ArticleHaematologica2021
Genetic manipulation of primary human natural killer cells to investigate the functional and oncogenic roles of PRDM1.
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- PRDM1-mediated epigenetic and transcriptional repression mechanisms: a key hub in immune differentiation, tumor progression, and inflammatory responses.Frontiers in immunology · 2026Review
- Article
- Genetic and Epigenetic Aberrations ofCurrent issues in molecular biology · 2025Article
- MYC overexpression in natural killer cell lymphoma: prognostic and therapeutic implications.Haematologica · 2024Article
- Natural Killer Cell-Based Immunotherapy against Glioblastoma.International journal of molecular sciences · 2023Review
- Intravascular NK/T-Cell Lymphoma: What We Know about This Diagnostically Challenging, Aggressive Disease.Cancers · 2022Review
- Genomic profiling identifies distinct genetic subtypes in extra-nodal natural killer/T-cell lymphoma.Leukemia · 2022Article
- The identification of gene signatures in patients with extranodal NK/T-cell lymphoma from a pair of twins.BMC cancer · 2021Article
- PRDM1 decreases sensitivity of human NK cells to IL2-induced cell expansion by directly repressing CD25 (IL2RA).Journal of leukocyte biology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Extra-nodal natural killer/T-cell lymphoma, nasal type (ENKTCL) is a highly aggressive lymphoma, where the tumor suppressor gene (TSG) PRDM1 is frequently lost/inactivated. We employed two different CRISPR/Cas9 approaches to generate PRDM1-/- primary NK cells to study its role in NK-cell homeostasis. PRDM1-/- NK cells showed a marked increase in cloning efficiency, higher proliferation rate and less apoptosis compared with their wild type counterparts. Gene expression profiling demonstrated a marked enrichment in pathways associated with proliferation, cell cycle, MYC, MYB and TCR/NK signaling in PRDM1-/- NK cells, but pathways associated with normal cellular functions including cytotoxic functions were down-regulated, suggesting that the loss of PRDM1 shifted NK cells toward proliferation and survival rather than the performance of its normal functions. We were also able to further modify a PRDM1 deleted clone to introduce heterozygous deletions of common TSG in ENKTCL such as TP53, DDX3X, or PTPN6. We have established an in vitro model to elucidate the major pathways through which PRDM1 mediates its homeostatic control of NK-cells. This approach can be applied to the study of other relevant genetic lesions and oncogenic collaborations in lymphoma pathogenesis.
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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.