Nodal T-cell lymphoma transdifferentiated from mantle cell lymphoma with Epstein-Barr virus infection.

Autor: Barone PD, Tam W, Geyer JT, Leonard JP, Phillips A, Ouseph MM
Jazyk: angličtina
Zdroj: Pathobiology : journal of immunopathology, molecular and cellular biology [Pathobiology] 2024 Oct 15, pp. 1-16. Date of Electronic Publication: 2024 Oct 15.
DOI: 10.1159/000541974
Abstrakt: Introduction: We report a case of mantle cell lymphoma (MCL) with apparent lineage switch to an EBV-positive T-cell lymphoma. Although lineage switch is a well-documented phenomenon in some hematolymphoid diseases, such as acute leukemias or histiocytic/dendritic cell neoplasms, lineage switch from mature B to T cell lymphoma is exceedingly rare.
Case Presentation: A 55-year-old man with an established history of MCL presented to our institution. Peripheral blood flow cytometry was consistent with MCL. Biopsy of a lumbar vertebral fracture site demonstrated mantle cell lymphoma, EBV-associated, with large cells reminiscent of high-grade transformation (BCL1-positive). Two months later, a lymph node biopsy demonstrated an EBV-positive T-cell lymphoma without phenotypic evidence of B-cell lymphoma (BCL1-negative). Cytogenetic testing revealed CCND1::IGH fusion in all three specimens. IGH/IGK clonality testing revealed conserved monoclonal peaks in all three samples; TCR clonality testing revealed monoclonal peaks in the T cell lymphoma, only. NGS-based molecular genetic studies revealed shared mutations between the three samples, consistent with a clonal relationship suggesting evolution from mantle cell lymphoma to T cell lymphoma.
Conclusions: This case demonstrates that lineage switch from mature B to mature T-cell phenotype is possible in certain settings. Whether lineage switch in this case was potentiated by EBV infection is unclear. The loss of BCL-1 expression in the T-cell lymphoma, despite conservation of the CCND1::IGH fusion, may be attributable to the downregulation of the IGH promoter as part of the shift from B to T-cell phenotype.
(The Author(s). Published by S. Karger AG, Basel.)
Databáze: MEDLINE