TY - JOUR
T1 - Chromosomal aberrations in nasopharyngeal carcinoma analyzed by comparative genomic hybridization
AU - Chen, Yann Jang
AU - Ko, Jenq Yuh
AU - Chen, Pei Jer
AU - Shu, Chih Hung
AU - Hsu, Ming Ta
AU - Tsai, Shih Feng
AU - Lin, Chi Hung
PY - 1999/6
Y1 - 1999/6
N2 - To investigate the genomic imbalances associated with nasopharyngeal carcinoma (NPC), we have performed chromosome analysis by comparative genomic hybridization (CGH) on 51 tumors, including 25 primary and 26 recurrent tumors. The most common copy number increases occurred on chromosome arms 12p (59%), 1q (47%), 17q (47%), 11q (41%), and 12q (35%). The minimal overlapping regions were at 12p12-13, 1q21-22, 17q21, 17q25, 11q13, and 12q13. The most frequent losses were from chromosome arms 3p (53%), 9p (41%), 13q (41%), 14q (35%), and 11q (29%). The minimal overlapping regions were at 3p12-14, 3p25- 26, 9p21-23, 13q21-32, 14q12-21, and 11q14-23. Compared with the primary cancers, no additional chromosomal change was found in the recurrent tumors; however, the most frequent gain in the recurrent NPCs was at 11q13 (53%) instead of 12p in the primary tumors. An increase of gene alterations correlated with clinical stage. Our results provide a first comprehensive view of the genomic changes associated with NPC and reveal several new sites of genomic imbalance, indicating the possible involvement of novel oncogenes/tumor suppressor genes in the carcinogenesis of NPC.
AB - To investigate the genomic imbalances associated with nasopharyngeal carcinoma (NPC), we have performed chromosome analysis by comparative genomic hybridization (CGH) on 51 tumors, including 25 primary and 26 recurrent tumors. The most common copy number increases occurred on chromosome arms 12p (59%), 1q (47%), 17q (47%), 11q (41%), and 12q (35%). The minimal overlapping regions were at 12p12-13, 1q21-22, 17q21, 17q25, 11q13, and 12q13. The most frequent losses were from chromosome arms 3p (53%), 9p (41%), 13q (41%), 14q (35%), and 11q (29%). The minimal overlapping regions were at 3p12-14, 3p25- 26, 9p21-23, 13q21-32, 14q12-21, and 11q14-23. Compared with the primary cancers, no additional chromosomal change was found in the recurrent tumors; however, the most frequent gain in the recurrent NPCs was at 11q13 (53%) instead of 12p in the primary tumors. An increase of gene alterations correlated with clinical stage. Our results provide a first comprehensive view of the genomic changes associated with NPC and reveal several new sites of genomic imbalance, indicating the possible involvement of novel oncogenes/tumor suppressor genes in the carcinogenesis of NPC.
UR - http://www.scopus.com/inward/record.url?scp=84984538774&partnerID=8YFLogxK
U2 - 10.1002/(SICI)1098-2264(199906)25:2<169::AID-GCC13>3.0.CO;2-I
DO - 10.1002/(SICI)1098-2264(199906)25:2<169::AID-GCC13>3.0.CO;2-I
M3 - Article
C2 - 10338001
AN - SCOPUS:84984538774
SN - 1045-2257
VL - 25
SP - 169
EP - 175
JO - Genes Chromosomes and Cancer
JF - Genes Chromosomes and Cancer
IS - 2
ER -