CHROMOSOMAL-ABNORMALITIES IN NODAL AND EXTRANODAL CD30-CELL LYMPHOMAS- INFREQUENT DETECTION OF THE T(2-5) IN EXTRANODAL LYMPHOMAS( ANAPLASTIC LARGE)

Citation
G. Ott et al., CHROMOSOMAL-ABNORMALITIES IN NODAL AND EXTRANODAL CD30-CELL LYMPHOMAS- INFREQUENT DETECTION OF THE T(2-5) IN EXTRANODAL LYMPHOMAS( ANAPLASTIC LARGE), Genes, chromosomes & cancer, 22(2), 1998, pp. 114-121
Citations number
29
Categorie Soggetti
Oncology,"Genetics & Heredity
Journal title
ISSN journal
10452257
Volume
22
Issue
2
Year of publication
1998
Pages
114 - 121
Database
ISI
SICI code
1045-2257(1998)22:2<114:CINAEC>2.0.ZU;2-Q
Abstract
To determine the significance of the t(2;5)(p23;q35) translocation in nodal and extranodal anaplastic large cell lymphoma (ALCL), we perform ed cytogenetic, molecular genetic, and immunohistochemical analyses of tumor tissues fl-om I I patients with CD30+ ALCL. Three of five patie nts with nodal ALCL had additional infiltration of the skin. Six patie nts had extranodal ALCL, two had primary intestinal ALCL, three had a primary cutaneous ALCL, and one had osseous ALCL. Cytogenetic investig ation detected the t(2;5) in all patients with nodal ALCL but not extr anodal ALCL. Tumor cells in t(2;5)+ lesions also stained immunohistoch emically for p80(NPM/ALK), whereas no staining for p80(NPM/ALK) was de tected in extranodal ALCL. Two extranodal lesions had NPM/ALK fusion t ranscripts detected by nested reverse transcriptase-polymerase chain r eaction. Fluorescence in situ hybridization analysis of these two lymp homas showed in one case a significant number (4%) of cells with a spl it hybridization signal, indicative of disruption of the NPM gene. Add itional recurrent breakpoints observed in extranodal ALCL were 1p36, 6 p25, and 8q24. Loss of genetic material occurred at 6q in one extranod al ALCL. Our results suggest that the t(2:5) more frequently plays a p athogenetic role in primary nodal than in extranodal ALCL and that thi s translocation may not be the primary event in some CD30+ ALCL. (C) 1 998 Wiley-Liss, Inc.