ArticleThe Journal of clinical investigation2018
PRDM16 isoforms differentially regulate normal and leukemic hematopoiesis and inflammatory gene signature.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Pooled it
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- RORγtScience immunology · 2026Article
- Sequential RNA polymerase II activation drives human hematopoiesis.Cell reports · 2026Article
- PRDM16 expression is an independent prognostic factor in AML with the double-mutant NPM1/FLT3-ITD genotype.Annals of hematology · 2026Article
- Dexamethasone added to induction and post-remission therapy in older patients with newly diagnosed acute myeloid leukemia: a multicenter, phase II trial (DEXAML-02).Haematologica · 2025Article
- Development and validation of a prognostic prediction model based on coagulation-related genes and clinical factors in acute leukemia.Translational pediatrics · 2025Article
- PRDM16, a new kid on the block in cardiovascular health and disease.Cardiovascular research · 2025Review
- Article
- Clinical value of serum PRDM16 in early diagnosis and prognosis assessment of lung adenocarcinoma.Molecular biology reports · 2025Article
- Overexpression of PRDM16 attenuates acute kidney injury progression: genetic and pharmacological approaches.MedComm · 2024Article
- Dysregulated innate immune signaling cooperates with RUNX1 mutations to transform an MDS-like disease to AML.iScience · 2024Article
- Proteomics to predict relapse in patients with myelodysplastic neoplasms undergoing allogeneic hematopoietic cell transplantation.Biomarker research · 2024Article
- A PRDM16-driven signal regulates body composition in testosterone-treated hypogonadal men.Frontiers in endocrinology · 2024Article
- PRDM16 regulates arterial development and vascular integrity.Frontiers in physiology · 2023Article
- Genome-wide DNA methylation analysis in pediatric acute myeloid leukemia.Blood advances · 2022Article
- Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia.Blood cancer discovery · 2022Article
- Article
- Acute Myeloid Leukemia-Related Proteins Modified by Ubiquitin and Ubiquitin-like Proteins.International journal of molecular sciences · 2022Review
- LncRNA Hmrhl regulates expression of cancer related genes in chronic myelogenous leukemia through chromatin association.NAR cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
PRDM16 is a transcriptional coregulator involved in translocations in acute myeloblastic leukemia (AML), myelodysplastic syndromes, and T acute lymphoblastic leukemia that is highly expressed in and required for the maintenance of hematopoietic stem cells (HSCs), and can be aberrantly expressed in AML. Prdm16 is expressed as full-length (fPrdm16) and short (sPrdm16) isoforms, the latter lacking the N-terminal PR domain. The role of both isoforms in normal and malignant hematopoiesis is unclear. We show here that fPrdm16 was critical for HSC maintenance, induced multiple genes involved in GTPase signaling, and repressed inflammation, while sPrdm16 supported B cell development biased toward marginal zone B cells and induced an inflammatory signature. In a mouse model of human MLL-AF9 leukemia, fPrdm16 extended latency, while sPrdm16 shortened latency and induced a strong inflammatory signature, including several cytokines and chemokines that are associated with myelodysplasia and with a worse prognosis in human AML. Finally, in human NPM1-mutant and in MLL-translocated AML, high expression of PRDM16, which negatively impacts outcome, was associated with inflammatory gene expression, thus corroborating the mouse data. Our observations demonstrate distinct roles for Prdm16 isoforms in normal HSCs and AML, and identify sPrdm16 as one of the drivers of prognostically adverse inflammation in leukemia.
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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.