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Molecular histogenesis of plasmablastic lymphoma of the oral cavity
Author(s) -
Gaidano Gianluca,
Cerri Michaela,
Capello Daniela,
Berra Eva,
Deambrogi Clara,
Rossi Davide,
Larocca Luigi Maria,
Campo Elias,
Gloghini Annunziata,
Tirelli Umberto,
Carbone Antonino
Publication year - 2002
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2002.03872.x
Subject(s) - plasmablastic lymphoma , histogenesis , biology , lymphoma , somatic hypermutation , phenotype , b cell , germinal center , microbiology and biotechnology , gene , antibody , cancer research , immunology , genetics , immunohistochemistry
Summary. Plasmablastic lymphoma (PBL) of the oral cavity is an aggressive B‐cell lymphoma associated with human immunodeficiency virus infection. Although the lymphoma phenotype is consistent with late B‐cell maturation, the molecular histogenesis of PBL is unknown. We investigated PBL of the oral cavity ( n = 12) for mutations of immunoglobulin variable heavy chain (IgV H ) and BCL ‐6 genes, which are acquired by B cells at the time of germinal centre (GC) transit, and for expression of BCL‐6, MUM‐1 and CD138, which distinguish GC B cells from post‐GC B cells. Somatic IgV H hypermutation occurred in 4/10 PBL whereas 6/10 PBL displayed germline IgV H genes. Among PBL carrying hypermutated IgV H genes, the pattern of IgV H mutations was consistent with antigen stimulation in two cases. Mutations of the BCL ‐6 gene were restricted to 1/12 patients with PBL of the oral cavity. All cases of PBL of the oral cavity displayed the BCL‐6 – /MUM‐1 + /CD138 + phenotype that is consistent with late stage of B‐cell differentiation. Overall, these data indicate that, despite a common phenotype and an apparently similar degree of differentiation, PBL of the oral cavity are characterized by histogenetic heterogeneity. A subset of PBL of the oral cavity carried the molecular clues of GC transit and conceivably originated from a B‐cell subset corresponding to post‐GC B cells. Conversely, another fraction of these lymphomas were devoid of somatic IgV H mutations and appeared to originate from naive B cells that have undergone preterminal differentiation independent of GC transit.