Recurrent DNA copy number changes in 1q, 4q, 6q, 9p, 13q, 14q and 22q detected by comparative genomic hybridization in malignant mesothelioma

被引:76
作者
Bjorkqvist, AM
Tammilehto, L
Anttila, S
Mattson, K
Knuutila, S
机构
[1] UNIV HELSINKI,HAARTMAN INST,DEPT MED GENET,FIN-00014 HELSINKI,FINLAND
[2] FINNISH INST OCCUPAT HLTH,DEPT EPIDEMIOL & BIOSTAT,FIN-00250 HELSINKI,FINLAND
[3] FINNISH INST OCCUPAT HLTH,DEPT OCCUPAT MED,FIN-00250 HELSINKI,FINLAND
[4] UNIV HELSINKI,CENT HOSP,DEPT INTERNAL MED,DIV PULM MED & CLIN PHYSIOL,FIN-00290 HELSINKI,FINLAND
关键词
mesothelioma; comparative genomic hybridization; gain; loss; DNA sequence;
D O I
10.1038/bjc.1997.91
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Comparative genomic hybridization (CGH) analyses were performed on 27 human pleural mesothelioma tumour specimens, consisting of 18 frozen tumours and nine paraffin-embedded tumours, to screen for gains and losses of DNA sequences. Copy number changes were detected in 15 of the 27 specimens with a range from one to eight per specimen. On average, more losses than gains of genetic material were observed. The loss of DNA sequences occurred most commonly in the short arm of chromosome 9 (p21-pter), in 60% of the abnormal specimens. Other losses among the abnormal specimens were frequently detected in the long arms of chromosomes 4 (q31.1-qter, 20%), 6 (q22-q24, 33%), 13 (33%), 14 (q24-qter, 33%) and 22 (q13, 20%). A gain in DNA sequences was found in the long arm of chromosome 1 (cen-qter) in 33% of the abnormal specimens. Our analysis is the first genome-wide screening for gains and losses of DNA sequences using comparative genomic hybridization in malignant pleural mesothelioma rumours. The recurrent DNA sequence changes detected in this study suggest that the corresponding chromosomal areas most probably contain genes important for the initiation and progression of mesothelioma.
引用
收藏
页码:523 / 527
页数:5
相关论文
共 39 条
[1]   MALIGNANT MESOTHELIOMA - PROGNOSTIC VARIABLES IN A REGISTRY OF 180 PATIENTS, THE DANA-FARBER-CANCER-INSTITUTE AND BRIGHAM-AND-WOMENS-HOSPITAL EXPERIENCE OVER 2 DECADES, 1965-1985 [J].
ANTMAN, K ;
SHEMIN, R ;
RYAN, L ;
KLEGAR, K ;
OSTEEN, R ;
HERMAN, T ;
LEDERMAN, G ;
CORSON, J .
JOURNAL OF CLINICAL ONCOLOGY, 1988, 6 (01) :147-153
[2]  
CAIRNS P, 1993, ONCOGENE, V8, P1083
[3]   MOLECULAR DELETION OF 9P SEQUENCES IN NONSMALL CELL LUNG-CANCER AND MALIGNANT MESOTHELIOMA [J].
CENTER, R ;
LUKEIS, R ;
DIETZSCH, E ;
GILLESPIE, M ;
GARSON, OM .
GENES CHROMOSOMES & CANCER, 1993, 7 (01) :47-53
[4]  
CHENG JQ, 1994, CANCER RES, V54, P5547
[5]  
CHENG JQ, 1993, CANCER RES, V53, P4761
[6]  
DIAZ MO, 1990, NEW ENGL J MED, V322, P77, DOI 10.1056/NEJM199001113220202
[7]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[8]   RECURRING LOSS INVOLVING CHROMOSOME-1, CHROMOSOME-3, AND CHROMOSOME-22 IN MALIGNANT MESOTHELIOMA - POSSIBLE SITES OF TUMOR SUPPRESSOR GENES [J].
FLEJTER, WL ;
LI, FP ;
ANTMAN, KH ;
TESTA, JR .
GENES CHROMOSOMES & CANCER, 1989, 1 (02) :148-154
[9]   HOMOZYGOUS DELETIONS WITHIN HUMAN-CHROMOSOME BAND-9P21 IN MELANOMA [J].
FOUNTAIN, JW ;
KARAYIORGOU, M ;
ERNSTOFF, MS ;
KIRKWOOD, JM ;
VLOCK, DR ;
TITUSERNSTOFF, L ;
BOUCHARD, B ;
VIJAYASARADHI, S ;
HOUGHTON, AN ;
LAHTI, J ;
KIDD, VJ ;
HOUSMAN, DE ;
DRACOPOLI, NC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) :10557-10561
[10]  
GERWIN BI, 1987, CANCER RES, V47, P6180