Evidence map›Paper›PMID 12931213›Full record

ArticleLeukemia2003

Translocations t(11;18)(q21;q21) and t(14;18)(q32;q21) are the main chromosomal abnormalities involving MLT/MALT1 in MALT lymphomas.

E M Murga Penas, K Hinz, K Röser, C Copie-Bergman, I Wlodarska, P Marynen, A Hagemeijer, P Gaulard, T Löning, D K Hossfeld and 1 more

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Article in Leukemia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
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  4. Rare central nervous system lymphomas.British journal of haematology · 2022
    Review
  5. The Social Norm of Hematopoietic Stem Cells and Dysregulation in Leukemia.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Genetics of primary intraocular tumors.Ocular immunology and inflammation · 2012
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Delving deeper into MALT lymphoma biology.The Journal of clinical investigation · 2006
    Article
4 · The record

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5 · Who and what money

Authors and funding

11 authors at 4 institutions in 3 countries.

E M Murga PenasDepartment of Medicine, Hamburg, Germany.
K Hinz
K Röser
C Copie-Bergman
I Wlodarska
P Marynen
A Hagemeijer
P Gaulard
T Löning
D K Hossfeld
J Dierlamm
Centre Hospitalier Universitaire Henri-Mondor · FRKU Leuven · BEUniversität Hamburg · DEVlaams Instituut voor Biotechnologie · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recently discovered MLT/MALT1 gene is fused with the API2 gene in the t(11;18)(q21;q21), which characterizes about one-third of MALT lymphomas. In order to screen for variant translocations and amplifications of MLT/MALT1, we have developed a novel, undirected two-color interphase fluorescence in situ hybridization (FISH) assay with two PAC clones flanking MLT/MALT1. This assay was applied to 108 marginal zone B-cell lymphomas (MZBCLs), including 72 extranodal MALT lymphomas, 17 nodal, and 19 splenic MZBCL. In 19 MALT lymphomas (26%), but in none of the nodal or splenic MZBCL, separated hybridization signals of the MLT/MALT1 flanking probes, were found. Further FISH analyses showed that 12 of these 19 cases displayed the classical t(11;18) and the remaining seven cases revealed the novel t(14;18)(q32;q21), involving the MLT/MALT1 and IGH genes. The frequency at which these translocations occurred varied significantly with the primary location of disease. The t(11;18) was mainly detected in gastrointestinal MALT lymphomas, whereas the t(14;18) occurred in MALT lymphomas of the parotid gland and the conjunctiva. Amplification of MLT/MALT1 was not observed in any of the lymphomas analyzed. We conclude that the translocations t(11;18)(q21;q21) and t(14;18)(q21;q32) represent the main structural aberrations involving MLT/MALT1 in MALT lymphomas, whereas true amplifications of MLT/MALT1 occur rarely in MZBCL.

Indexed as

Chromosome AberrationsChromosomes, Human, Pair 11Chromosomes, Human, Pair 14Chromosomes, Human, Pair 18Translocation, GeneticBreast NeoplasmsCaspasesChromosome MappingGastrointestinal NeoplasmsHumansIn Situ Hybridization, FluorescenceLymphoma, B-Cell, Marginal ZoneMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsParotid NeoplasmsProteinsCaspasesMALT1 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsProteins

Identifiers

PMID12931213
OpenAlexW2072149766

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.