Integrative analysis of RUNX1 downstream pathways and target genes
Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of th...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Michaud, Joëlle [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2008 |
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| Schlagwörter: |
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| Anmerkung: |
© Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: BMC genomics - London : BioMed Central, 2000, 9(2008), 1 vom: 31. Juli |
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| Übergeordnetes Werk: |
volume:9 ; year:2008 ; number:1 ; day:31 ; month:07 |
| Links: |
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| DOI / URN: |
10.1186/1471-2164-9-363 |
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| Katalog-ID: |
SPR027037479 |
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| 100 | 1 | |a Michaud, Joëlle |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Integrative analysis of RUNX1 downstream pathways and target genes |
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| 520 | |a Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. | ||
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| 700 | 1 | |a Simpson, Ken M |4 aut | |
| 700 | 1 | |a Escher, Robert |4 aut | |
| 700 | 1 | |a Buchet-Poyau, Karine |4 aut | |
| 700 | 1 | |a Beissbarth, Tim |4 aut | |
| 700 | 1 | |a Carmichael, Catherine |4 aut | |
| 700 | 1 | |a Ritchie, Matthew E |4 aut | |
| 700 | 1 | |a Schütz, Frédéric |4 aut | |
| 700 | 1 | |a Cannon, Ping |4 aut | |
| 700 | 1 | |a Liu, Marjorie |4 aut | |
| 700 | 1 | |a Shen, Xiaofeng |4 aut | |
| 700 | 1 | |a Ito, Yoshiaki |4 aut | |
| 700 | 1 | |a Raskind, Wendy H |4 aut | |
| 700 | 1 | |a Horwitz, Marshall S |4 aut | |
| 700 | 1 | |a Osato, Motomi |4 aut | |
| 700 | 1 | |a Turner, David R |4 aut | |
| 700 | 1 | |a Speed, Terence P |4 aut | |
| 700 | 1 | |a Kavallaris, Maria |4 aut | |
| 700 | 1 | |a Smyth, Gordon K |4 aut | |
| 700 | 1 | |a Scott, Hamish S |4 aut | |
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10.1186/1471-2164-9-363 doi (DE-627)SPR027037479 (SPR)1471-2164-9-363-e DE-627 ger DE-627 rakwb eng Michaud, Joëlle verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. Unaffected Individual (dpeaa)DE-He213 Core Binding Factor (dpeaa)DE-He213 Overexpression System (dpeaa)DE-He213 Leukemia Development (dpeaa)DE-He213 Conserve Binding Site (dpeaa)DE-He213 Simpson, Ken M aut Escher, Robert aut Buchet-Poyau, Karine aut Beissbarth, Tim aut Carmichael, Catherine aut Ritchie, Matthew E aut Schütz, Frédéric aut Cannon, Ping aut Liu, Marjorie aut Shen, Xiaofeng aut Ito, Yoshiaki aut Raskind, Wendy H aut Horwitz, Marshall S aut Osato, Motomi aut Turner, David R aut Speed, Terence P aut Kavallaris, Maria aut Smyth, Gordon K aut Scott, Hamish S aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 31. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:31 month:07 https://dx.doi.org/10.1186/1471-2164-9-363 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 1 31 07 |
| spelling |
10.1186/1471-2164-9-363 doi (DE-627)SPR027037479 (SPR)1471-2164-9-363-e DE-627 ger DE-627 rakwb eng Michaud, Joëlle verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. Unaffected Individual (dpeaa)DE-He213 Core Binding Factor (dpeaa)DE-He213 Overexpression System (dpeaa)DE-He213 Leukemia Development (dpeaa)DE-He213 Conserve Binding Site (dpeaa)DE-He213 Simpson, Ken M aut Escher, Robert aut Buchet-Poyau, Karine aut Beissbarth, Tim aut Carmichael, Catherine aut Ritchie, Matthew E aut Schütz, Frédéric aut Cannon, Ping aut Liu, Marjorie aut Shen, Xiaofeng aut Ito, Yoshiaki aut Raskind, Wendy H aut Horwitz, Marshall S aut Osato, Motomi aut Turner, David R aut Speed, Terence P aut Kavallaris, Maria aut Smyth, Gordon K aut Scott, Hamish S aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 31. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:31 month:07 https://dx.doi.org/10.1186/1471-2164-9-363 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 1 31 07 |
| allfields_unstemmed |
10.1186/1471-2164-9-363 doi (DE-627)SPR027037479 (SPR)1471-2164-9-363-e DE-627 ger DE-627 rakwb eng Michaud, Joëlle verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. Unaffected Individual (dpeaa)DE-He213 Core Binding Factor (dpeaa)DE-He213 Overexpression System (dpeaa)DE-He213 Leukemia Development (dpeaa)DE-He213 Conserve Binding Site (dpeaa)DE-He213 Simpson, Ken M aut Escher, Robert aut Buchet-Poyau, Karine aut Beissbarth, Tim aut Carmichael, Catherine aut Ritchie, Matthew E aut Schütz, Frédéric aut Cannon, Ping aut Liu, Marjorie aut Shen, Xiaofeng aut Ito, Yoshiaki aut Raskind, Wendy H aut Horwitz, Marshall S aut Osato, Motomi aut Turner, David R aut Speed, Terence P aut Kavallaris, Maria aut Smyth, Gordon K aut Scott, Hamish S aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 31. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:31 month:07 https://dx.doi.org/10.1186/1471-2164-9-363 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 1 31 07 |
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10.1186/1471-2164-9-363 doi (DE-627)SPR027037479 (SPR)1471-2164-9-363-e DE-627 ger DE-627 rakwb eng Michaud, Joëlle verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. Unaffected Individual (dpeaa)DE-He213 Core Binding Factor (dpeaa)DE-He213 Overexpression System (dpeaa)DE-He213 Leukemia Development (dpeaa)DE-He213 Conserve Binding Site (dpeaa)DE-He213 Simpson, Ken M aut Escher, Robert aut Buchet-Poyau, Karine aut Beissbarth, Tim aut Carmichael, Catherine aut Ritchie, Matthew E aut Schütz, Frédéric aut Cannon, Ping aut Liu, Marjorie aut Shen, Xiaofeng aut Ito, Yoshiaki aut Raskind, Wendy H aut Horwitz, Marshall S aut Osato, Motomi aut Turner, David R aut Speed, Terence P aut Kavallaris, Maria aut Smyth, Gordon K aut Scott, Hamish S aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 31. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:31 month:07 https://dx.doi.org/10.1186/1471-2164-9-363 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 1 31 07 |
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10.1186/1471-2164-9-363 doi (DE-627)SPR027037479 (SPR)1471-2164-9-363-e DE-627 ger DE-627 rakwb eng Michaud, Joëlle verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. Unaffected Individual (dpeaa)DE-He213 Core Binding Factor (dpeaa)DE-He213 Overexpression System (dpeaa)DE-He213 Leukemia Development (dpeaa)DE-He213 Conserve Binding Site (dpeaa)DE-He213 Simpson, Ken M aut Escher, Robert aut Buchet-Poyau, Karine aut Beissbarth, Tim aut Carmichael, Catherine aut Ritchie, Matthew E aut Schütz, Frédéric aut Cannon, Ping aut Liu, Marjorie aut Shen, Xiaofeng aut Ito, Yoshiaki aut Raskind, Wendy H aut Horwitz, Marshall S aut Osato, Motomi aut Turner, David R aut Speed, Terence P aut Kavallaris, Maria aut Smyth, Gordon K aut Scott, Hamish S aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 31. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:31 month:07 https://dx.doi.org/10.1186/1471-2164-9-363 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 1 31 07 |
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Michaud, Joëlle @@aut@@ Simpson, Ken M @@aut@@ Escher, Robert @@aut@@ Buchet-Poyau, Karine @@aut@@ Beissbarth, Tim @@aut@@ Carmichael, Catherine @@aut@@ Ritchie, Matthew E @@aut@@ Schütz, Frédéric @@aut@@ Cannon, Ping @@aut@@ Liu, Marjorie @@aut@@ Shen, Xiaofeng @@aut@@ Ito, Yoshiaki @@aut@@ Raskind, Wendy H @@aut@@ Horwitz, Marshall S @@aut@@ Osato, Motomi @@aut@@ Turner, David R @@aut@@ Speed, Terence P @@aut@@ Kavallaris, Maria @@aut@@ Smyth, Gordon K @@aut@@ Scott, Hamish S @@aut@@ |
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Michaud, Joëlle |
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Michaud, Joëlle misc Unaffected Individual misc Core Binding Factor misc Overexpression System misc Leukemia Development misc Conserve Binding Site Integrative analysis of RUNX1 downstream pathways and target genes |
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Michaud, Joëlle Simpson, Ken M Escher, Robert Buchet-Poyau, Karine Beissbarth, Tim Carmichael, Catherine Ritchie, Matthew E Schütz, Frédéric Cannon, Ping Liu, Marjorie Shen, Xiaofeng Ito, Yoshiaki Raskind, Wendy H Horwitz, Marshall S Osato, Motomi Turner, David R Speed, Terence P Kavallaris, Maria Smyth, Gordon K Scott, Hamish S |
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integrative analysis of runx1 downstream pathways and target genes |
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Integrative analysis of RUNX1 downstream pathways and target genes |
| abstract |
Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Background The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFβ, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFβ. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications. © Michaud et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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Simpson, Ken M Escher, Robert Buchet-Poyau, Karine Beissbarth, Tim Carmichael, Catherine Ritchie, Matthew E Schütz, Frédéric Cannon, Ping Liu, Marjorie Shen, Xiaofeng Ito, Yoshiaki Raskind, Wendy H Horwitz, Marshall S Osato, Motomi Turner, David R Speed, Terence P Kavallaris, Maria Smyth, Gordon K Scott, Hamish S |
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In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. Conclusion This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. 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