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MAPK and JAK-STAT pathways dysregulation in plasmablastic lymphoma.
Joan Enric Ramis-Zaldivar1, Blanca Gonzalez-Farre1, Alina Nicolae2
1Hematopathology Unit, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Madrid.
Haematologica
|May 6, 2021
Summary
Plasmablastic lymphoma (PBL) is a complex cancer. This study reveals its genetic landscape, identifying key mutations and pathways, and highlighting differences based on Epstein-Barr virus (EBV) status.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- Plasmablastic lymphoma (PBL) is an aggressive B-cell lymphoma with challenging differential diagnoses.
- The genomic landscape of PBL remains incompletely understood.
Purpose of the Study:
- To characterize the genetic and molecular heterogeneity of Plasmablastic lymphoma.
- To identify novel molecular targets and understand EBV's role in PBL pathogenesis.
Main Methods:
- Integrated genomic analysis of 34 PBL cases.
- Utilized fluorescence in situ hybridization, targeted gene sequencing (94 genes), and copy-number arrays.
Main Results:
- PBL exhibits high genetic complexity, including frequent MYC translocations (87%) and mutations in STAT3 (37%), NRAS/TP53 (33%).
- MYC alterations cooperate with MAPK and JAK-STAT signaling pathways.
- Epstein-Barr virus (EBV)-negative PBL shows higher mutational burden and distinct mutation profiles compared to EBV-positive cases.
Conclusions:
- This study elucidates the distinct molecular heterogeneity of PBL.
- Identified novel molecular targets and differential genetic profiles influenced by EBV infection.
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