TY - JOUR
T1 - Genetic alterations in primary cutaneous CD30+anaplastic large cell lymphoma
AU - Mao, X
AU - Orchard, G
AU - Lillington, D M
AU - Russell-Jones, K
AU - Young, B D
AU - Whittaker, S
PY - 2003/6/1
Y1 - 2003/6/1
N2 - Primary cutaneous CD30+ ahaplastic large tell lymphoma (C-ALCL) represents a distinct clinical subtype of CD30+ anaplastic large cell lymphomas. The etiology and underlying molecular pathogenesis of C-ALCL remain unclear. This study aimed to investigate genetic changes in C-ALCL. Comparative genomic hybridization (CGH) analysis of 23 DNA samples from 15 C-ALCL cases identified chromosome imbalances, (CI) in 10 samples I from eight cases (43%). The mean number of CI per sample Was 2.09 +/- 3.86, with gains (2.00 +/- 3.85) more common than losses (0.09 +/- 0.29). The most frequent C! were gains of 1/1p and 5 (50%), and 6, 7, 8/8p, and 19 (38%). Microarray-based CGH analysis of six DNA. samples from five cases. with CI revealed genomic imbalances (GI) in all of the cases studied. This included oncogene copy number gains of FGFR1 (8p11) in three cases, and NRAS (1p13.2), MYCN (2p24.1); RAF1 (3p25), CTSB (8p22), FES (15q26.1) and CBFA2 (21q22.3) in two cases. Real-time PCR analysis of nine DNA samples from eight cases With Cl and GI detected amplifications of CTSB and RAF1 in seven cases (88%), REL (2p13p12) and JUNB (19p13.2) in six cases (75%), and MYCN and YES I, (18p11.3) in four cases (50%), Immunohistochemical staining of paraffin sections from six cases demonstrated expression of JUNB protein in five cases and BCL2 in three cases. These results reveal a consistent pattern of genetic alterations in C-ALCL and. provide the molecular basis for further investigation of this disease. (C) 2003 Wiley-Liss, Inc.
AB - Primary cutaneous CD30+ ahaplastic large tell lymphoma (C-ALCL) represents a distinct clinical subtype of CD30+ anaplastic large cell lymphomas. The etiology and underlying molecular pathogenesis of C-ALCL remain unclear. This study aimed to investigate genetic changes in C-ALCL. Comparative genomic hybridization (CGH) analysis of 23 DNA samples from 15 C-ALCL cases identified chromosome imbalances, (CI) in 10 samples I from eight cases (43%). The mean number of CI per sample Was 2.09 +/- 3.86, with gains (2.00 +/- 3.85) more common than losses (0.09 +/- 0.29). The most frequent C! were gains of 1/1p and 5 (50%), and 6, 7, 8/8p, and 19 (38%). Microarray-based CGH analysis of six DNA. samples from five cases. with CI revealed genomic imbalances (GI) in all of the cases studied. This included oncogene copy number gains of FGFR1 (8p11) in three cases, and NRAS (1p13.2), MYCN (2p24.1); RAF1 (3p25), CTSB (8p22), FES (15q26.1) and CBFA2 (21q22.3) in two cases. Real-time PCR analysis of nine DNA samples from eight cases With Cl and GI detected amplifications of CTSB and RAF1 in seven cases (88%), REL (2p13p12) and JUNB (19p13.2) in six cases (75%), and MYCN and YES I, (18p11.3) in four cases (50%), Immunohistochemical staining of paraffin sections from six cases demonstrated expression of JUNB protein in five cases and BCL2 in three cases. These results reveal a consistent pattern of genetic alterations in C-ALCL and. provide the molecular basis for further investigation of this disease. (C) 2003 Wiley-Liss, Inc.
UR - http://www.scopus.com/inward/record.url?scp=0038070423&partnerID=8YFLogxK
U2 - 10.1002/gcc.10184
DO - 10.1002/gcc.10184
M3 - Article
VL - 37
SP - 176
EP - 185
JO - Genes Chromosomes and Cancer
JF - Genes Chromosomes and Cancer
IS - 2
ER -
