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Phenotypic evolution in a case of peripheral T‐cell lymphoma suggests the presence of tumor heterogeneity
Author(s) -
AlIbraheemi Alyaa,
KanagalShamanna Rashmi,
Patel Keyur P.,
Konoplev Sergej N.,
Mehta Pramod,
Medeiros L. Jeffrey,
Miranda Roberto N.
Publication year - 2013
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/cup.12112
Subject(s) - immunophenotyping , lymphoma , peripheral t cell lymphoma , cd8 , pathology , t cell , gene rearrangement , immunology , phenotype , medicine , biology , antigen , immune system , gene , genetics
Peripheral T‐cell lymphoma ( PTCL ), not otherwise specified ( NOS ), represents a heterogeneous group of nodal and extranodal lymphomas that express a variety of T‐cell antigens indicative of mature T‐cell lineage. Most cases of PTCL express CD4 and lack CD8 expression and have a T‐helper immunophenotype. Although the immunophenotype of PTCL is usually stable over time, immunophenotypic switch or evolution from T‐helper to T‐suppressor or vice versa has been rarely reported. Herein, we report a patient who presented with nasal PTCL , NOS , that was CD8 + and negative for Epstein–Barr virus, with concurrent skin lesions that had a CD8 +/ TIA ‐1+ T‐cell immunophenotype. Patient received multi‐agent chemotherapy and matched unrelated donor stem cell transplant, and subsequently suffered a cutaneous relapse with a CD4 +/ TIA ‐1(−) immunophenotype. Molecular analysis of the neoplasm biopsied at presentation showed one monoclonal T‐cell receptor gamma gene rearrangement, and a second oligoclonal peak. At the time of CD4 ‐positive recurrence, the oligoclonal peak was rather prominent, suggesting that the emergence of this peak is related with the phenotypic evolution from CD8 + to CD4 + predominant. These results highlight the utility of sequential immunophenotypic and molecular analysis of PTCL cases at the time of relapse to better understand the mechanisms of disease.