TY - JOUR
T1 - Comparative genomic hybridization analysis of primary cutaneous B-cell lymphomas: Identification of common genomic alterations in disease pathogenesis
AU - Mao, X
AU - Lillington, D
AU - Child, F
AU - Russell-Jones, R
AU - Young, B
AU - Whittaker, S
PY - 2002/10
Y1 - 2002/10
N2 - To investigate genetic alterations in primary cutaneous B-cell lymphomas (PCBCLs), we have analyzed 29 cases of PCBCL. Comparative genomic hybridization showed chromosome imbalances (CIs) in 12 cases (41%). The mean number of CIs per sample was 2.05 +/- 2.97, with gains (1.48 +/- 2.38) more frequent than losses (0.56 +/- 1.40). The common regions of gains were 18/18q (50%), 7/7p (42%), 3/3q (33%), 20 (33%), 1p (25%), 12/12q (25%), and 13/13q (25%), whereas loss of 6q was frequent (42%). Among the different subsets of PCBCLs, CI was seen in 50% of diffuse large-cell lymphomas (DLCLs), 33% of marginal zone lymphomas, and 8% of follicle center cell lymphomas and unclassified lymphomas. A similar pattern of Cl was observed in these lymphomas, but loss of 6q and gains of 3/3q were present only in DLCLs. Microarray-based genomic analysis of four DLCL cases identified oncogene gains of SAS/CDK4 (12q13.3) in three cases and MYCLI (1p34.3), MYC (8q24), FGFR2 (10q26), BCL2 (18q21.3), CSEIL (20q13), and PDGFB (22q12-13) in two cases, whereas losses of AKTI (14q32.3), IGFRI (15q25-26), and JUN8 (19p13.2) were identified in three cases, and losses of FGR (1p36), ESR (6q25.1), ABLI (9q34.1), TOP2A (17q21-22), ERBB2 (17q21.2), CCNEI (19q13.1), and BCR (22q11) were each identified in two cases. In addition, real-time-polymerase chain reaction detected amplification of BCL2 in 5 of 29 cases. These findings suggest that there are complex but consistent genetic alterations associated with the pathogenesis of PCBCLs. (C) 2002 Wiley-Liss, Inc.
AB - To investigate genetic alterations in primary cutaneous B-cell lymphomas (PCBCLs), we have analyzed 29 cases of PCBCL. Comparative genomic hybridization showed chromosome imbalances (CIs) in 12 cases (41%). The mean number of CIs per sample was 2.05 +/- 2.97, with gains (1.48 +/- 2.38) more frequent than losses (0.56 +/- 1.40). The common regions of gains were 18/18q (50%), 7/7p (42%), 3/3q (33%), 20 (33%), 1p (25%), 12/12q (25%), and 13/13q (25%), whereas loss of 6q was frequent (42%). Among the different subsets of PCBCLs, CI was seen in 50% of diffuse large-cell lymphomas (DLCLs), 33% of marginal zone lymphomas, and 8% of follicle center cell lymphomas and unclassified lymphomas. A similar pattern of Cl was observed in these lymphomas, but loss of 6q and gains of 3/3q were present only in DLCLs. Microarray-based genomic analysis of four DLCL cases identified oncogene gains of SAS/CDK4 (12q13.3) in three cases and MYCLI (1p34.3), MYC (8q24), FGFR2 (10q26), BCL2 (18q21.3), CSEIL (20q13), and PDGFB (22q12-13) in two cases, whereas losses of AKTI (14q32.3), IGFRI (15q25-26), and JUN8 (19p13.2) were identified in three cases, and losses of FGR (1p36), ESR (6q25.1), ABLI (9q34.1), TOP2A (17q21-22), ERBB2 (17q21.2), CCNEI (19q13.1), and BCR (22q11) were each identified in two cases. In addition, real-time-polymerase chain reaction detected amplification of BCL2 in 5 of 29 cases. These findings suggest that there are complex but consistent genetic alterations associated with the pathogenesis of PCBCLs. (C) 2002 Wiley-Liss, Inc.
UR - http://www.scopus.com/inward/record.url?scp=0036778619&partnerID=8YFLogxK
U2 - 10.1002/gcc.10104
DO - 10.1002/gcc.10104
M3 - Article
VL - 35
SP - 144
EP - 155
JO - Genes Chromosomes and Cancer
JF - Genes Chromosomes and Cancer
IS - 2
ER -