Morphological, ultrastructural, and genetic characterization of an unusual T-cell lymphoma in a patient with sinus histiocytosis with massive lymphadenopathy
Autor: | Jonathan E. Kolitz, Prasad Koduru, Daniel R. Budman, M. J. Siques, Myron Susin, M. Soni, E. Amorosi, Saul Teichberg, T. Sun |
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Rok vydání: | 1995 |
Předmět: |
Male
Pathology medicine.medical_specialty Lymph node biopsy Gene Expression Hypereosinophilia Biology Gene Rearrangement T-Lymphocyte Lymphoma T-Cell Immunophenotyping medicine T-cell lymphoma Humans Gene Rearrangement B-Lymphocyte Lymphatic Diseases medicine.diagnostic_test Interleukins Sinus Histiocytosis with Massive Lymphadenopathy Hematology Gene rearrangement Middle Aged medicine.disease Lymphoma Clone Cells Histiocytosis Karyotyping Lymph Nodes medicine.symptom Histiocytosis Sinus |
Zdroj: | American journal of hematology. 48(3) |
ISSN: | 0361-8609 |
Popis: | Sinus histiocytosis with massive lymphadenopathy (SHML) is a rare benign disease of unknown etiology. It is rarely associated with malignant lymphoma. This report documents the first case of a T-cell lymphoma, which developed in a patient with a 10-year history of SHML. The disease was complicated by hypereosinophilia and massive retroperitoneal lymphadenopathy. Histological examination of a cervical lymph node biopsy during the terminal phase identified a lymphoma composed of cells with morphological plasmacytoid features. Ultrastructurally, the tumor cells showed poorly developed cytoplasm, nuclei with peripheral chromatin clumping, and inconspicuous nucleoli. Cytogenetic studies showed two related clones. On immunohistochemical staining tumor cells were positive with monoclonal antibodies (mAb) CD3 and CD45RO. Southern blotting analysis identified clonal rearrangements in the T-cell receptor (TCR) alpha, beta and gamma genes. Thus, T-cell lineage of the tumor cells was established. In situ hybridization of interleukin-2 (IL-2) and interleukin-5 (IL-5) cDNA probes on tissue sections identified the synthesis of IL-5 by the eosinophils, suggesting an autocrine pathway of eosinophilopoiesis leading to hypereosinophilia in this patient. |
Databáze: | OpenAIRE |
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