Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia
Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes ( BCL9 , CSF1R , DAZAP1 , HNRNPUL1 and SS18 ) in 22 B progenitor ALL (B-ALL) cases...
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| Vydané v: | Nature communications Ročník 7; číslo 1; s. 13331 - 10 |
|---|---|
| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
London
Nature Publishing Group UK
08.11.2016
Nature Publishing Group Nature Portfolio |
| Predmet: | |
| ISSN: | 2041-1723, 2041-1723 |
| On-line prístup: | Získať plný text |
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| Abstract | Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between
MEF2D
(myocyte enhancer factor 2D) and five genes (
BCL9
,
CSF1R
,
DAZAP1
,
HNRNPUL1
and
SS18
) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is
MEF2D-BCL9
. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with
MEF2D
rearrangements, which include an additional fusion partner,
FOXJ2
; thus,
MEF2D-
rearranged cases comprise 5.3% of cases lacking recurring alterations.
MEF2D-
rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of
HDAC9
expression and sensitive to histone deacetylase inhibitor treatment. Thus,
MEF2D-
rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered.
Acute lymphoblastic leukaemia is characterized by chromosomal rearrangements. Here, the authors carry out RNA-sequencing on a large cohort of patients and identify recurrent rearrangements of
MEF2D
, which lead to increased transcriptional activity of the gene, and cellular transformation
in vitro
. |
|---|---|
| AbstractList | Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between
MEF2D
(myocyte enhancer factor 2D) and five genes (
BCL9
,
CSF1R
,
DAZAP1
,
HNRNPUL1
and
SS18
) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is
MEF2D-BCL9
. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with
MEF2D
rearrangements, which include an additional fusion partner,
FOXJ2
; thus,
MEF2D-
rearranged cases comprise 5.3% of cases lacking recurring alterations.
MEF2D-
rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of
HDAC9
expression and sensitive to histone deacetylase inhibitor treatment. Thus,
MEF2D-
rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered.
Acute lymphoblastic leukaemia is characterized by chromosomal rearrangements. Here, the authors carry out RNA-sequencing on a large cohort of patients and identify recurrent rearrangements of
MEF2D
, which lead to increased transcriptional activity of the gene, and cellular transformation
in vitro
. Acute lymphoblastic leukaemia is characterized by chromosomal rearrangements. Here, the authors carry out RNA-sequencing on a large cohort of patients and identify recurrent rearrangements of MEF2D, which lead to increased transcriptional activity of the gene, and cellular transformation in vitro. Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes ( BCL9 , CSF1R , DAZAP1 , HNRNPUL1 and SS18 ) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9 . Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2 ; thus, MEF2D- rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D- rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D- rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered. Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered.Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered. Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered. Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered. Acute lymphoblastic leukaemia is characterized by chromosomal rearrangements. Here, the authors carry out RNA-sequencing on a large cohort of patients and identify recurrent rearrangements of MEF2D, which lead to increased transcriptional activity of the gene, and cellular transformation in vitro. |
| ArticleNumber | 13331 |
| Author | Harvey, Richard C. Stonerock, Eileen Moorman, Anthony V. Marra, Marco Luger, Selina M. McCastlain, Kelly Gianni, Francesca Maloney, Kelly Pei, Deqing Radich, Jerald P. P. Hunger, Stephen Churchman, Michelle Gastier-Foster, Julie M. Willman, Cheryl L. Bloomfield, Clara D. Mullighan, Charles G. Liu, Yu Payne-Turner, Debbie Chen, I-Ming Konopleva, Marina Kantarjian, Hagop M. Wood, Brent Kohlschmidt, Jessica Mungall, Andrew J. Angiolillo, Anne Devidas, Meenakshi Rowe, Jacob M. Shao, Ying Dai, Yunfeng Bhatia, Ravi Spinelli, Orietta Salzer, Wanda L. Aldoss, Ibrahim Mattano Jr, Leonard A. Moore, Richard Borowitz, Michael Minden, Mark D. Iacobucci, Ilaria Paietta, Elisabeth Roberts, Kathryn Larsen, Eric E. Gu, Zhaohui Marcucci, Guido Stock, Wendy L. Loh, Mignon Ma, Yussanne Fielding, Adele K. Li, Yongjin Reshmi, Shalini C. Burke, Michael J. Patel, Bella Mungall, Karen L. Valentine, Marcus Forman, Stephen J. Kornblau, Steven Mrózek, Krzysztof |
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New Mexico Cancer Center – sequence: 7 givenname: Kelly orcidid: 0000-0001-7868-3049 surname: McCastlain fullname: McCastlain, Kelly organization: Department of Pathology and Hematological Malignancies Program, St Jude Children’s Research Hospital – sequence: 8 givenname: Shalini C. surname: Reshmi fullname: Reshmi, Shalini C. organization: The Research Institute, Nationwide Children’s Hospital – sequence: 9 givenname: Debbie surname: Payne-Turner fullname: Payne-Turner, Debbie organization: Department of Pathology and Hematological Malignancies Program, St Jude Children’s Research Hospital – sequence: 10 givenname: Ilaria surname: Iacobucci fullname: Iacobucci, Ilaria organization: Department of Pathology and Hematological Malignancies Program, St Jude Children’s Research Hospital – sequence: 11 givenname: Ying surname: Shao fullname: Shao, Ying organization: Department of Pathology and Hematological Malignancies Program, St Jude Children’s Research Hospital, Department of 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Devidas, Meenakshi organization: Department of Biostatistics, Colleges of Medicine and Public Health & Health Professions, University of Florida – sequence: 23 givenname: Yunfeng surname: Dai fullname: Dai, Yunfeng organization: Department of Biostatistics, Colleges of Medicine and Public Health & Health Professions, University of Florida – sequence: 24 givenname: Brent surname: Wood fullname: Wood, Brent organization: Department of Laboratory Medicine, University of Washington – sequence: 25 givenname: Michael surname: Borowitz fullname: Borowitz, Michael organization: Department of Pathology, Johns Hopkins Medical Institutions – sequence: 26 givenname: Eric E. surname: Larsen fullname: Larsen, Eric E. organization: Maine Children’s Cancer Program – sequence: 27 givenname: Kelly surname: Maloney fullname: Maloney, Kelly organization: Pediatric Hematology/Oncology/BMT, University of Colorado School of Medicine and Children’s Hospital Colorado – sequence: 28 givenname: Leonard A. 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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27824051$$D View this record in MEDLINE/PubMed |
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| Snippet | Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements... Acute lymphoblastic leukaemia is characterized by chromosomal rearrangements. Here, the authors carry out RNA-sequencing on a large cohort of patients and... |
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| Title | Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia |
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