Rearrangement of CRLF2 in B-progenitor– and Down syndrome–associated acute lymphoblastic leukemia
Charles Mullighan and colleagues report a recurrent rearrangement of CRLF2 in B-progenitor and Down syndrome-associated acute lymphoblastic leukemia. Their genetic and functional evidence indicates that CRLF2 cooperates with activated JAK2 to promote leukemogenesis. Aneuploidy and translocations are...
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| Published in: | Nature genetics Vol. 41; no. 11; pp. 1243 - 1246 |
|---|---|
| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
New York
Nature Publishing Group US
01.11.2009
Nature Publishing Group |
| Subjects: | |
| ISSN: | 1061-4036, 1546-1718, 1546-1718 |
| Online Access: | Get full text |
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| Abstract | Charles Mullighan and colleagues report a recurrent rearrangement of
CRLF2
in B-progenitor and Down syndrome-associated acute lymphoblastic leukemia. Their genetic and functional evidence indicates that CRLF2 cooperates with activated JAK2 to promote leukemogenesis.
Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of
P2RY8
with the coding region of
CRLF2
. We identified the
P2RY8-CRLF2
fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome.
CRLF2
alteration was associated with activating
JAK
mutations, and expression of human
P2RY8-CRLF2
together with mutated mouse
Jak2
resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. |
|---|---|
| AbstractList | Charles Mullighan and colleagues report a recurrent rearrangement of
CRLF2
in B-progenitor and Down syndrome-associated acute lymphoblastic leukemia. Their genetic and functional evidence indicates that CRLF2 cooperates with activated JAK2 to promote leukemogenesis.
Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of
P2RY8
with the coding region of
CRLF2
. We identified the
P2RY8-CRLF2
fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome.
CRLF2
alteration was associated with activating
JAK
mutations, and expression of human
P2RY8-CRLF2
together with mutated mouse
Jak2
resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of P2RY8 with the coding region of CRLF2. We identified the P2RY8-CRLF2 fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome. CRLF2 alteration was associated with activating JAK mutations, and expression of human P2RY8-CRLF2 together with mutated mouse Jak2 resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL.Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of P2RY8 with the coding region of CRLF2. We identified the P2RY8-CRLF2 fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome. CRLF2 alteration was associated with activating JAK mutations, and expression of human P2RY8-CRLF2 together with mutated mouse Jak2 resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of P2RY8 with the coding region of CRLF2. We identified the P2RY8-CRLF2 fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome. CRLF2 alteration was associated with activating JAK mutations, and expression of human P2RY8-CRLF2 together with mutated mouse Jak2 resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. [PUBLICATION ABSTRACT] Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring chromosomal alterations. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of P2RY8 with the coding region of CRLF2. We identified the P2RY8-CRLF2 fusion in 7% of individuals with B-progenitor ALL and 53% of individuals with ALL associated with Down syndrome. CRLF2 alteration was associated with activating JAK mutations, and expression of human P2RY8-CRLF2 together with mutated mouse Jak2 resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3 cells overexpressing interleukin-7 receptor alpha. Our findings indicate that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many patients lack a recurring chromosomal alteration. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, non-coding exon of P2RY8 to the coding region of CRLF2 (which encodes cytokine receptor like factor 2, or thymic stromal lymphopoietin receptor). The P2RY8-CRLF2 fusion was identified in 7% of B-progenitor ALL cases, and was identified in over 50% of ALL cases arising in patients with Down syndrome (53% of 75 cases). CRLF2 alteration was associated with the presence of activating JAK mutations, and expression of P2RY8-CRLF2 together with JAK2 mutants resulted in constitutive Jak-Stat activation and cytokine-independent growth of Ba/F3-IL7R cells, indicating that these two genetic lesions together contribute to leukemogenesis in B-progenitor ALL. |
| Audience | Academic |
| Author | Harvey, Richard C Raimondi, Susana C Basso, Giuseppe Downing, James R Liu, Wei Cheng, Jinjun Willman, Cheryl L Heerema, Nyla A Williams, Richard T Collins-Underwood, J Racquel Meyer, Julia Pui, Ching-Hon Carroll, Andrew J Rabin, Karen R Phillips, Letha A A Zhang, Jinghui Coustan-Smith, Elaine Ma, Jing Pession, Andrea Hunger, Stephen P Loudin, Michael G Mikhail, Fady M Carroll, William L Mullighan, Charles G |
| AuthorAffiliation | 4 Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Rockville, MD 8 Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 9 New York University Cancer Institute, New York University Langone Medical Center, New York, NY 10 Pathology, College of Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH 6 Department of Oncology, St Jude Children’s Research Hospital, Memphis, TN 11 Department of Pediatrics, University of Padua, Padua, Italy 3 Department of Biostatistics, St Jude Children’s Research Hospital, Memphis, TN 2 Department of Pediatrics, Section of Hematology-Oncology, Baylor College of Medicine, Houston, TX 12 Department of Pediatrics, University of Bologna, Hematology and Oncology Unit “Lalla Seragnoli”, Bologna, Italy 7 University of New Mexico Cancer Research & Treatment Center, UNM Cancer Research Facility, Albuquerque, NM 13 Section of Pediatric Hematology/Oncology/Bone Mar |
| AuthorAffiliation_xml | – name: 10 Pathology, College of Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH – name: 13 Section of Pediatric Hematology/Oncology/Bone Marrow Transplantation and Center for Cancer and Blood Disorders, University of Colorado Denver School of Medicine, The Children’s Hospital, Aurora, CO – name: 5 The Hartwell Center for Bioinformatics and Biotechnology, St Jude Children’s Research Hospital, Memphis, TN – name: 9 New York University Cancer Institute, New York University Langone Medical Center, New York, NY – name: 12 Department of Pediatrics, University of Bologna, Hematology and Oncology Unit “Lalla Seragnoli”, Bologna, Italy – name: 8 Department of Genetics, University of Alabama at Birmingham, Birmingham, AL – name: 4 Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health, Rockville, MD – name: 11 Department of Pediatrics, University of Padua, Padua, Italy – name: 1 Department of Pathology, St Jude Children’s Research Hospital, Memphis, TN – name: 3 Department of Biostatistics, St Jude Children’s Research Hospital, Memphis, TN – name: 7 University of New Mexico Cancer Research & Treatment Center, UNM Cancer Research Facility, Albuquerque, NM – name: 2 Department of Pediatrics, Section of Hematology-Oncology, Baylor College of Medicine, Houston, TX – name: 6 Department of Oncology, St Jude Children’s Research Hospital, Memphis, TN |
| Author_xml | – sequence: 1 givenname: Charles G surname: Mullighan fullname: Mullighan, Charles G email: charles.mullighan@stjude.org organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 2 givenname: J Racquel surname: Collins-Underwood fullname: Collins-Underwood, J Racquel organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 3 givenname: Letha A A surname: Phillips fullname: Phillips, Letha A A organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 4 givenname: Michael G surname: Loudin fullname: Loudin, Michael G organization: Department of Pediatrics, Section of Hematology-Oncology, Baylor College of Medicine – sequence: 5 givenname: Wei surname: Liu fullname: Liu, Wei organization: Department of Biostatistics, St. Jude Children's Research Hospital – sequence: 6 givenname: Jinghui surname: Zhang fullname: Zhang, Jinghui organization: Center for Biomedical Informatics and Information Technology, National Cancer Institute, National Institutes of Health – sequence: 7 givenname: Jing surname: Ma fullname: Ma, Jing organization: The Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital – sequence: 8 givenname: Elaine surname: Coustan-Smith fullname: Coustan-Smith, Elaine organization: Department of Oncology, St. Jude Children's Research Hospital – sequence: 9 givenname: Richard C surname: Harvey fullname: Harvey, Richard C organization: University of New Mexico Cancer Research & Treatment Center, University of New Mexico Cancer Research Facility – sequence: 10 givenname: Cheryl L surname: Willman fullname: Willman, Cheryl L organization: University of New Mexico Cancer Research & Treatment Center, University of New Mexico Cancer Research Facility – sequence: 11 givenname: Fady M surname: Mikhail fullname: Mikhail, Fady M organization: Department of Genetics, University of Alabama at Birmingham – sequence: 12 givenname: Julia surname: Meyer fullname: Meyer, Julia organization: New York University Cancer Institute, New York University Langone Medical Center – sequence: 13 givenname: Andrew J surname: Carroll fullname: Carroll, Andrew J organization: Department of Genetics, University of Alabama at Birmingham – sequence: 14 givenname: Richard T surname: Williams fullname: Williams, Richard T organization: Department of Oncology, St. Jude Children's Research Hospital – sequence: 15 givenname: Jinjun surname: Cheng fullname: Cheng, Jinjun organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 16 givenname: Nyla A surname: Heerema fullname: Heerema, Nyla A organization: Department of Pathology, College of Medicine, The Ohio State University Comprehensive Cancer Center – sequence: 17 givenname: Giuseppe surname: Basso fullname: Basso, Giuseppe organization: Department of Pediatrics, University of Padua – sequence: 18 givenname: Andrea surname: Pession fullname: Pession, Andrea organization: Department of Pediatrics, University of Bologna, Hematology and Oncology Unit 'Lalla Seràgnoli' – sequence: 19 givenname: Ching-Hon surname: Pui fullname: Pui, Ching-Hon organization: Department of Oncology, St. Jude Children's Research Hospital – sequence: 20 givenname: Susana C surname: Raimondi fullname: Raimondi, Susana C organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 21 givenname: Stephen P surname: Hunger fullname: Hunger, Stephen P organization: Section of Pediatric Hematology, Oncology and Bone Marrow Transplantation and Center for Cancer and Blood Disorders, University of Colorado Denver School of Medicine, The Children's Hospital – sequence: 22 givenname: James R surname: Downing fullname: Downing, James R organization: Department of Pathology, St. Jude Children's Research Hospital – sequence: 23 givenname: William L surname: Carroll fullname: Carroll, William L organization: New York University Cancer Institute, New York University Langone Medical Center – sequence: 24 givenname: Karen R surname: Rabin fullname: Rabin, Karen R organization: Department of Pediatrics, Section of Hematology-Oncology, Baylor College of Medicine |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22103334$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19838194$$D View this record in MEDLINE/PubMed |
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| CODEN | NGENEC |
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| Snippet | Charles Mullighan and colleagues report a recurrent rearrangement of
CRLF2
in B-progenitor and Down syndrome-associated acute lymphoblastic leukemia. Their... Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many individuals with this cancer lack recurring... Aneuploidy and translocations are hallmarks of B-progenitor acute lymphoblastic leukemia (ALL), but many patients lack a recurring chromosomal alteration. Here... |
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| StartPage | 1243 |
| SubjectTerms | Acute lymphocytic leukemia Agriculture Amino Acid Sequence Animal Genetics and Genomics Animals Base Sequence Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Cancer Research Cell cycle Cell Line Chromosome aberrations Chromosome Deletion Chromosomes Down syndrome Down Syndrome - complications Down Syndrome - genetics Fundamental and applied biological sciences. Psychology Gene Function Gene mutations Gene Rearrangement Genetic aspects Genetics Genetics of eukaryotes. Biological and molecular evolution Genomics Health aspects Hematologic and hematopoietic diseases Hospitals Human Genetics Humans Janus Kinase 2 - genetics Janus Kinase 2 - metabolism Kinases letter Leukemia Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical genetics Medical research Medical sciences Mice Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor Cell Lymphoblastic Leukemia-Lymphoma - complications Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Receptors, Cytokine - chemistry Receptors, Cytokine - genetics Receptors, Cytokine - metabolism Receptors, Purinergic P2 - genetics Receptors, Purinergic P2 - metabolism Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Risk factors Studies |
| Title | Rearrangement of CRLF2 in B-progenitor– and Down syndrome–associated acute lymphoblastic leukemia |
| URI | https://link.springer.com/article/10.1038/ng.469 https://www.ncbi.nlm.nih.gov/pubmed/19838194 https://www.proquest.com/docview/222680055 https://www.proquest.com/docview/21214320 https://www.proquest.com/docview/733668975 https://pubmed.ncbi.nlm.nih.gov/PMC2783810 |
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