Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature

Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how...

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Published in:	Cell reports (Cambridge) Vol. 12; no. 5; pp. 821 - 836
Main Authors:	Cauchy, Pierre, James, Sally R., Zacarias-Cabeza, Joaquin, Ptasinska, Anetta, Imperato, Maria Rosaria, Assi, Salam A., Piper, Jason, Canestraro, Martina, Hoogenkamp, Maarten, Raghavan, Manoj, Loke, Justin, Akiki, Susanna, Clokie, Samuel J., Richards, Stephen J., Westhead, David R., Griffiths, Michael J., Ott, Sascha, Bonifer, Constanze, Cockerill, Peter N.
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 04.08.2015 Cell Press Elsevier
Subjects:	Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism fms-Like Tyrosine Kinase 3 - genetics fms-Like Tyrosine Kinase 3 - metabolism Gene Expression Regulation, Leukemic Humans Leukemia, Myeloid, Acute - enzymology Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - pathology Male MAP Kinase Signaling System Mitogen-Activated Protein Kinase Kinases - genetics Mitogen-Activated Protein Kinase Kinases - metabolism Mutation Protein Structure, Tertiary Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism
ISSN:	2211-1247, 2211-1247
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Abstract	Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML. [Display omitted] •FLT3-ITD signaling is associated with a common gene expression signature•FLT3-ITD-specific gene expression is associated with a common chromatin signature•FLT3-ITD AML displays chronic activation of the inducible transcription factor AP-1•AP-1 cooperates with RUNX1 to shape the epigenome of FLT3-ITD AML Cauchy et al. identify a specific gene expression and regulatory signature associated with aberrant signaling in acute myeloid leukemia with FLT3-ITD mutations. In FLT3-ITD AML, the inducible transcription factor AP-1 is chronically activated and cooperates with RUNX1, shaping the epigenome to transactivate specific target genes.
AbstractList	Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML. Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML. • FLT3-ITD signaling is associated with a common gene expression signature • FLT3-ITD-specific gene expression is associated with a common chromatin signature • FLT3-ITD AML displays chronic activation of the inducible transcription factor AP-1 • AP-1 cooperates with RUNX1 to shape the epigenome of FLT3-ITD AML Cauchy et al. identify a specific gene expression and regulatory signature associated with aberrant signaling in acute myeloid leukemia with FLT3-ITD mutations. In FLT3-ITD AML, the inducible transcription factor AP-1 is chronically activated and cooperates with RUNX1, shaping the epigenome to transactivate specific target genes. Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML.Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML. Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML. [Display omitted] •FLT3-ITD signaling is associated with a common gene expression signature•FLT3-ITD-specific gene expression is associated with a common chromatin signature•FLT3-ITD AML displays chronic activation of the inducible transcription factor AP-1•AP-1 cooperates with RUNX1 to shape the epigenome of FLT3-ITD AML Cauchy et al. identify a specific gene expression and regulatory signature associated with aberrant signaling in acute myeloid leukemia with FLT3-ITD mutations. In FLT3-ITD AML, the inducible transcription factor AP-1 is chronically activated and cooperates with RUNX1, shaping the epigenome to transactivate specific target genes.
Author	Westhead, David R. Bonifer, Constanze Loke, Justin Piper, Jason Zacarias-Cabeza, Joaquin Cockerill, Peter N. Clokie, Samuel J. Canestraro, Martina Ptasinska, Anetta Imperato, Maria Rosaria Hoogenkamp, Maarten Raghavan, Manoj Richards, Stephen J. Griffiths, Michael J. Assi, Salam A. Ott, Sascha Cauchy, Pierre James, Sally R. Akiki, Susanna
AuthorAffiliation	1 School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK 2 Section of Experimental Haematology, Leeds Institute for Molecular Medicine, University of Leeds, Leeds LS9 7TF, UK 5 West Midlands Regional Genetics Laboratory, Birmingham Women’s NHS Foundation Trust, Birmingham B15 2TG, UK 3 Warwick Systems Biology Centre, University of Warwick, Coventry CV4 7AL, UK 4 Centre for Clinical Haematology, Queen Elizabeth Hospital, Birmingham B15 2TH, UK 8 School of Immunity and Infection, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK 6 Haematological Malignancy Diagnostic Service, St. James’s University Hospital, Leeds LS9 7TF, UK 7 School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK
AuthorAffiliation_xml	– name: 3 Warwick Systems Biology Centre, University of Warwick, Coventry CV4 7AL, UK – name: 2 Section of Experimental Haematology, Leeds Institute for Molecular Medicine, University of Leeds, Leeds LS9 7TF, UK – name: 7 School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK – name: 5 West Midlands Regional Genetics Laboratory, Birmingham Women’s NHS Foundation Trust, Birmingham B15 2TG, UK – name: 8 School of Immunity and Infection, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – name: 4 Centre for Clinical Haematology, Queen Elizabeth Hospital, Birmingham B15 2TH, UK – name: 1 School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – name: 6 Haematological Malignancy Diagnostic Service, St. James’s University Hospital, Leeds LS9 7TF, UK
Author_xml	– sequence: 1 givenname: Pierre surname: Cauchy fullname: Cauchy, Pierre organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 2 givenname: Sally R. surname: James fullname: James, Sally R. organization: Section of Experimental Haematology, Leeds Institute for Molecular Medicine, University of Leeds, Leeds LS9 7TF, UK – sequence: 3 givenname: Joaquin surname: Zacarias-Cabeza fullname: Zacarias-Cabeza, Joaquin organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 4 givenname: Anetta surname: Ptasinska fullname: Ptasinska, Anetta organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 5 givenname: Maria Rosaria surname: Imperato fullname: Imperato, Maria Rosaria organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 6 givenname: Salam A. surname: Assi fullname: Assi, Salam A. organization: Section of Experimental Haematology, Leeds Institute for Molecular Medicine, University of Leeds, Leeds LS9 7TF, UK – sequence: 7 givenname: Jason surname: Piper fullname: Piper, Jason organization: Warwick Systems Biology Centre, University of Warwick, Coventry CV4 7AL, UK – sequence: 8 givenname: Martina surname: Canestraro fullname: Canestraro, Martina organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 9 givenname: Maarten surname: Hoogenkamp fullname: Hoogenkamp, Maarten organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 10 givenname: Manoj surname: Raghavan fullname: Raghavan, Manoj organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 11 givenname: Justin surname: Loke fullname: Loke, Justin organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 12 givenname: Susanna surname: Akiki fullname: Akiki, Susanna organization: West Midlands Regional Genetics Laboratory, Birmingham Women’s NHS Foundation Trust, Birmingham B15 2TG, UK – sequence: 13 givenname: Samuel J. surname: Clokie fullname: Clokie, Samuel J. organization: West Midlands Regional Genetics Laboratory, Birmingham Women’s NHS Foundation Trust, Birmingham B15 2TG, UK – sequence: 14 givenname: Stephen J. surname: Richards fullname: Richards, Stephen J. organization: Haematological Malignancy Diagnostic Service, St. James’s University Hospital, Leeds LS9 7TF, UK – sequence: 15 givenname: David R. surname: Westhead fullname: Westhead, David R. organization: School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK – sequence: 16 givenname: Michael J. surname: Griffiths fullname: Griffiths, Michael J. organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 17 givenname: Sascha surname: Ott fullname: Ott, Sascha organization: Warwick Systems Biology Centre, University of Warwick, Coventry CV4 7AL, UK – sequence: 18 givenname: Constanze surname: Bonifer fullname: Bonifer, Constanze email: c.bonifer@bham.ac.uk organization: School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK – sequence: 19 givenname: Peter N. surname: Cockerill fullname: Cockerill, Peter N. email: p.n.cockerill@bham.ac.uk organization: School of Immunity and Infection, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK
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Snippet	Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a...
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SubjectTerms	Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism fms-Like Tyrosine Kinase 3 - genetics fms-Like Tyrosine Kinase 3 - metabolism Gene Expression Regulation, Leukemic Humans Leukemia, Myeloid, Acute - enzymology Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - pathology Male MAP Kinase Signaling System Mitogen-Activated Protein Kinase Kinases - genetics Mitogen-Activated Protein Kinase Kinases - metabolism Mutation Protein Structure, Tertiary Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism
Title	Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature
URI	https://dx.doi.org/10.1016/j.celrep.2015.06.069 https://www.ncbi.nlm.nih.gov/pubmed/26212328 https://www.proquest.com/docview/1702656693 https://pubmed.ncbi.nlm.nih.gov/PMC4726916 https://doaj.org/article/890fdb6f789647a8a26cb2cb15a4e709
Volume	12
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