Distinct comparative genomic hybridisation profiles in gastric mucosa-associated lymphoid tissue lymphomas with and without t(11;18)(q21;q21)

Yuanping Zhou, Hongtao Ye, Jose I. Martin-Subero, Rifat Hamoudi, Yong Jie Lu, Rubin Wang, Reiner Siebert, Janet Shipley, Peter G. Isaacson, Ahmet Dogan, Ming Qing Du

Research output: Contribution to journalArticle

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Abstract

t(11;18)(q21;q21) occurs specifically in mucosa-associated lymphoid tissue (MALT) lymphoma and the translocation generates a functional API2-MALT1 fusion product that activates nuclear factor (NF)κB. t(11;18) positive lymphomas usually lack the chromosomal aberrations and microsatellite alterations frequently seen in the translocation-negative MALT lymphomas. To further understand their genetic differences, we investigated gastric MALT lymphomas with and without t(11;18) by comparative genomic hybridisation. In general, both chromosomal gains and losses were far more frequent in t(11;18)-negative (median = 3.4 imbalances) than t(11;18)-positive cases (median = 1.6 imbalances), with gains being more frequent than losses. Recurrent chromosomal gains involving whole or major parts of a chromosome were seen for chromosomes 3, 12, 18 and 22 (23%, 19%, 19% and 27% respectively). Discrete recurrent chromosomal gains were found at 9q34 (11/26 = 42%). Bioinformatic analysis of genes mapping to 9q34 revealed potential targets. Among them, TRAF2 and CARD9 are known interaction partners of BCL10, playing a role in NFκB activation. Interphase fluorescent in situ hybridisation confirmed genomic gain of the TRAF2, CARD9 and MALT1 loci in 5/6 and 2/2 cases showing chromosomal gains at 9q34 and 18q21 respectively. The results further highlight the genetic difference between MALT lymphomas with and without t(11;18). Moreover, our findings suggest that genomic gain of genes that modulate NFκB activation, such as MALT1, TRAF2 and CARD9, may play a role in the pathogenesis of the translocation-negative MALT lymphoma.

Original languageEnglish (US)
Pages (from-to)35-42
Number of pages8
JournalBritish Journal of Haematology
Volume133
Issue number1
DOIs
StatePublished - Apr 2006
Externally publishedYes

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Marginal Zone B-Cell Lymphoma
Comparative Genomic Hybridization
Gastric Mucosa
TNF Receptor-Associated Factor 2
Chromosomes, Human, Pair 22
Chromosomes, Human, Pair 12
Chromosomes, Human, Pair 3
Chromosome Mapping
Interphase
Computational Biology
Fluorescence In Situ Hybridization
Chromosome Aberrations
Microsatellite Repeats
Lymphoma
Chromosomes
Genes

Keywords

  • CARD9
  • Comparative genomic hybridisation
  • MALT1
  • Mucosa-associated lymphoid tissue lymphoma
  • t(11;18)
  • TRAF2

ASJC Scopus subject areas

  • Hematology

Cite this

Distinct comparative genomic hybridisation profiles in gastric mucosa-associated lymphoid tissue lymphomas with and without t(11;18)(q21;q21). / Zhou, Yuanping; Ye, Hongtao; Martin-Subero, Jose I.; Hamoudi, Rifat; Lu, Yong Jie; Wang, Rubin; Siebert, Reiner; Shipley, Janet; Isaacson, Peter G.; Dogan, Ahmet; Du, Ming Qing.

In: British Journal of Haematology, Vol. 133, No. 1, 04.2006, p. 35-42.

Research output: Contribution to journalArticle

Zhou, Y, Ye, H, Martin-Subero, JI, Hamoudi, R, Lu, YJ, Wang, R, Siebert, R, Shipley, J, Isaacson, PG, Dogan, A & Du, MQ 2006, 'Distinct comparative genomic hybridisation profiles in gastric mucosa-associated lymphoid tissue lymphomas with and without t(11;18)(q21;q21)', British Journal of Haematology, vol. 133, no. 1, pp. 35-42. https://doi.org/10.1111/j.1365-2141.2006.05969.x
Zhou, Yuanping ; Ye, Hongtao ; Martin-Subero, Jose I. ; Hamoudi, Rifat ; Lu, Yong Jie ; Wang, Rubin ; Siebert, Reiner ; Shipley, Janet ; Isaacson, Peter G. ; Dogan, Ahmet ; Du, Ming Qing. / Distinct comparative genomic hybridisation profiles in gastric mucosa-associated lymphoid tissue lymphomas with and without t(11;18)(q21;q21). In: British Journal of Haematology. 2006 ; Vol. 133, No. 1. pp. 35-42.
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abstract = "t(11;18)(q21;q21) occurs specifically in mucosa-associated lymphoid tissue (MALT) lymphoma and the translocation generates a functional API2-MALT1 fusion product that activates nuclear factor (NF)κB. t(11;18) positive lymphomas usually lack the chromosomal aberrations and microsatellite alterations frequently seen in the translocation-negative MALT lymphomas. To further understand their genetic differences, we investigated gastric MALT lymphomas with and without t(11;18) by comparative genomic hybridisation. In general, both chromosomal gains and losses were far more frequent in t(11;18)-negative (median = 3.4 imbalances) than t(11;18)-positive cases (median = 1.6 imbalances), with gains being more frequent than losses. Recurrent chromosomal gains involving whole or major parts of a chromosome were seen for chromosomes 3, 12, 18 and 22 (23{\%}, 19{\%}, 19{\%} and 27{\%} respectively). Discrete recurrent chromosomal gains were found at 9q34 (11/26 = 42{\%}). Bioinformatic analysis of genes mapping to 9q34 revealed potential targets. Among them, TRAF2 and CARD9 are known interaction partners of BCL10, playing a role in NFκB activation. Interphase fluorescent in situ hybridisation confirmed genomic gain of the TRAF2, CARD9 and MALT1 loci in 5/6 and 2/2 cases showing chromosomal gains at 9q34 and 18q21 respectively. The results further highlight the genetic difference between MALT lymphomas with and without t(11;18). Moreover, our findings suggest that genomic gain of genes that modulate NFκB activation, such as MALT1, TRAF2 and CARD9, may play a role in the pathogenesis of the translocation-negative MALT lymphoma.",
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AU - Lu, Yong Jie

AU - Wang, Rubin

AU - Siebert, Reiner

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