impaired persistence, infiltration, and function in PDAC.
methodsWe established a direct reprogramming strategy to generate cytotoxic NK cells (1 F-NKs) by targeting BCL11B, a transcription factor essential for T cell lineage commitment, using shRNA or CRISPR/Cas9 in peripheral blood mononuclear cells (PBMCs). A genome-wide CRISPR/Cas9 screen identified tumor-intrinsic modulators of NK resistance. Functional and in vivo studies assesses the efficacy of 1 F-NKs alone and in combination with mesothelin (MSLN)-CAR engineering and PKMYT1 inhibition.
resultsBCL11B depletion enabled the generation of CD56
conclusionsThis study presents a synergistic immunotherapy platform that integrates NK reprogramming, CAR engineering, and tumor sensitization. The combinatorial approach significantly enhances antitumor efficacy in PDAC and offers a promising strategy for overcoming immune resistance in solid tumors.
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