Premium
Chromosomal abnormalities in nodal and extranodal CD30+ anaplastic large cell lymphomas: Infrequent detection of the t(2;5) in extranodal lymphomas
Author(s) -
Ott German,
Katzenberger Tiemo,
Siebert Reiner,
Decoteau John F.,
Fletcher Jonathan A.,
Knoll Joan H. M.,
Kalla Jörg,
Rosenwald Andreas,
Ott M. Michaela,
WeberMatthiesen Klaus,
Kadin Marshall E.,
MüllerHermelink Hans Konrad
Publication year - 1998
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199806)22:2<114::aid-gcc5>3.0.co;2-#
Subject(s) - anaplastic large cell lymphoma , cd30 , pathology , lymphoma , large cell , nodal , medicine , biology , cancer , adenocarcinoma
To determine the significance of the t(2;5)(p23;q35) translocation in nodal and extranodal anaplastic large cell lymphoma (ALCL), we performed cytogenetic, molecular genetic, and immunohistochemical analyses of tumor tissues from 11 patients with CD30+ ALCL. Three of five patients with nodal ALCL had additional infiltration of the skin. Six patients had extranodal ALCL, two had primary intestinal ALCL, three had a primary cutaneous ALCL, and one had osseous ALCL. Cytogenetic investigation detected the t(2;5) in all patients with nodal ALCL but not extranodal ALCL. Tumor cells in t(2;5)+ lesions also stained immunohistochemically for p80 NPM/ALK , whereas no staining for p80 NPM/ALK was detected in extranodal ALCL. Two extranodal lesions had NPM/ALK fusion transcripts detected by nested reverse transcriptase–polymerase chain reaction. Fluorescence in situ hybridization analysis of these two lymphomas showed in one case a significant number (4%) of cells with a split hybridization signal, indicative of disruption of the NPM gene. Additional recurrent breakpoints observed in extranodal ALCL were 1p36, 6p25, and 8q24. Loss of genetic material occurred at 6q in one extranodal ALCL. Our results suggest that the t(2;5) more frequently plays a pathogenetic role in primary nodal than in extranodal ALCL and that this translocation may not be the primary event in some CD30+ ALCL. Genes Chromosomes Cancer 22:114–121, 1998. © 1998 Wiley‐Liss, Inc.