ArticleBlood2019
PRDM16s transforms megakaryocyte-erythroid progenitors into myeloid leukemia-initiating cells.
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Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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Who cites it
28 citing papers in PubMed, 30 citations in OpenAlex.
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Genome-wide association study in 21,271 individuals identifies 9 novel loci associated with circulating CD34HemaSphere · 2026Article
- The Roles of the PRDM Family in the Neuro-Motor System.Biomolecules · 2026Review
- Investigation of the expression and potential mechanistic role of BYSL in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- PRDM16 expression is an independent prognostic factor in AML with the double-mutant NPM1/FLT3-ITD genotype.Annals of hematology · 2026Article
- Metabolic reprogramming by PRDM16 drives cytarabine resistance in acute myeloid leukemia.Haematologica · 2025Article
- Prognostic Risk Model of Megakaryocyte-Erythroid Progenitor (MEP) Signature Based on AHSP and MYB in Acute Myeloid Leukemia.Biomedicines · 2025Article
- DOGMA-seq and multimodal, single-cell analysis in acute myeloid leukemia.International review of cell and molecular biology · 2025Review
- Overexpression of PRDM16 attenuates acute kidney injury progression: genetic and pharmacological approaches.MedComm · 2024Article
- Versatility of megakaryocytes in homeostasis and disease.Blood science (Baltimore, Md.) · 2024Review
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- Kmt2c restricts G-CSF-driven HSC mobilization and granulocyte production in a methyltransferase-independent manner.Cell reports · 2024Article
- Super-enhancer omics in stem cell.Molecular cancer · 2024Review
- Dysregulated innate immune signaling cooperates with RUNX1 mutations to transform an MDS-like disease to AML.iScience · 2024Article
- UBTF tandem duplications are rare but recurrent alterations in adult AML and associated with younger age, myelodysplasia, and inferior outcome.Blood cancer journal · 2023Article
- Super enhancers: Pathogenic roles and potential therapeutic targets for acute myeloid leukemia (AML).Genes & diseases · 2022Review
- Genome-wide DNA methylation analysis in pediatric acute myeloid leukemia.Blood advances · 2022Article
- Isolation, Maintenance and Expansion of Adult Hematopoietic Stem/Progenitor Cells and Leukemic Stem Cells.Cancers · 2022Review
- An oncogenic enhancer encodes selective selenium dependency in AML.Cell stem cell · 2022Article
- Impact ofPharmacogenomics and personalized medicine · 2022Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Tianyuan HuDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Kiyomi MoritaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Matthew C HillProgram in Developmental Biology, Baylor College of Medicine, Houston, TX.
Yajian JiangProgram in Developmental Biology, Baylor College of Medicine, Houston, TX.
Ayumi KitanoDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Yusuke SaitoDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Feng WangDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Xizeng MaoDepartment of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX.
Kevin A HoegenauerDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Kazuhiro MorishitaDivision of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
James F MartinProgram in Developmental Biology, Baylor College of Medicine, Houston, TX.
P Andrew FutrealDepartment of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX.
Koichi TakahashiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Daisuke NakadaDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USUniversity of Miyazaki · JP
Funding
Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8MTumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9MUniversity of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7MVirology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7MHematology Training ProgramT32DK060445 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2002 to 2023
$8.3MPitx2 in atrial fibrillationR01HL118761 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MARTIN, JAMES F · 2014 to 2025
$6.1MMETABOLIC REGULATION IN LEUKEMIA-INITIATING CELLSR01CA193235 · NCI · BAYLOR COLLEGE OF MEDICINE · PI NAKADA, DAISUKE · 2015 to 2024
$4.6MHippo and Wnt Signaling in Cardiac RegenerationR01HL127717 · NHLBI · TEXAS HEART INSTITUTE · PI MARTIN, JAMES F · 2016 to 2023
$4.4MOptical elastography for assessment of myocardial regenerationR01HL130804 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LARIN, KIRILL V, MARTIN, JAMES F · 2016 to 2019
$2.9MMesenchymal Stromal Cells Regulate Hematopoietic Stem Cell AgingR01DK107413 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI NAKADA, DAISUKE · 2016 to 2020
$2.2MBD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430kNCI NIH HHS P30 CA016672NCI NIH HHS P30 CA125123NCI NIH HHS P50 CA100632NCI NIH HHS R01 CA193235NCRR NIH HHS S10 RR024574NHLBI NIH HHS R01 HL118761NHLBI NIH HHS R01 HL127717NHLBI NIH HHS R01 HL130804NIAID NIH HHS P30 AI036211NIDDK NIH HHS R01 DK107413NIDDK NIH HHS T32 DK060445
Abstract
Oncogenic mutations confer on cells the ability to propagate indefinitely, but whether oncogenes alter the cell fate of these cells is unknown. Here, we show that the transcriptional regulator PRDM16s causes oncogenic fate conversion by transforming cells fated to form platelets and erythrocytes into myeloid leukemia stem cells (LSCs).
Indexed as
AnimalsCell Transformation, NeoplasticDNA-Binding ProteinsGene Expression Regulation, LeukemicGene Regulatory NetworksHumansLeukemia, Myeloid, AcuteMegakaryocyte-Erythroid Progenitor CellsMice, Inbred C57BLProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTranscription FactorsTranslocation, GeneticDNA-Binding ProteinsPRDM16 protein, humanPrdm16 protein, mouseProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTranscription Factors
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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.