Trisomies 8 and 20 characterize a subgroup of benign fibrous lesions arising in both soft tissue and bone

被引:66
作者
Bridge, JA
Swarts, SJ
Buresh, C
Nelson, M
Degenhardt, JM
Spanier, S
Maale, G
Meloni, A
Lynch, JC
Neff, JR
机构
[1] Univ Nebraska, Med Ctr, Dept Pathol, Omaha, NE 68198 USA
[2] Univ Nebraska, Med Ctr, Dept Microbiol, Omaha, NE 68198 USA
[3] Univ Nebraska, Med Ctr, Dept Orthopaed Surg, Omaha, NE 68198 USA
[4] Univ Nebraska, Med Ctr, Dept Pediat, Omaha, NE 68198 USA
[5] Univ Nebraska, Med Ctr, Dept Prevent & Soc Med, Omaha, NE 68198 USA
[6] Univ Florida, Dept Orthopaed Surg, Gainesville, FL USA
[7] Texas SW Hosp, Dept Orthopaed Surg, Dallas, TX USA
[8] Univ Utah, Dept Mol Cytogenet, Salt Lake City, UT USA
关键词
D O I
10.1016/S0002-9440(10)65319-9
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Trisomy 8 and trisomy 20 are nonrandom aberrations in desmoid tumors, The presence of these trisomies in related benign fibrous lesions of bone has not been previously addressed. In this study, 22 specimens from 19 patients diagnosed with desmoid tumor, desmoplastic fibroma, periosteal desmoid tumor, osteofibrous dysplasia, or fibrous dysplasia were examined by cytogenetic analysis of short-term cultures and bi-color fluorescence in situ hybridization of cytological touch preparations or paraffin-embedded tissue with centromeric probes for chromosomes 8 and 20. Trisomy 8 and trisomy 20 were detected by molecular cytogenetic methodologies In 15 specimens, Including 10 primary bone lesions. Traditional cytogenetic analysis revealed trisomy 8 in two cases of osteofibrous dysplasia. Our findings demonstrate that trisomy 8 and trisomy 20 are also nonrandom aberrations in histologically similar, but clinically distinct, benign fibrous lesions of bone.
引用
收藏
页码:729 / 733
页数:5
相关论文
共 27 条
[1]   LOCALIZATION OF THE GENE FOR FAMILIAL ADENOMATOUS POLYPOSIS ON CHROMOSOME-5 [J].
BODMER, WF ;
BAILEY, CJ ;
BODMER, J ;
BUSSEY, HJR ;
ELLIS, A ;
GORMAN, P ;
LUCIBELLO, FC ;
MURDAY, VA ;
RIDER, SH ;
SCAMBLER, P ;
SHEER, D ;
SOLOMON, E ;
SPURR, NK .
NATURE, 1987, 328 (6131) :614-616
[2]  
Breiner JA, 1999, CANCER GENET CYTOGEN, V108, P176
[3]   Deletion 5q in desmoid tumor and fluorescence in situ hybridization for chromosome 8 and/or 20 copy number [J].
Bridge, JA ;
Meloni, AM ;
Neff, JR ;
Deboer, J ;
Pickering, D ;
Dalence, C ;
Jeffrey, B ;
Sandberg, AA .
CANCER GENETICS AND CYTOGENETICS, 1996, 92 (02) :150-151
[4]  
BRIDGE JA, 1989, CLIN ORTHOP RELAT R, P272
[5]  
BRIDGE JA, 1992, CANCER-AM CANCER SOC, V69, P430, DOI 10.1002/1097-0142(19920115)69:2<430::AID-CNCR2820690226>3.0.CO
[6]  
2-H
[7]   BIOLOGIC AND CLINICAL-SIGNIFICANCE OF CYTOGENETIC AND MOLECULAR CYTOGENETIC ABNORMALITIES IN BENIGN AND MALIGNANT CARTILAGINOUS LESIONS [J].
BRIDGE, JA ;
BHATIA, PS ;
ANDERSON, JR ;
NEFF, JR .
CANCER GENETICS AND CYTOGENETICS, 1993, 69 (02) :79-90
[8]  
BRIDGE JA, 1994, CANCER, V73, P1746, DOI 10.1002/1097-0142(19940315)73:6<1746::AID-CNCR2820730632>3.0.CO
[9]  
2-W
[10]   Trisomy 7 and trisomy 8 in dividing and non-dividing tumor cells in Dupuytren's disease [J].
Dal Cin, P ;
De Smet, L ;
Sciot, R ;
Van Damme, B ;
Van den Berghe, H .
CANCER GENETICS AND CYTOGENETICS, 1999, 108 (02) :137-140