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The pathogenesis of large cell transformation in cutaneous T‐cell lymphoma is not associated with t(2;5)(p23;q35) chromosomal translocation
Author(s) -
Li Guoqing,
Salhany Kevin E.,
Rook Alain H.,
Lessin Stuart R.
Publication year - 1997
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/j.1600-0560.1997.tb00814.x
Subject(s) - chromosomal translocation , pathogenesis , pathology , lymphoma , cell , medicine , biology , cancer research , genetics , gene
In 20%–50% of the advanced cutaneous T‐cell lymphomas (CTCL), malignant T cells undergo large cell transformation (LOT). The malignant T cells of LCT in CTCL can share morphologic and immunophenotypic similarities with CD30 (Ki‐1)‐positive anaplastic large cell lymphoma (ALCL), suggesting a common mechanism of pathogenesis. The t(2;5) (p23;q35) translocation, resulting in the fusion of the nucleophosmin (NPM) gene and the anaplastic lymphoma kinase (ALK) gene, is associated with primary CD30+ ALCL. To determine whether acquisition of this chromosomal translocation is involved in the pathogenesis of LCT in CTCL, we examined 12 tumor samples from 9 CTCL patients, including 8 with LCT‐CTCL and one with concurrent CTCL and Hodgkin's disease, for the presence of the t(2;5) translocation. Numerous CD30+ large cells were present in 4 LCT‐CTCL consistent with secondary CD30+ ALCL; CD30 was expressed by <10% of the large cells in another case and was negative in the other 3 lymphomas. Using primers spanning the NPM/ALK fusion junction, PCR amplification following reverse transcription (RT) of mRNA failed to show the products of NPM/ALK fusion in all samples tested. Thus, the t(2;5) (p23;q35) translocation does not appear to be involved in the molecular pathogenesis of LCT in CTCL, including CD30+ cases.