Numerical aberrations of chromosome 7 detected in 15 mu m paraffin embedded tissue sections of primary cutaneous melanomas by fluorescence in situ hybridization and confocal laser scanning microscopy

被引:11
作者
DAlessandro, I
Zitzelsberger, H
Hutzler, P
Lehmann, L
Braselmann, H
Chimenti, S
Hofler, H
机构
[1] GSF,NATL RES CTR ENVIRONM & HLTH,INST RADIOBIOL,D-85758 OBERSCHLEISSHEIM,GERMANY
[2] GSF,NATL RES CTR ENVIRONM & HLTH,INST PATHOL,D-85758 OBERSCHLEISSHEIM,GERMANY
[3] UNIV AQUILA,DEPT DERMATOL,I-67100 LAQUILA,ITALY
[4] UNIV MUNICH,INST RADIOBIOL,MUNICH,GERMANY
[5] TECH UNIV MUNICH,INST PATHOL,D-8000 MUNICH,GERMANY
关键词
D O I
10.1111/j.1600-0560.1997.tb01099.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Fluorescence in situ hybridization (FISH) to sections of formalin-fixed paraffin-embedded archival tissues allows the detection of gene or chromosome copy number changes in interphase cell nuclei within the histological context and thus may be of particular interest in tumor pathology. In this report, we describe the application of FISH to thick (15 mu m) paraffin sections of 7 primary cutaneous malignant melanomas. A chromosome 7-specific centromeric DNA probe was used to detect numerical aberrations of chromosome 7. By optical sectioning using confocal laser scanning microscopy (CLSM) only complete, uncut interphase cell nuclei were scored. The mean percentage (+/-SEM) of melanoma cell nuclei with three hybridization spots was (20.7+/-2.8)%; (6.8+/-1.0)% of nuclei showed one spot and (5.0+/-1.2)% four or more spots. The frequency distribution of spot numbers among melanoma cell nuclei and normal keratinocyte nuclei was significantly different (chi(2) = 176.8, df = 5, p<0.001). Trisomy 7 was detected in all 7 cases analyzed, mostly associated with monosomy 7 or polysomy 7. The approach used in our study and the data obtained could be useful for further studies designed to investigate a possible involvement of chromosome 7 in melanocytic tumor progression. (C) Munksgaard 1997.
引用
收藏
页码:70 / 75
页数:6
相关论文
共 18 条
[1]  
ALCARAZ A, 1994, CANCER RES, V54, P3998
[2]   CYTOGENETIC ANALYSIS OF MELANOCYTES FROM PREMALIGNANT NEVI AND MELANOMAS [J].
COWAN, JM ;
HALABAN, R ;
FRANCKE, U .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1988, 80 (14) :1159-1164
[3]   DNA IN-SITU HYBRIDIZATION AS A DIAGNOSTIC-TOOL IN THE DISCRIMINATION OF MELANOMA AND SPITZ NEVUS [J].
DEWIT, PE ;
KERSTENS, HMJ ;
PODDIGHE, PJ ;
VANMUIJEN, GNP ;
RUITER, DJ .
JOURNAL OF PATHOLOGY, 1994, 173 (03) :227-233
[4]   INSITU DETECTION OF SUPERNUMERARY ABERRATIONS OF CHROMOSOME-SPECIFIC REPETITIVE DNA TARGETS IN INTERPHASE NUCLEI IN HUMAN-MELANOMA CELL-LINES AND TISSUE-SECTIONS [J].
DEWIT, PEJ ;
HOPMAN, AHN ;
VANMUIJEN, GNP ;
SMEETS, DFCM ;
BECK, JLM ;
MOESKER, O ;
RUITER, DJ .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1992, 98 (04) :450-458
[5]  
DOLONWARD J, 1984, NATURE, V307, P521
[6]   CONFOCAL LASER-SCANNING MICROSCOPY - A NEW OPTICAL MICROSCOPIC TECHNIQUE FOR APPLICATIONS IN PATHOLOGY AND DERMATOLOGY [J].
FINKPUCHES, R ;
HOFMANNWELLENHOF, R ;
SMOLLE, J ;
KERL, H .
JOURNAL OF CUTANEOUS PATHOLOGY, 1995, 22 (03) :252-259
[7]  
GRAY JW, 1992, CANCER, V69, P1536, DOI 10.1002/1097-0142(19920315)69:6+<1536::AID-CNCR2820691306>3.0.CO
[8]  
2-J
[9]   MAPPING OF THE HUMAN-GENE FOR EPIDERMAL GROWTH-FACTOR RECEPTOR (EGFR) ON THE P13-]Q22 REGION OF CHROMOSOME-7 [J].
KONDO, I ;
SHIMIZU, N .
CYTOGENETICS AND CELL GENETICS, 1983, 35 (01) :9-14
[10]   EXPRESSION OF THE RECEPTOR FOR EPIDERMAL GROWTH-FACTOR CORRELATES WITH INCREASED DOSAGE OF CHROMOSOME-7 IN MALIGNANT-MELANOMA [J].
KOPROWSKI, H ;
HERLYN, M ;
BALABAN, G ;
PARMITER, A ;
ROSS, A ;
NOWELL, P .
SOMATIC CELL AND MOLECULAR GENETICS, 1985, 11 (03) :297-302