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Bianca Schuhmacher1, Julia Bein1, Tobias Rausch2,3

  • 1Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.

Haematologica
|September 15, 2018
PubMed
Summary

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This summary is machine-generated.

T-cell/histiocyte-rich large B-cell lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma share recurrent genetic mutations, suggesting they may be part of the same disease spectrum. Key genes like JUNB were frequently mutated in both conditions.

Area of Science:

  • Hematology
  • Oncology
  • Genetics

Background:

  • T-cell/histiocyte-rich large B-cell lymphoma (THRLBCL) and nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) are rare lymphomas with overlapping histopathology.
  • Despite distinct tumor microenvironments and clinical behaviors, shared tumor cell similarities suggest a potential disease spectrum relationship.

Purpose of the Study:

  • To investigate shared genetic mutations between THRLBCL and NLPHL to determine if they represent variants of the same disease.
  • To identify specific genes and mutation patterns implicated in the pathogenesis of these related lymphomas.

Main Methods:

  • Ultra-deep targeted resequencing was performed on 11 typical and 6 histopathological variants of NLPHL, along with 9 THRLBCL cases.
  • Analysis focused on identifying recurrently mutated genes and assessing mutation frequencies across the studied lymphoma entities.

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Main Results:

  • Genes recurrently mutated in NLPHL were found at similar frequencies in THRLBCL.
  • JUNB, DUSP2, SGK1, SOCS1, and CREBBP were the most frequently mutated genes, with higher mutation rates in THRLBCL and NLPHL variants.
  • Mutations in JUNB, DUSP2, SGK1, and SOCS1 were enriched at somatic hypermutation hotspots, indicating a role for aberrant somatic hypermutation in pathogenesis.
  • JUNB mutations, rare in other lymphomas, were notably frequent in both THRLBCL (5/9) and NLPHL (5/17).

Conclusions:

  • The shared genetic landscape, particularly recurrent mutations in specific genes, strongly supports a close relationship between THRLBCL and NLPHL.
  • These findings suggest that THRLBCL and NLPHL may exist on a disease spectrum, linked by common genetic alterations and potentially aberrant somatic hypermutation.
  • The high frequency of JUNB mutations in both entities provides a specific genetic marker supporting their close relationship.