The immunoglobulin heavy chain gene 3′ enhancers induce Bcl2 deregulation and lymphomagenesis in murine B cells

Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain ( Igh ) locus, resulting in the deregulated expression of Bcl2 . Our previous studies have shown that the Igh 3′ enhancers deregulate...

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Published inLeukemia Vol. 25; no. 9; pp. 1484 - 1493
Main Authors Xiang, H, Noonan, E J, Wang, J, Duan, H, Ma, L, Michie, S, Boxer, L M
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.09.2011
Nature Publishing Group
Subjects
3' Untranslated Regions - genetics
692/420/2489/68
692/699/67/1990/291/1621/1915
Animals
B cells
B-cell lymphoma
B-Lymphocytes - pathology
Biological and medical sciences
Blotting, Southern
Blotting, Western
Cancer Research
Cell Cycle
Cell Differentiation
Cell Survival
Cells, Cultured
Chains
Chromosome aberrations
Chromosome translocations
Chromosomes
Cloning
Critical Care Medicine
Deoxyribonuclease
Deregulation
Enhancer Elements, Genetic - genetics
Enhancers
Female
Flow Cytometry
Fluorescent Antibody Technique
Gene expression
Gene targeting
Genes, Immunoglobulin Heavy Chain - genetics
Heavy chains
Hematologic and hematopoietic diseases
Hematology
Humans
Immunoglobulins
In vivo methods and tests
Intensive
Internal Medicine
Leukemia
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Loci
Lymphocytes B
Lymphoma
Lymphoma, B-Cell - etiology
Lymphoma, B-Cell - pathology
Male
Medical genetics
Medical sciences
Medicine
Medicine & Public Health
Mice
Mice, Transgenic
mRNA
Oncology
original-article
Physiological aspects
Polymerase Chain Reaction
Promoter Regions, Genetic - genetics
Proteins
Proto-Oncogene Proteins - physiology
Proto-Oncogene Proteins c-bcl-2
Translocation
United States
Palo Alto California
United States > US
mouse models
BCL2
t(14;18)
enhancer
lymphoma
Chromosomal aberration
Animal model
Carcinogenesis
Lymphoproliferative syndrome
Genetics
Protooncogene
Chromosome translocation
Heavy peptide chain
Immunoglobulins
Hematology
Rodentia
Malignant hemopathy
B-Lymphocyte
Lymphoid neoplasm
Igh enhancer
Lymphoma
Vertebrata
Mammalia
Abnormal chromosome E18
Mouse
Animal
C-Onc gene
Abnormal chromosome D14
Abnormal chromosome
Cancer
Online AccessGet full text

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Abstract Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain ( Igh ) locus, resulting in the deregulated expression of Bcl2 . Our previous studies have shown that the Igh 3′ enhancers deregulate the Bcl2 expression in vitro . However, the effects of the Igh 3′ enhancer elements on Bcl2 expression in vivo are not known. To investigate the role of the Igh 3′ enhancers in Bcl2 deregulation, we used gene targeting to generate knock-in mice in which four DNase I-hypersensitive regions from the murine Igh 3′ region were integrated 3′ of the Bcl2 locus. Increased levels of Bcl2 mRNA and protein were observed in the B cells of Igh-3′E-bcl2 mice. B cells from Igh-3′E-bcl2 mice showed an extended survival in vitro compared with B cells from wild-type (Wt) mice. The Bcl2 promoter shift from P1 (the 5′ promoter) to P2 (the 3′ promoter) was observed in B cells from Igh-3′E-bcl2 mice, similar to human t(14;18) lymphomas. The IgH-3′E-bcl2 mice developed monoclonal B-cell follicular lymphomas, which were slowly progressive. These studies show that the Igh 3′ enhancers have an important role in the deregulation of Bcl2 and B-cell lymphomagenesis in vivo .
AbstractList Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain (Igh) locus, resulting in the deregulated expression of Bcl2. Our previous studies have shown that the Igh 3' enhancers deregulate the Bcl2 expression in vitro. However, the effects of the Igh 3' enhancer elements on Bcl2 expression in vivo are not known. To investigate the role of the Igh 3' enhancers in Bcl2 deregulation, we used gene targeting to generate knock-in mice in which four DNase I-hypersensitive regions from the murine Igh 3' region were integrated 3' of the Bcl2 locus. Increased levels of Bcl2 mRNA and protein were observed in the B cells of Igh-3'E-bcl2 mice. B cells from Igh-3'E-bcl2 mice showed an extended survival in vitro compared with B cells from wild-type (Wt) mice. The Bcl2 promoter shift from P1 (the 5' promoter) to P2 (the 3' promoter) was observed in B cells from Igh-3'E-bcl2 mice, similar to human t(14;18) lymphomas. The IgH-3'E-bcl2 mice developed monoclonal B-cell follicular lymphomas, which were slowly progressive. These studies show that the Igh 3' enhancers have an important role in the deregulation of Bcl2 and B-cell lymphomagenesis in vivo.
Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain (Igh) locus, resulting in the deregulated expression of Bcl2. Our previous studies have shown that the Igh 3' enhancers deregulate the Bcl2 expression in vitro. However, the effects of the Igh 3' enhancer elements on Bcl2 expression in vivo are not known. To investigate the role of the Igh 3' enhancers in Bcl2 deregulation, we used gene targeting to generate knock-in mice in which four DNase I-hypersensitive regions from the murine Igh 3' region were integrated 3' of the Bcl2 locus. Increased levels of Bcl2 mRNA and protein were observed in the B cells of Igh-3'E-bcl2 mice. B cells from Igh-3'E-bcl2 mice showed an extended survival in vitro compared with B cells from wild-type (Wt) mice. The Bcl2 promoter shift from P1 (the 5' promoter) to P2 (the 3' promoter) was observed in B cells from Igh-3'E-bcl2 mice, similar to human t(14;18) lymphomas. The IgH-3'E-bcl2 mice developed monoclonal B-cell follicular lymphomas, which were slowly progressive. These studies show that the Igh 3' enhancers have an important role in the deregulation of Bcl2 and B-cell lymphomagenesis in vivo. doi: 10.1038/leu.2011.115; published online 24 May 2011 Keywords: lymphoma; BCL2; t(14;18); Igh enhancer; mouse models
Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain ( Igh ) locus, resulting in the deregulated expression of Bcl2 . Our previous studies have shown that the Igh 3’ enhancers deregulate Bcl2 expression in vitro . However, the effects of the Igh 3’ enhancer elements on Bcl2 expression in vivo are not known. To investigate the role of the Igh 3’ enhancers in Bcl2 deregulation, we used gene targeting to generate knock-in mice in which four DNase I hypersensitive regions from the murine Igh 3’ region were integrated 3’ of the Bcl2 locus. Increased levels of Bcl2 mRNA and protein were observed in the B cells of Igh-3’E-bcl2 mice. B cells from Igh-3’E-bcl2 mice demonstrated an extended survival in vitro compared with B cells from wild-type mice. The Bcl2 promoter shift from P1 (the 5’ promoter) to P2 (the 3’ promoter) was observed in B cells from Igh-3’E-bcl2 mice, similar to human t(14;18) lymphomas. The IgH-3’E-bcl2 mice developed monoclonal B-cell follicular lymphomas, which were slowly progressive. These studies demonstrate that the Igh 3’ enhancers play an important role in the deregulation of Bcl2 and B-cell lymphomagenesis in vivo .
Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin heavy chain ( Igh ) locus, resulting in the deregulated expression of Bcl2 . Our previous studies have shown that the Igh 3′ enhancers deregulate the Bcl2 expression in vitro . However, the effects of the Igh 3′ enhancer elements on Bcl2 expression in vivo are not known. To investigate the role of the Igh 3′ enhancers in Bcl2 deregulation, we used gene targeting to generate knock-in mice in which four DNase I-hypersensitive regions from the murine Igh 3′ region were integrated 3′ of the Bcl2 locus. Increased levels of Bcl2 mRNA and protein were observed in the B cells of Igh-3′E-bcl2 mice. B cells from Igh-3′E-bcl2 mice showed an extended survival in vitro compared with B cells from wild-type (Wt) mice. The Bcl2 promoter shift from P1 (the 5′ promoter) to P2 (the 3′ promoter) was observed in B cells from Igh-3′E-bcl2 mice, similar to human t(14;18) lymphomas. The IgH-3′E-bcl2 mice developed monoclonal B-cell follicular lymphomas, which were slowly progressive. These studies show that the Igh 3′ enhancers have an important role in the deregulation of Bcl2 and B-cell lymphomagenesis in vivo .
Audience Academic
Author Xiang, H
Wang, J
Michie, S
Boxer, L M
Ma, L
Duan, H
Noonan, E J
AuthorAffiliation 3 Department of Pathology, Stanford University School of Medicine, Stanford, California 94305
1 Center for Molecular Biology in Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304
2 Department of Medicine, Stanford University School of Medicine, Stanford, California 94305
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Issue 9
Keywords mouse models
BCL2
t(14;18)
enhancer
lymphoma
Chromosomal aberration
Animal model
Carcinogenesis
Lymphoproliferative syndrome
Genetics
Protooncogene
Chromosome translocation
Heavy peptide chain
Immunoglobulins
Hematology
Rodentia
Malignant hemopathy
B-Lymphocyte
Lymphoid neoplasm
Igh enhancer
Lymphoma
Vertebrata
Mammalia
Abnormal chromosome E18
Mouse
Animal
C-Onc gene
Abnormal chromosome D14
Abnormal chromosome
Cancer
Language English
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PMID 21606958
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pubmed_primary_21606958
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PublicationCentury 2000
PublicationDate 2011-09-01
PublicationDateYYYYMMDD 2011-09-01
PublicationDate_xml – month: 09
  year: 2011
  text: 2011-09-01
  day: 01
PublicationDecade 2010
PublicationPlace London
PublicationPlace_xml – name: London
– name: Avenel, NJ
– name: England
PublicationTitle Leukemia
PublicationTitleAbbrev Leukemia
PublicationTitleAlternate Leukemia
PublicationYear 2011
Publisher Nature Publishing Group UK
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
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Snippet Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin...
Human follicular B-cell lymphoma is associated with the t(14;18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin...
Human follicular B-cell lymphoma is associated with the t(14; 18) chromosomal translocation that juxtaposes the Bcl2 proto-oncogene with the immunoglobulin...
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SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 1484
SubjectTerms 3' Untranslated Regions - genetics
692/420/2489/68
692/699/67/1990/291/1621/1915
Animals
B cells
B-cell lymphoma
B-Lymphocytes - pathology
Biological and medical sciences
Blotting, Southern
Blotting, Western
Cancer Research
Cell Cycle
Cell Differentiation
Cell Survival
Cells, Cultured
Chains
Chromosome aberrations
Chromosome translocations
Chromosomes
Cloning
Critical Care Medicine
Deoxyribonuclease
Deregulation
Enhancer Elements, Genetic - genetics
Enhancers
Female
Flow Cytometry
Fluorescent Antibody Technique
Gene expression
Gene targeting
Genes, Immunoglobulin Heavy Chain - genetics
Heavy chains
Hematologic and hematopoietic diseases
Hematology
Humans
Immunoglobulins
In vivo methods and tests
Intensive
Internal Medicine
Leukemia
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Loci
Lymphocytes B
Lymphoma
Lymphoma, B-Cell - etiology
Lymphoma, B-Cell - pathology
Male
Medical genetics
Medical sciences
Medicine
Medicine & Public Health
Mice
Mice, Transgenic
mRNA
Oncology
original-article
Physiological aspects
Polymerase Chain Reaction
Promoter Regions, Genetic - genetics
Proteins
Proto-Oncogene Proteins - physiology
Proto-Oncogene Proteins c-bcl-2
Translocation
Title The immunoglobulin heavy chain gene 3′ enhancers induce Bcl2 deregulation and lymphomagenesis in murine B cells
URI https://link.springer.com/article/10.1038/leu.2011.115
https://www.ncbi.nlm.nih.gov/pubmed/21606958
https://www.proquest.com/docview/2645717873
https://www.proquest.com/docview/888294812
https://search.proquest.com/docview/888089848
https://search.proquest.com/docview/968174167
https://pubmed.ncbi.nlm.nih.gov/PMC3162065
Volume 25
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