Integrative analysis of RUNX1 downstream pathways and target genes

<p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Liu Marjorie [verfasserIn] Cannon Ping [verfasserIn] Schütz Frédéric [verfasserIn] Ritchie Matthew E [verfasserIn] Carmichael Catherine [verfasserIn] Beissbarth Tim [verfasserIn] Buchet-Poyau Karine [verfasserIn] Escher Robert [verfasserIn] Simpson Ken M [verfasserIn] Michaud Joëlle [verfasserIn] Shen Xiaofeng [verfasserIn] Ito Yoshiaki [verfasserIn] Raskind Wendy H [verfasserIn] Horwitz Marshall S [verfasserIn] Osato Motomi [verfasserIn] Turner David R [verfasserIn] Speed Terence P [verfasserIn] Kavallaris Maria [verfasserIn] Smyth Gordon K [verfasserIn] Scott Hamish S [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2008

Übergeordnetes Werk:	In: BMC Genomics - BMC, 2003, 9(2008), 1, p 363
Übergeordnetes Werk:	volume:9 ; year:2008 ; number:1, p 363

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2164-9-363

Katalog-ID:	DOAJ042977932

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p<
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700	0		\|a Ritchie Matthew E \|e verfasserin \|4 aut
700	0		\|a Carmichael Catherine \|e verfasserin \|4 aut
700	0		\|a Beissbarth Tim \|e verfasserin \|4 aut
700	0		\|a Buchet-Poyau Karine \|e verfasserin \|4 aut
700	0		\|a Escher Robert \|e verfasserin \|4 aut
700	0		\|a Simpson Ken M \|e verfasserin \|4 aut
700	0		\|a Michaud Joëlle \|e verfasserin \|4 aut
700	0		\|a Shen Xiaofeng \|e verfasserin \|4 aut
700	0		\|a Ito Yoshiaki \|e verfasserin \|4 aut
700	0		\|a Raskind Wendy H \|e verfasserin \|4 aut
700	0		\|a Horwitz Marshall S \|e verfasserin \|4 aut
700	0		\|a Osato Motomi \|e verfasserin \|4 aut
700	0		\|a Turner David R \|e verfasserin \|4 aut
700	0		\|a Speed Terence P \|e verfasserin \|4 aut
700	0		\|a Kavallaris Maria \|e verfasserin \|4 aut
700	0		\|a Smyth Gordon K \|e verfasserin \|4 aut
700	0		\|a Scott Hamish S \|e verfasserin \|4 aut
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author_variant	l m lm c p cp s f sf r m e rme c c cc b t bt b p k bpk e r er s k m skm m j mj s x sx i y iy r w h rwh h m s hms o m om t d r tdr s t p stp k m km s g k sgk s h s shs
matchkey_str	article:14712164:2008----::nertvaayiorn1ontemaha
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callnumber-subject-code	TP
publishDate	2008
allfields	10.1186/1471-2164-9-363 doi (DE-627)DOAJ042977932 (DE-599)DOAJ95b48b9303154120a994862031596f13 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Liu Marjorie verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Biotechnology Genetics Cannon Ping verfasserin aut Schütz Frédéric verfasserin aut Ritchie Matthew E verfasserin aut Carmichael Catherine verfasserin aut Beissbarth Tim verfasserin aut Buchet-Poyau Karine verfasserin aut Escher Robert verfasserin aut Simpson Ken M verfasserin aut Michaud Joëlle verfasserin aut Shen Xiaofeng verfasserin aut Ito Yoshiaki verfasserin aut Raskind Wendy H verfasserin aut Horwitz Marshall S verfasserin aut Osato Motomi verfasserin aut Turner David R verfasserin aut Speed Terence P verfasserin aut Kavallaris Maria verfasserin aut Smyth Gordon K verfasserin aut Scott Hamish S verfasserin aut In BMC Genomics BMC, 2003 9(2008), 1, p 363 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:9 year:2008 number:1, p 363 https://doi.org/10.1186/1471-2164-9-363 kostenfrei https://doaj.org/article/95b48b9303154120a994862031596f13 kostenfrei http://www.biomedcentral.com/1471-2164/9/363 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 363
spelling	10.1186/1471-2164-9-363 doi (DE-627)DOAJ042977932 (DE-599)DOAJ95b48b9303154120a994862031596f13 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Liu Marjorie verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Biotechnology Genetics Cannon Ping verfasserin aut Schütz Frédéric verfasserin aut Ritchie Matthew E verfasserin aut Carmichael Catherine verfasserin aut Beissbarth Tim verfasserin aut Buchet-Poyau Karine verfasserin aut Escher Robert verfasserin aut Simpson Ken M verfasserin aut Michaud Joëlle verfasserin aut Shen Xiaofeng verfasserin aut Ito Yoshiaki verfasserin aut Raskind Wendy H verfasserin aut Horwitz Marshall S verfasserin aut Osato Motomi verfasserin aut Turner David R verfasserin aut Speed Terence P verfasserin aut Kavallaris Maria verfasserin aut Smyth Gordon K verfasserin aut Scott Hamish S verfasserin aut In BMC Genomics BMC, 2003 9(2008), 1, p 363 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:9 year:2008 number:1, p 363 https://doi.org/10.1186/1471-2164-9-363 kostenfrei https://doaj.org/article/95b48b9303154120a994862031596f13 kostenfrei http://www.biomedcentral.com/1471-2164/9/363 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 363
allfields_unstemmed	10.1186/1471-2164-9-363 doi (DE-627)DOAJ042977932 (DE-599)DOAJ95b48b9303154120a994862031596f13 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Liu Marjorie verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Biotechnology Genetics Cannon Ping verfasserin aut Schütz Frédéric verfasserin aut Ritchie Matthew E verfasserin aut Carmichael Catherine verfasserin aut Beissbarth Tim verfasserin aut Buchet-Poyau Karine verfasserin aut Escher Robert verfasserin aut Simpson Ken M verfasserin aut Michaud Joëlle verfasserin aut Shen Xiaofeng verfasserin aut Ito Yoshiaki verfasserin aut Raskind Wendy H verfasserin aut Horwitz Marshall S verfasserin aut Osato Motomi verfasserin aut Turner David R verfasserin aut Speed Terence P verfasserin aut Kavallaris Maria verfasserin aut Smyth Gordon K verfasserin aut Scott Hamish S verfasserin aut In BMC Genomics BMC, 2003 9(2008), 1, p 363 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:9 year:2008 number:1, p 363 https://doi.org/10.1186/1471-2164-9-363 kostenfrei https://doaj.org/article/95b48b9303154120a994862031596f13 kostenfrei http://www.biomedcentral.com/1471-2164/9/363 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 363
allfieldsGer	10.1186/1471-2164-9-363 doi (DE-627)DOAJ042977932 (DE-599)DOAJ95b48b9303154120a994862031596f13 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Liu Marjorie verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Biotechnology Genetics Cannon Ping verfasserin aut Schütz Frédéric verfasserin aut Ritchie Matthew E verfasserin aut Carmichael Catherine verfasserin aut Beissbarth Tim verfasserin aut Buchet-Poyau Karine verfasserin aut Escher Robert verfasserin aut Simpson Ken M verfasserin aut Michaud Joëlle verfasserin aut Shen Xiaofeng verfasserin aut Ito Yoshiaki verfasserin aut Raskind Wendy H verfasserin aut Horwitz Marshall S verfasserin aut Osato Motomi verfasserin aut Turner David R verfasserin aut Speed Terence P verfasserin aut Kavallaris Maria verfasserin aut Smyth Gordon K verfasserin aut Scott Hamish S verfasserin aut In BMC Genomics BMC, 2003 9(2008), 1, p 363 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:9 year:2008 number:1, p 363 https://doi.org/10.1186/1471-2164-9-363 kostenfrei https://doaj.org/article/95b48b9303154120a994862031596f13 kostenfrei http://www.biomedcentral.com/1471-2164/9/363 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 363
allfieldsSound	10.1186/1471-2164-9-363 doi (DE-627)DOAJ042977932 (DE-599)DOAJ95b48b9303154120a994862031596f13 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Liu Marjorie verfasserin aut Integrative analysis of RUNX1 downstream pathways and target genes 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p< Biotechnology Genetics Cannon Ping verfasserin aut Schütz Frédéric verfasserin aut Ritchie Matthew E verfasserin aut Carmichael Catherine verfasserin aut Beissbarth Tim verfasserin aut Buchet-Poyau Karine verfasserin aut Escher Robert verfasserin aut Simpson Ken M verfasserin aut Michaud Joëlle verfasserin aut Shen Xiaofeng verfasserin aut Ito Yoshiaki verfasserin aut Raskind Wendy H verfasserin aut Horwitz Marshall S verfasserin aut Osato Motomi verfasserin aut Turner David R verfasserin aut Speed Terence P verfasserin aut Kavallaris Maria verfasserin aut Smyth Gordon K verfasserin aut Scott Hamish S verfasserin aut In BMC Genomics BMC, 2003 9(2008), 1, p 363 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:9 year:2008 number:1, p 363 https://doi.org/10.1186/1471-2164-9-363 kostenfrei https://doaj.org/article/95b48b9303154120a994862031596f13 kostenfrei http://www.biomedcentral.com/1471-2164/9/363 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 363
language	English
source	In BMC Genomics 9(2008), 1, p 363 volume:9 year:2008 number:1, p 363
sourceStr	In BMC Genomics 9(2008), 1, p 363 volume:9 year:2008 number:1, p 363
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Biotechnology Genetics
isfreeaccess_bool	true
container_title	BMC Genomics
authorswithroles_txt_mv	Liu Marjorie @@aut@@ Cannon Ping @@aut@@ Schütz Frédéric @@aut@@ Ritchie Matthew E @@aut@@ Carmichael Catherine @@aut@@ Beissbarth Tim @@aut@@ Buchet-Poyau Karine @@aut@@ Escher Robert @@aut@@ Simpson Ken M @@aut@@ Michaud Joëlle @@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@@
publishDateDaySort_date	2008-01-01T00:00:00Z
hierarchy_top_id	326644954
id	DOAJ042977932
language_de	englisch
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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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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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callnumber-first	T - Technology
author	Liu Marjorie
spellingShingle	Liu Marjorie misc TP248.13-248.65 misc QH426-470 misc Biotechnology misc Genetics Integrative analysis of RUNX1 downstream pathways and target genes
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topic_title	TP248.13-248.65 QH426-470 Integrative analysis of RUNX1 downstream pathways and target genes
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title	Integrative analysis of RUNX1 downstream pathways and target genes
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title_full	Integrative analysis of RUNX1 downstream pathways and target genes
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author_browse	Liu Marjorie Cannon Ping Schütz Frédéric Ritchie Matthew E Carmichael Catherine Beissbarth Tim Buchet-Poyau Karine Escher Robert Simpson Ken M Michaud Joëlle 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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title_sort	integrative analysis of runx1 downstream pathways and target genes
callnumber	TP248.13-248.65
title_auth	Integrative analysis of RUNX1 downstream pathways and target genes
abstract	<p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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.</p<
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title_short	Integrative analysis of RUNX1 downstream pathways and target genes
url	https://doi.org/10.1186/1471-2164-9-363 https://doaj.org/article/95b48b9303154120a994862031596f13 http://www.biomedcentral.com/1471-2164/9/363 https://doaj.org/toc/1471-2164
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up_date	2024-07-03T15:02:34.905Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ042977932</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230501194044.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2008 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1471-2164-9-363</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ042977932</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ95b48b9303154120a994862031596f13</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">TP248.13-248.65</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QH426-470</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Liu Marjorie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Integrative analysis of RUNX1 downstream pathways and target genes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2008</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a"><p<Abstract</p< <p<Background</p< <p<The <it<RUNX1 </it<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.</p< <p<Results</p< <p<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 <it<RUNX1 </it<or its cofactor, <it<CBFβ</it<. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous <it<RUNX1 </it<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.</p< <p<Conclusion</p< <p<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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Integrative analysis of RUNX1 downstream pathways and target genes

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