{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:22:07Z","timestamp":1791206527884,"version":"4.1.0"},"reference-count":51,"publisher":"American Society of Hematology","issue":"3","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The transcription factor PU.1 is required for normal blood cell development. PU.1 regulates the expression of a number of crucial myeloid genes, such as the macrophage colony-stimulating factor (M-CSF) receptor, the granulocyte colony-stimulating factor (G-CSF) receptor, and the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor. Myeloid cells derived from PU.1\u2212\/\u2212 mice are blocked at the earliest stage of myeloid differentiation, similar to the blast cells that are the hallmark of human acute myeloid leukemia (AML). These facts led us to hypothesize that molecular abnormalities involving the PU.1 gene could contribute to the development of AML. We identified 10 mutant alleles of the PU.1 gene in 9 of 126 AML patients. The PU.1 mutations comprised 5 deletions affecting the DNA-binding domain, and 5 point mutations in 1) the DNA-binding domain (2 patients), 2) the PEST domain (2 patients), and 3) the transactivation domain (one patient). DNA binding to and transactivation of the M-CSF receptor promoter, a direct PU.1 target gene, were deficient in the 7 PU.1 mutants that affected the DNA-binding domain. In addition, these mutations decreased the ability of PU.1 to synergize with PU.1-interacting proteins such as AML1 or c-Jun in the activation of PU.1 target genes. This is the first report of mutations in the PU.1 gene in human neoplasia and suggests that disruption of PU.1 function contributes to the block in differentiation found in AML patients.<\/jats:p>","DOI":"10.1182\/blood.v100.3.998","type":"journal-article","created":{"date-parts":[[2002,10,11]],"date-time":"2002-10-11T18:33:52Z","timestamp":1034361232000},"page":"998-1007","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":208,"title":["Heterozygous PU.1 mutations are associated with acute myeloid leukemia"],"prefix":"10.1182","volume":"100","author":[{"given":"Beatrice U.","family":"Mueller","sequence":"first","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Pabst","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Motomi","family":"Osato","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norio","family":"Asou","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M.","family":"Johansen","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark D.","family":"Minden","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard","family":"Behre","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Hiddemann","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiaki","family":"Ito","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel G.","family":"Tenen","sequence":"additional","affiliation":[{"name":"From the Harvard Institutes of Medicine, Harvard Medical School, Boston, MA; the Department of Internal Medicine, Kumamoto University, Japan; the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan; the Department of Medicine and Medical Biophysics, University of Toronto, Canada; the Department of Medicine III, Grosshadern, Clinical Cooperative Group Acute Myeloid Leukemia of the National Research Center for Environment and Health (GSF), Munich, 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Genet."},{"key":"2020021221084058200_B7","doi-asserted-by":"crossref","first-page":"2862","DOI":"10.1182\/blood.V96.8.2862","article-title":"High incidence of biallelic point mutations in the Runt domain of the AML1\/PEP2\u03b1B gene in M0 acute myeloid leukemia and in myeloid malignancies with acquired trisomy 21.","volume":"96","author":"Preudhomme","year":"2000","journal-title":"Blood."},{"key":"2020021221084058200_B8","doi-asserted-by":"crossref","first-page":"263","DOI":"10.1038\/85820","article-title":"Dominant negative mutations of CEBPA, encoding CCAAT\/Enhancer Binding Protein-\u03b1 (C\/EBP\u03b1), in acute myeloid leukemia.","volume":"27","author":"Pabst","year":"2001","journal-title":"Nat Genet."},{"key":"2020021221084058200_B9","doi-asserted-by":"crossref","first-page":"1364","DOI":"10.1182\/blood.V99.4.1364","article-title":"In vitro analyses of known and novel RUNX1\/AML1 mutations in dominant familial platelet disorder with predisposition to acute myelogenous leukemia 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mice.","volume":"91","author":"Anderson","year":"1998","journal-title":"Blood."},{"key":"2020021221084058200_B25","doi-asserted-by":"crossref","first-page":"1576","DOI":"10.1182\/blood.V92.5.1576","article-title":"Neutrophils deficient in PU.1 do not terminally differentiate or become functionally competent.","volume":"92","author":"Anderson","year":"1998","journal-title":"Blood."},{"key":"2020021221084058200_B26","doi-asserted-by":"crossref","first-page":"4456","DOI":"10.1093\/emboj\/17.15.4456","article-title":"PU.1 regulates both cytokine dependent proliferation and differentiation of granulocyte\/macrophage progenitors.","volume":"17","author":"DeKoter","year":"1998","journal-title":"EMBO J."},{"key":"2020021221084058200_B27","doi-asserted-by":"crossref","first-page":"2310","DOI":"10.1182\/blood.V94.7.2310.419k34_2310_2318","article-title":"PU.1 and the granulocyte- and macrophage colony-stimulating factor receptors play distinct roles in late-stage myeloid cell differentiation.","volume":"94","author":"Anderson","year":"1999","journal-title":"Blood."},{"key":"2020021221084058200_B28","doi-asserted-by":"crossref","first-page":"3915","DOI":"10.1128\/MCB.18.7.3915","article-title":"Multiple functional domains of AML1: PU.1 and C\/EBP\u03b1 cooperate with different regions of AML1.","volume":"18","author":"Petrovick","year":"1998","journal-title":"Mol Cell Biol."},{"key":"2020021221084058200_B29","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1093\/oso\/9780195124507.003.0033","article-title":"Regulatory interactions between transcription factors and their role in hematopoietic lineage determination.","volume-title":"Hematopoiesis: A Developmental Approach.","author":"Nerlov","year":"2001"},{"key":"2020021221084058200_B30","doi-asserted-by":"crossref","first-page":"560","DOI":"10.1182\/blood.V94.2.560","article-title":"C\/EBP\u03b1 bypasses granulocyte colony-stimulating factor signals to rapidly induce PU.1 gene expression, stimulate granulocytic differentiation, and limit proliferation in 32D cl3 myeloblasts.","volume":"94","author":"Wang","year":"1999","journal-title":"Blood."},{"key":"2020021221084058200_B31","doi-asserted-by":"crossref","first-page":"3940","DOI":"10.1128\/MCB.19.6.3940","article-title":"Dimeric RFX proteins contribute to the activity and lineage-specificity of the interleukin-5 receptor \u03b1 promoter through activation and repression domains.","volume":"19","author":"Iwama","year":"1999","journal-title":"Mol Cell Biol."},{"key":"2020021221084058200_B32","doi-asserted-by":"crossref","first-page":"2499","DOI":"10.1093\/nar\/19.9.2499","article-title":"A rapid micropreparation technique for extraction of DNA-binding proteins from limiting numbers of mammalian cells.","volume":"19","author":"Andrews","year":"1991","journal-title":"Nucl Acids Res."},{"key":"2020021221084058200_B33","doi-asserted-by":"crossref","first-page":"1173","DOI":"10.1084\/jem.188.6.1173","article-title":"Upregulation of interleukin 6 and granulocyte colony-stimulating factor receptors by transcription factor CCAAT enhancer binding protein \u03b1 (C\/EBP\u03b1) is critical for granulopoiesis.","volume":"188","author":"Zhang","year":"1998","journal-title":"J Exp Med."},{"key":"2020021221084058200_B34","first-page":"454","article-title":"Luciferase reporter gene vectors for analysis of promoters and enhancers.","volume":"6","author":"Nordeen","year":"1988","journal-title":"Biotechniques."},{"key":"2020021221084058200_B35","doi-asserted-by":"crossref","first-page":"4939","DOI":"10.1074\/jbc.274.8.4939","article-title":"c-Jun is a JNK-independent coactivator of the PU.1 transcription factor.","volume":"274","author":"Behre","year":"1999","journal-title":"J Biol Chem."},{"key":"2020021221084058200_B36","doi-asserted-by":"crossref","first-page":"3789","DOI":"10.1128\/MCB.21.11.3789-3806.2001","article-title":"c-myc is a critical target for C\/EBP\u03b1 in granulopoiesis.","volume":"21","author":"Johansen","year":"2001","journal-title":"Mol Cell Biol."},{"key":"2020021221084058200_B37","doi-asserted-by":"crossref","first-page":"8392","DOI":"10.1073\/pnas.90.18.8392","article-title":"Production of high-titer helper-free retroviruses by transient transfection.","volume":"90","author":"Pear","year":"1993","journal-title":"Proc Natl Acad Sci U S A."},{"key":"2020021221084058200_B38","first-page":"1095","article-title":"Lymphoid- and myeloid-specific activity of the PU.1 promoter is determined by the combinatorial action of octamer and ets transcription factors.","volume":"11","author":"Kistler","year":"1995","journal-title":"Oncogene."},{"key":"2020021221084058200_B39","doi-asserted-by":"crossref","first-page":"8705","DOI":"10.1073\/pnas.96.15.8705","article-title":"Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1.","volume":"96","author":"Zhang","year":"1999","journal-title":"Proc Natl Acad Sci U S 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Biol."},{"key":"2020021221084058200_B46","doi-asserted-by":"crossref","first-page":"368","DOI":"10.1128\/MCB.12.1.368","article-title":"PU.1 recruits a second nuclear factor to a site important for immunoglobulin kappa 3\u2032 enhancer activity.","volume":"12","author":"Pongubala","year":"1992","journal-title":"Mol Cell Biol."},{"key":"2020021221084058200_B47","doi-asserted-by":"crossref","first-page":"1622","DOI":"10.1126\/science.8456286","article-title":"Effect of PU.1 phosphorylation on interaction with NF-EM5 and transcriptional activation.","volume":"259","author":"Pongubala","year":"1993","journal-title":"Science."},{"key":"2020021221084058200_B48","doi-asserted-by":"crossref","first-page":"6468","DOI":"10.4049\/jimmunol.163.12.6468","article-title":"Protein-protein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors.","volume":"163","author":"Meraro","year":"1999","journal-title":"J Immunol."},{"key":"2020021221084058200_B49","doi-asserted-by":"crossref","first-page":"2908","DOI":"10.1182\/blood.V97.9.2908","article-title":"PU.1 exhibits partial functional redundancy with Spi-B, but not with Ets-1 or Elf-1.","volume":"97","author":"Garrett-Sinha","year":"2001","journal-title":"Blood."},{"key":"2020021221084058200_B50","doi-asserted-by":"crossref","first-page":"57","DOI":"10.1038\/35049577","article-title":"Diversification of haematopoietic stem cells to specific lineages.","volume":"1","author":"Orkin","year":"2000","journal-title":"Nat Rev Genet."},{"key":"2020021221084058200_B51","doi-asserted-by":"crossref","first-page":"569","DOI":"10.1073\/pnas.94.2.569","article-title":"Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein \u03b1-deficient mice.","volume":"94","author":"Zhang","year":"1997","journal-title":"Proc Natl Acad Sci U S 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