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Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms

Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms
Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms
This study was undertaken to further elucidate the biological mechanisms underlying the frequent event of transformation of follicular lymphoma (FL) to diffuse large B-cell lymphoma (t-FL). The gene expression profiles of 20 paired lymph node biopsies, derived from the same patient pre- and post-transformation, were analysed using the Lymphochip cDNA microarray. TP53 mutation analysis was performed and copy number alterations at the c-REL and CDNK2A examined. Immunohistochemistry was performed on an independent panel of paired transformation paraffin-embedded samples. Transformed follicular lymphoma was predominantly of the germinal centre B-like phenotype both at the mRNA and protein level. Despite this homogeneity, transformation proceeded by at least two pathways. One mechanism was characterised by high proliferation, as assessed by the co-ordinately expressed genes of the proliferation signature. This group was associated with the presence of recurrent oncogenic abnormalities. In the remaining cases, proliferation was not increased and transformation proceeded by alternative routes as yet undetermined. Genes involved in cellular proliferation prevailed amongst those that were significantly increased upon transformation and T cell and follicular dendritic-associated genes predominated amongst those that decreased. t-FL is a germinal centre B (GCB)-like malignancy that evolves by two pathways, one that is similar in proliferation rate to the antecedent FL and the other that has a higher proliferation rate and is characterised by the presence of recognised oncogenic abnormalities.
0007-1048
286-293
Davies, Andrew J.
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Rosenwald, Aandreas
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Wright, George
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Lee, Abigail
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Last, Kim W.
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Weisenburger, Denis D.
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Chan, Wing C.
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Delabie, Jan
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Braziel, Rita M.
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Campo, Elias
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Gascoyne, Randy D.
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Jaffe, Elaine S.
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Muller-Hermelink, H. Konrad
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Ott, German
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Calaminici, Maria
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Norton, Andrew J.
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Goff, Lindsey K.
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Fitzgibbon, Jude
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Staudt, Lindsey M
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Lister, T. Andrew
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Davies, Andrew J.
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Rosenwald, Aandreas
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Wright, George
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Lee, Abigail
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Last, Kim W.
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Weisenburger, Denis D.
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Chan, Wing C.
ecd09099-ea35-4522-8f69-4b95fc839dd8
Delabie, Jan
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Braziel, Rita M.
56405a22-6cac-416e-bd8b-9bffa2cac0a1
Campo, Elias
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Gascoyne, Randy D.
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Jaffe, Elaine S.
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Muller-Hermelink, H. Konrad
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Ott, German
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Calaminici, Maria
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Norton, Andrew J.
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Goff, Lindsey K.
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Fitzgibbon, Jude
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Staudt, Lindsey M
4fcb3083-2688-453e-9c7f-1e7c5e09bbbb
Lister, T. Andrew
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Davies, Andrew J., Rosenwald, Aandreas, Wright, George, Lee, Abigail, Last, Kim W., Weisenburger, Denis D., Chan, Wing C., Delabie, Jan, Braziel, Rita M., Campo, Elias, Gascoyne, Randy D., Jaffe, Elaine S., Muller-Hermelink, H. Konrad, Ott, German, Calaminici, Maria, Norton, Andrew J., Goff, Lindsey K., Fitzgibbon, Jude, Staudt, Lindsey M and Lister, T. Andrew (2007) Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms. British Journal of Haematology, 136 (2), 286-293. (doi:10.1111/j.1365-2141.2006.06439.x).

Record type: Article

Abstract

This study was undertaken to further elucidate the biological mechanisms underlying the frequent event of transformation of follicular lymphoma (FL) to diffuse large B-cell lymphoma (t-FL). The gene expression profiles of 20 paired lymph node biopsies, derived from the same patient pre- and post-transformation, were analysed using the Lymphochip cDNA microarray. TP53 mutation analysis was performed and copy number alterations at the c-REL and CDNK2A examined. Immunohistochemistry was performed on an independent panel of paired transformation paraffin-embedded samples. Transformed follicular lymphoma was predominantly of the germinal centre B-like phenotype both at the mRNA and protein level. Despite this homogeneity, transformation proceeded by at least two pathways. One mechanism was characterised by high proliferation, as assessed by the co-ordinately expressed genes of the proliferation signature. This group was associated with the presence of recurrent oncogenic abnormalities. In the remaining cases, proliferation was not increased and transformation proceeded by alternative routes as yet undetermined. Genes involved in cellular proliferation prevailed amongst those that were significantly increased upon transformation and T cell and follicular dendritic-associated genes predominated amongst those that decreased. t-FL is a germinal centre B (GCB)-like malignancy that evolves by two pathways, one that is similar in proliferation rate to the antecedent FL and the other that has a higher proliferation rate and is characterised by the presence of recognised oncogenic abnormalities.

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Published date: January 2007

Identifiers

Local EPrints ID: 73280
URI: http://eprints.soton.ac.uk/id/eprint/73280
ISSN: 0007-1048
PURE UUID: 95a08a85-71be-4452-a0c3-b7a947abfe13
ORCID for Andrew J. Davies: ORCID iD orcid.org/0000-0002-7517-6938

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Date deposited: 04 Mar 2010
Last modified: 14 Mar 2024 02:54

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Contributors

Author: Aandreas Rosenwald
Author: George Wright
Author: Abigail Lee
Author: Kim W. Last
Author: Denis D. Weisenburger
Author: Wing C. Chan
Author: Jan Delabie
Author: Rita M. Braziel
Author: Elias Campo
Author: Randy D. Gascoyne
Author: Elaine S. Jaffe
Author: H. Konrad Muller-Hermelink
Author: German Ott
Author: Maria Calaminici
Author: Andrew J. Norton
Author: Lindsey K. Goff
Author: Jude Fitzgibbon
Author: Lindsey M Staudt
Author: T. Andrew Lister

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