Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma

Alyssa Bouska, Timothy W. McKeithan, Karen E. Deffenbacher, Cynthia Lachel, George W. Wright, Javeed Iqbal, Lynette M. Smith, Weiwei Zhang, Can Kucuk, Andrea Rinaldi, Francesco Bertoni, Jude Fitzgibbon, Kai Fu, Dennis D. Weisenburger, Timothy C. Greiner, Bhavana J. Dave, Randy D. Gascoyne, Andreas Rosenwald, German Ott, Elias CampoLisa M. Rimsza, Jan Delabie, Elaine S. Jaffe, Rita Braziel, Joseph M. Connors, Louis M. Staudt, Wing Chung Chan

Research output: Contribution to journalArticle

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Abstract

Follicular lymphoma (FL), the second most common type of non-Hodgkin lymphoma in the western world, is characterized by the t(14;18) translocation, which is present in up to 90% of cases. We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Common recurrent chromosomal abnormalities in FL included gains of 2, 5, 7, 6p, 8, 12, 17q, 18, 21, and X and losses on 6q and 17p. We also observed many frequent small abnormalities, including losses of 1p36.33-p36.31, 6q23.3-q24.1, and 10q23.1-q25.1 and gains of 2p16.1-p15, 8q24.13-q24.3, and 12q12-q13.13, and identified candidate genes that may be driving this selection. Recurrent abnormalities more frequent in tFL samples included gains of 3q27.3-q28 and chromosome 11 and losses of 9p21.3 and 15q. Four abnormalities, gain of X or Xp and losses of 6q23.2-24.1 or 6q13-15, predicted overall survival. Abnormalities associated with transformation of the disease likely impair immune surveillance, activate the nuclear factor-κB pathway, and deregulate p53 and B-cell transcription factors.

Original languageEnglish (US)
Pages (from-to)1681-1690
Number of pages10
JournalBlood
Volume123
Issue number11
DOIs
StatePublished - Mar 13 2014

Fingerprint

Follicular Lymphoma
Genes
Genome
Chromosome Aberrations
Cells
Chromosomes
Polymorphism
Chromosomes, Human, Pair 11
Western World
Lymphoma, Large B-Cell, Diffuse
Transcription Factors
Nucleotides
Non-Hodgkin's Lymphoma
Single Nucleotide Polymorphism
Lymphoma
B-Lymphocytes

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology

Cite this

Bouska, A., McKeithan, T. W., Deffenbacher, K. E., Lachel, C., Wright, G. W., Iqbal, J., ... Chan, W. C. (2014). Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma. Blood, 123(11), 1681-1690. https://doi.org/10.1182/blood-2013-05-500595

Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma. / Bouska, Alyssa; McKeithan, Timothy W.; Deffenbacher, Karen E.; Lachel, Cynthia; Wright, George W.; Iqbal, Javeed; Smith, Lynette M.; Zhang, Weiwei; Kucuk, Can; Rinaldi, Andrea; Bertoni, Francesco; Fitzgibbon, Jude; Fu, Kai; Weisenburger, Dennis D.; Greiner, Timothy C.; Dave, Bhavana J.; Gascoyne, Randy D.; Rosenwald, Andreas; Ott, German; Campo, Elias; Rimsza, Lisa M.; Delabie, Jan; Jaffe, Elaine S.; Braziel, Rita; Connors, Joseph M.; Staudt, Louis M.; Chan, Wing Chung.

In: Blood, Vol. 123, No. 11, 13.03.2014, p. 1681-1690.

Research output: Contribution to journalArticle

Bouska, A, McKeithan, TW, Deffenbacher, KE, Lachel, C, Wright, GW, Iqbal, J, Smith, LM, Zhang, W, Kucuk, C, Rinaldi, A, Bertoni, F, Fitzgibbon, J, Fu, K, Weisenburger, DD, Greiner, TC, Dave, BJ, Gascoyne, RD, Rosenwald, A, Ott, G, Campo, E, Rimsza, LM, Delabie, J, Jaffe, ES, Braziel, R, Connors, JM, Staudt, LM & Chan, WC 2014, 'Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma', Blood, vol. 123, no. 11, pp. 1681-1690. https://doi.org/10.1182/blood-2013-05-500595
Bouska A, McKeithan TW, Deffenbacher KE, Lachel C, Wright GW, Iqbal J et al. Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma. Blood. 2014 Mar 13;123(11):1681-1690. https://doi.org/10.1182/blood-2013-05-500595
Bouska, Alyssa ; McKeithan, Timothy W. ; Deffenbacher, Karen E. ; Lachel, Cynthia ; Wright, George W. ; Iqbal, Javeed ; Smith, Lynette M. ; Zhang, Weiwei ; Kucuk, Can ; Rinaldi, Andrea ; Bertoni, Francesco ; Fitzgibbon, Jude ; Fu, Kai ; Weisenburger, Dennis D. ; Greiner, Timothy C. ; Dave, Bhavana J. ; Gascoyne, Randy D. ; Rosenwald, Andreas ; Ott, German ; Campo, Elias ; Rimsza, Lisa M. ; Delabie, Jan ; Jaffe, Elaine S. ; Braziel, Rita ; Connors, Joseph M. ; Staudt, Louis M. ; Chan, Wing Chung. / Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma. In: Blood. 2014 ; Vol. 123, No. 11. pp. 1681-1690.
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abstract = "Follicular lymphoma (FL), the second most common type of non-Hodgkin lymphoma in the western world, is characterized by the t(14;18) translocation, which is present in up to 90{\%} of cases. We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Common recurrent chromosomal abnormalities in FL included gains of 2, 5, 7, 6p, 8, 12, 17q, 18, 21, and X and losses on 6q and 17p. We also observed many frequent small abnormalities, including losses of 1p36.33-p36.31, 6q23.3-q24.1, and 10q23.1-q25.1 and gains of 2p16.1-p15, 8q24.13-q24.3, and 12q12-q13.13, and identified candidate genes that may be driving this selection. Recurrent abnormalities more frequent in tFL samples included gains of 3q27.3-q28 and chromosome 11 and losses of 9p21.3 and 15q. Four abnormalities, gain of X or Xp and losses of 6q23.2-24.1 or 6q13-15, predicted overall survival. Abnormalities associated with transformation of the disease likely impair immune surveillance, activate the nuclear factor-κB pathway, and deregulate p53 and B-cell transcription factors.",
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AU - Bouska, Alyssa

AU - McKeithan, Timothy W.

AU - Deffenbacher, Karen E.

AU - Lachel, Cynthia

AU - Wright, George W.

AU - Iqbal, Javeed

AU - Smith, Lynette M.

AU - Zhang, Weiwei

AU - Kucuk, Can

AU - Rinaldi, Andrea

AU - Bertoni, Francesco

AU - Fitzgibbon, Jude

AU - Fu, Kai

AU - Weisenburger, Dennis D.

AU - Greiner, Timothy C.

AU - Dave, Bhavana J.

AU - Gascoyne, Randy D.

AU - Rosenwald, Andreas

AU - Ott, German

AU - Campo, Elias

AU - Rimsza, Lisa M.

AU - Delabie, Jan

AU - Jaffe, Elaine S.

AU - Braziel, Rita

AU - Connors, Joseph M.

AU - Staudt, Louis M.

AU - Chan, Wing Chung

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N2 - Follicular lymphoma (FL), the second most common type of non-Hodgkin lymphoma in the western world, is characterized by the t(14;18) translocation, which is present in up to 90% of cases. We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Common recurrent chromosomal abnormalities in FL included gains of 2, 5, 7, 6p, 8, 12, 17q, 18, 21, and X and losses on 6q and 17p. We also observed many frequent small abnormalities, including losses of 1p36.33-p36.31, 6q23.3-q24.1, and 10q23.1-q25.1 and gains of 2p16.1-p15, 8q24.13-q24.3, and 12q12-q13.13, and identified candidate genes that may be driving this selection. Recurrent abnormalities more frequent in tFL samples included gains of 3q27.3-q28 and chromosome 11 and losses of 9p21.3 and 15q. Four abnormalities, gain of X or Xp and losses of 6q23.2-24.1 or 6q13-15, predicted overall survival. Abnormalities associated with transformation of the disease likely impair immune surveillance, activate the nuclear factor-κB pathway, and deregulate p53 and B-cell transcription factors.

AB - Follicular lymphoma (FL), the second most common type of non-Hodgkin lymphoma in the western world, is characterized by the t(14;18) translocation, which is present in up to 90% of cases. We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Common recurrent chromosomal abnormalities in FL included gains of 2, 5, 7, 6p, 8, 12, 17q, 18, 21, and X and losses on 6q and 17p. We also observed many frequent small abnormalities, including losses of 1p36.33-p36.31, 6q23.3-q24.1, and 10q23.1-q25.1 and gains of 2p16.1-p15, 8q24.13-q24.3, and 12q12-q13.13, and identified candidate genes that may be driving this selection. Recurrent abnormalities more frequent in tFL samples included gains of 3q27.3-q28 and chromosome 11 and losses of 9p21.3 and 15q. Four abnormalities, gain of X or Xp and losses of 6q23.2-24.1 or 6q13-15, predicted overall survival. Abnormalities associated with transformation of the disease likely impair immune surveillance, activate the nuclear factor-κB pathway, and deregulate p53 and B-cell transcription factors.

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