| Autor: |
Yuanping Zhou, Hongtao Ye, Martin-Subero, Jose I., Hamoudi, Rifat, Yong-Jie Lu, Wang, Rubin, Siebert, Reiner, Shipley, Janet, Isaacson, Peter G., Dogan, Ahmet, Ming-Qing Du |
| Předmět: |
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| Zdroj: |
British Journal of Haematology; Apr2006, Vol. 133 Issue 1, p35-42, 8p, 1 Diagram, 1 Chart |
| Abstrakt: |
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 NF κB 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 NF κB activation, such as MALT1, TRAF2 and CARD9, may play a role in the pathogenesis of the translocation-negative MALT lymphoma. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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