Role of activation‐induced cytidine deaminase in the progression of follicular lymphoma
Activation‐induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class‐switch recombination of the immunoglobulin gene, and for c‐myc translocation of germinal center‐derived B‐cell lymphoma. In the present study, we attempted to clarify the significance of AID associated...
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Published in | Cancer science Vol. 103; no. 3; pp. 415 - 421 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.03.2012
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Subjects | |
Online Access | Get full text |
ISSN | 1347-9032 1349-7006 1349-7006 |
DOI | 10.1111/j.1349-7006.2011.02186.x |
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Abstract | Activation‐induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class‐switch recombination of the immunoglobulin gene, and for c‐myc translocation of germinal center‐derived B‐cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c‐myc in the progression of follicular lymphoma (FL) using RT‐PCR and quantitative real‐time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c‐myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c‐myc. In order to examine the role of AID expression in rapidly progressive FL, the full‐length AID transcript was transfected into AID‐negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID‐expressing transfectants with a low proliferation rate and a significantly increased incidence of G0/G1 arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c‐myc is expressed. Switch‐off or low expression of AID after c‐myc amplification may correlate with the clinical outcomes of FL. (Cancer Sci 2012; 103: 415–421) |
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AbstractList | Activation‐induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class‐switch recombination of the immunoglobulin gene, and for
c‐myc
translocation of germinal center‐derived B‐cell lymphoma. In the present study, we attempted to clarify the significance of
AID
associated with
c‐myc
in the progression of follicular lymphoma (FL) using RT‐PCR and quantitative real‐time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of
c‐myc
and
AID
. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of
AID
, despite expressing high levels of
c‐myc
. In order to examine the role of AID expression in rapidly progressive FL, the full‐length
AID
transcript was transfected into
AID
‐negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of
AID
‐expressing transfectants with a low proliferation rate and a significantly increased incidence of G
0
/G
1
arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient
c‐myc
is expressed. Switch‐off or low expression of
AID
after
c‐myc
amplification may correlate with the clinical outcomes of FL. (
Cancer Sci
2012; 103: 415–421) Activation-induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class-switch recombination of the immunoglobulin gene, and for c-myc translocation of germinal center-derived B-cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c-myc in the progression of follicular lymphoma (FL) using RT-PCR and quantitative real-time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c-myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c-myc. In order to examine the role of AID expression in rapidly progressive FL, the full-length AID transcript was transfected into AID-negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID-expressing transfectants with a low proliferation rate and a significantly increased incidence of G(0)/G(1) arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c-myc is expressed. Switch-off or low expression of AID after c-myc amplification may correlate with the clinical outcomes of FL. Activation‐induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class‐switch recombination of the immunoglobulin gene, and for c‐myc translocation of germinal center‐derived B‐cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c‐myc in the progression of follicular lymphoma (FL) using RT‐PCR and quantitative real‐time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c‐myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c‐myc. In order to examine the role of AID expression in rapidly progressive FL, the full‐length AID transcript was transfected into AID‐negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID‐expressing transfectants with a low proliferation rate and a significantly increased incidence of G0/G1 arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c‐myc is expressed. Switch‐off or low expression of AID after c‐myc amplification may correlate with the clinical outcomes of FL. (Cancer Sci 2012; 103: 415–421) Activation-induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class-switch recombination of the immunoglobulin gene, and for c-myc translocation of germinal center-derived B-cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c-myc in the progression of follicular lymphoma (FL) using RT-PCR and quantitative real-time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c-myc and AID. The samples taken from a patient with FL who died within 2years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c-myc. In order to examine the role of AID expression in rapidly progressive FL, the full-length AID transcript was transfected into AID-negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID-expressing transfectants with a low proliferation rate and a significantly increased incidence of G0/G1 arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c-myc is expressed. Switch-off or low expression of AID after c-myc amplification may correlate with the clinical outcomes of FL. (Cancer Sci 2012; 103: 415-421) Activation-induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class-switch recombination of the immunoglobulin gene, and for c-myc translocation of germinal center-derived B-cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c-myc in the progression of follicular lymphoma (FL) using RT-PCR and quantitative real-time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c-myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c-myc. In order to examine the role of AID expression in rapidly progressive FL, the full-length AID transcript was transfected into AID-negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID-expressing transfectants with a low proliferation rate and a significantly increased incidence of G(0)/G(1) arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c-myc is expressed. Switch-off or low expression of AID after c-myc amplification may correlate with the clinical outcomes of FL.Activation-induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class-switch recombination of the immunoglobulin gene, and for c-myc translocation of germinal center-derived B-cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c-myc in the progression of follicular lymphoma (FL) using RT-PCR and quantitative real-time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c-myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c-myc. In order to examine the role of AID expression in rapidly progressive FL, the full-length AID transcript was transfected into AID-negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID-expressing transfectants with a low proliferation rate and a significantly increased incidence of G(0)/G(1) arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c-myc is expressed. Switch-off or low expression of AID after c-myc amplification may correlate with the clinical outcomes of FL. |
Author | Yamanouchi, Jun Sugita, Atsuro Matsushita, Natsuki Nakamura, Naoya Yakushijin, Yoshihiro Sakai, Akira Hato, Takaaki Azuma, Taichi Yasukawa, Masaki Shikata, Hisaharu |
AuthorAffiliation | 4 Department of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University Graduate School of Medicine, Hiroshima 6 Department of Pathology, Tokai University School of Medicine, Isehara 1 Department of Bioregulatory Medicine 3 Functional Genomics Core Laboratory, Ehime University Proteo‐Medicine Research Center, Toon 7 Division of Blood Transfusion and Cell Therapy, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon; Japan 2 Cancer Center, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon 5 Department of Pathology, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon |
AuthorAffiliation_xml | – name: 7 Division of Blood Transfusion and Cell Therapy, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon; Japan – name: 3 Functional Genomics Core Laboratory, Ehime University Proteo‐Medicine Research Center, Toon – name: 1 Department of Bioregulatory Medicine – name: 6 Department of Pathology, Tokai University School of Medicine, Isehara – name: 5 Department of Pathology, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon – name: 2 Cancer Center, Ehime University Hospital, Ehime University Graduate School of Medicine, Toon – name: 4 Department of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University Graduate School of Medicine, Hiroshima |
Author_xml | – sequence: 1 givenname: Hisaharu surname: Shikata fullname: Shikata, Hisaharu – sequence: 2 givenname: Yoshihiro surname: Yakushijin fullname: Yakushijin, Yoshihiro – sequence: 3 givenname: Natsuki surname: Matsushita fullname: Matsushita, Natsuki – sequence: 4 givenname: Akira surname: Sakai fullname: Sakai, Akira – sequence: 5 givenname: Atsuro surname: Sugita fullname: Sugita, Atsuro – sequence: 6 givenname: Naoya surname: Nakamura fullname: Nakamura, Naoya – sequence: 7 givenname: Jun surname: Yamanouchi fullname: Yamanouchi, Jun – sequence: 8 givenname: Taichi surname: Azuma fullname: Azuma, Taichi – sequence: 9 givenname: Takaaki surname: Hato fullname: Hato, Takaaki – sequence: 10 givenname: Masaki surname: Yasukawa fullname: Yasukawa, Masaki |
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SubjectTerms | Activation-induced cytidine deaminase Adult Aged Blotting, Western c-Myc protein Cancer Cell Proliferation Cell survival Class switching Cytidine Deaminase - genetics Cytidine Deaminase - metabolism Disease Progression double prime B-cell lymphoma Enzyme Activation Female Gene Expression Profiling Humans Immunoglobulins Immunohistochemistry Lymphoma, Follicular - genetics Lymphoma, Follicular - metabolism Lymphoma, Follicular - pathology Male Middle Aged Original Polymerase chain reaction Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism Real-Time Polymerase Chain Reaction Recombination Reverse Transcriptase Polymerase Chain Reaction somatic hypermutation Transcription Transfection Translocation |
Title | Role of activation‐induced cytidine deaminase in the progression of follicular lymphoma |
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