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MAPK and JAK-STAT pathways dysregulation in plasmablastic lymphoma

Ramis-Zaldivar, Joan Enric ; Gonzalez-Farre, Blanca ; Nicolae, Alina ; Pack, Svetlana ; Clot, Guillem ; Nadeu, Ferran ; Mottok, Anja ; Horn, Heike ; Song, Joo Y ; Fu, Kai ; Wright, George ; Gascoyne, Randy D. ; Chan, Wing C. ; Scott, David W. ; Feldman, Andrew L. ; Valera, Alexandra ; Enjuanes, Anna ; Braziel, Rita M. ; Smeland, Erlend B. ; Staudt, Louis M. ; Rosenwald, Andreas ; Rimsza, Lisa M. ; Ott, German ; Jaffe, Elaine S ; Salaverria, Itziar ; Campo, Elias

Haematologica (Roma), 2021-10, Vol.106 (10), p.2682-2693 [Periódico revisado por pares]

Fondazione Ferrata Storti

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  • Título:
    MAPK and JAK-STAT pathways dysregulation in plasmablastic lymphoma
  • Autor: Ramis-Zaldivar, Joan Enric ; Gonzalez-Farre, Blanca ; Nicolae, Alina ; Pack, Svetlana ; Clot, Guillem ; Nadeu, Ferran ; Mottok, Anja ; Horn, Heike ; Song, Joo Y ; Fu, Kai ; Wright, George ; Gascoyne, Randy D. ; Chan, Wing C. ; Scott, David W. ; Feldman, Andrew L. ; Valera, Alexandra ; Enjuanes, Anna ; Braziel, Rita M. ; Smeland, Erlend B. ; Staudt, Louis M. ; Rosenwald, Andreas ; Rimsza, Lisa M. ; Ott, German ; Jaffe, Elaine S ; Salaverria, Itziar ; Campo, Elias
  • É parte de: Haematologica (Roma), 2021-10, Vol.106 (10), p.2682-2693
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
    The copy-number data reported in this article have been deposited in the Gene Expression Omnibus database under accession number GSE155055. Sequencing data have been deposited in the European Nucleotide Archive (ENA, accession number ERP123243).
    Disclosures
    JER-Z performed research, analyzed data and wrote the manuscript; BG-F. performed morphological diagnoses, analyzed data and wrote the manuscript; GC, FN, AM, HH, GW, DWS, AV and AE performed research and analyzed data; AN, SP, JYS, KF, RDG, WCC, ALF, RMB, EBS, LMS, AR, LMR, GO and ESJ reviewed and interpreted pathological and/or clinical data; IS performed research, analyzed data, designed research and wrote the manuscript; EC performed morphological analyses, designed research and wrote the manuscript. All authors approved the final version of the manuscript.
    Contributions
    No conflicts of interest to disclose.
    Data-sharing statement
  • Descrição: Plasmablastic lymphoma (PBL) is an aggressive B-cell lymphoma with an immunoblastic/large-cell morphology and terminal B-cell differentiation. The differential diagnosis from Burkitt lymphoma, plasma cell myeloma and some variants of diffuse large B-cell lymphoma may be challenging because of the overlapping morphological, genetic and immunophenotypic features. Furthermore, the genomic landscape in PBL is not well known. To characterize the genetic and molecular heterogeneity of these tumors, we investigated 34 cases of PBL using an integrated approach, including fluorescence in situ hybridization, targeted sequencing of 94 B-cell lymphoma-related genes, and copy-number arrays. PBL were characterized by high genetic complexity including MYC translocations (87%), gains of 1q21.1-q44, trisomy 7, 8q23.2- q24.21, 11p13-p11.2, 11q14.2-q25, 12p and 19p13.3-p13.13, losses of 1p33, 1p31.1-p22.3, 13q and 17p13.3-p11.2, and recurrent mutations of STAT3 (37%), NRAS and TP53 (33%), MYC and EP300 (19%) and CARD11, SOCS1 and TET2 (11%). Pathway enrichment analysis suggested a cooperative action between MYC alterations and MAPK (49%) and JAK-STAT (40%) signaling pathways. Of note, Epstein-Barr virus (EBV)-negative PBL cases had higher mutational and copy-number load and more frequent TP53, CARD11 and MYC mutations, whereas EBVpositive PBL tended to have more mutations affecting the JAK-STAT pathway. In conclusion, these findings further unravel the distinctive molecular heterogeneity of PBL identifying novel molecular targets and the different genetic profile of these tumors in relation to EBV infection.
  • Editor: Fondazione Ferrata Storti
  • Idioma: Inglês;Norueguês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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