Biologic and clinical significance of cytogenetic and molecular cytogenetic abnormalities in benign and malignant cartilaginous lesions

Bridge, Julia A.; Bhatia, Paramjit; Anderson, James R.; Neff, James R.

doi:10.1016/0165-4608(93)90080-6

Cited by 102 publications

(54 citation statements)

References 57 publications

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“…Rearrangements of 6p2l, often as t(6;14)(p21;q24), were found in 10 of the 22 tumours reported so far, and various recombinations involving chromosome segment 12ql3-15 were seen in eight hamartomas (Fletcher et al, 1991(Fletcher et al, , 1992Johansson et al, 1992Johansson et al, , 1993Dal Cin et al, 1993). Also osteocartilaginous dxostoses show consistent chromosomal changes; five of six cytogenetically aberrant cases had lost band 8q24, often as the sole anomaly (Bridge et al, 1993;Mertens et al, 1994). Among the remaining 13 tumours-five chondromas (Teyssier, 1987;Teyssier and Ferre, 1989;Mandahl et al, 1990Mandahl et al, , 1993Bridge et al, 1993), four chondroblastomas (Mark et al, 1992;Bridge et al, 1993), two enchondromas (Bridge et al, 1992), and two chondromyxoid fibromas (Bridge et al, 1989;Tarkkanen et al, 1993)-the cytogenetic features are less distinct.…”

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confidence: 99%

“…Also osteocartilaginous dxostoses show consistent chromosomal changes; five of six cytogenetically aberrant cases had lost band 8q24, often as the sole anomaly (Bridge et al, 1993;Mertens et al, 1994). Among the remaining 13 tumours-five chondromas (Teyssier, 1987;Teyssier and Ferre, 1989;Mandahl et al, 1990Mandahl et al, , 1993Bridge et al, 1993), four chondroblastomas (Mark et al, 1992;Bridge et al, 1993), two enchondromas (Bridge et al, 1992), and two chondromyxoid fibromas (Bridge et al, 1989;Tarkkanen et al, 1993)-the cytogenetic features are less distinct. All had a near-diploid chromosome number (44-47 chromosomes) and relatively simple karyotypic changes, with breakpoints in 12ql3-15 (three tumours), trisomy 5, and rearrangements involving band 5ql3 (two tumours each) as the only recurrent features.…”

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Chromosome rearrangements in synovial chondromatous lesions

Mertens

Jonsson²,

Willén³

et al. 1996

Br J Cancer

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Summary Short-term cultures from one synovial chondroma and three cases of synovial chondromatosis, a lesion for which no previous karyotypic information exists, were cytogenetically analysed. Whereas the chondroma displayed the relatively simple karyotype 46,XY,add(12)(ql3),der(17)t(12;17)(ql3;q21), more complex changes were found in the three cases of chondromatosis: case 1, 47,XY,der(l)inv(l)(pl3q25) del (1) (q25q32), t (1; 12) (q25;q13), + 5,der (12) add (12) (pl 1) t (1; 12) (p22;q1 3); case 2, 47, XY,add (10) (q26), + 20/ 46, idem,-6/46,XY,t (2;4) (q33;q21), add (21) (pl1); and case 3, 44,XY,add(l)(p36),del(l)(pl3p22),add(6)(p25), del(7) (q22q32),del(10)(q21),add (11)

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confidence: 99%

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Chromosome rearrangements in synovial chondromatous lesions

Mertens

Jonsson²,

Willén³

et al. 1996

Br J Cancer

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“…As cartilaginous areas are not common despite the name 'EMC', making a diagnosis based solely on histopathological findings is often difficult. At present, the number of reported cytogenetic studies of EMC remains small due to the rarity of the tumor (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). We report an additional case of EMC and review the literature on cytogenetic studies.…”

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confidence: 99%

Extraskeletal myxoid chondrosarcoma of the thigh with a t(9;17) translocation

et al. 2011

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Abstract. Extraskeletal myxoid chondrosarcomas (EMC) are relatively rare. We report a case of EMC of the thigh. A 41-yearold man presented with a tumor history of more than 4 months. Following open biopsy, wide resection of the tumor was performed. Histopathologically, the tumor had a multinodular architecture consisting of myxomatous areas demarcated by fibrous septa. Proliferation of uniform, round tumor cells with oval nuclei was observed. Well-formed hyaline cartilage and rhabdoid-like cells were not visible. Immunohistochemically, the tumor cells were positive for vimentin and S-100. The composite karyotype was 46,XY,t(9;17)(q22;q11),t(9;21) (q21;p13), and the diagnosis of EMC was made. No recurrence of the mass or metastasis was observed during a follow-up period of 4 years and 7 months. Only 50 cytogenetic cases of EMC, including our case, have been reported in the English literature thus far. Clinical presentation, radiological features and histopathological and cytogenetic findings are described, and the relevant literature is reviewed.

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“…19 The number of hybridization signals for each specimen was assessed in 200 interphase nuclei with strong and well delineated signals by two different individuals. To exclude the possibility of triploidy, the biotinylated probe, D7Z1, which binds to the centromeric region of chromosome 7, was used.…”

Section: Fluorescence In Situ Hybridization (Fish)mentioning

confidence: 99%

Trisomies 8 and 20 Characterize a Subgroup of Benign Fibrous Lesions Arising in Both Soft Tissue and Bone

Bridge

Swarts

Buresh

et al. 1999

The American Journal of Pathology

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Desmoid tumor, desmoplastic fibroma, periosteal desmoid tumor, osteofibrous dysplasia and fibrous dysplasia are benign mesenchymal lesions arising in soft tissue or bone. Desmoid tumors, also known as aggressive fibromatosis or fibromatosis of soft tissue, may occur in extraabdominal, abdominal, or intra-abdominal locations. Desmoplastic fibroma and periosteal desmoid tumor, identical histologically, differ only by location. Desmoplastic fibroma and periosteal desmoid tumor are considered to represent the bone counterparts of desmoid tumors of soft tissue. A tumor-like proliferation of fibroosseous tissue is characteristic of osteofibrous dysplasia and fibrous dysplasia. The former is distinguished histologically by osteoblastic rimming of the bone trabeculae. Cytogenetic and molecular cytogenetic analyses of desmoid tumors are few and are particularly sparse or are nonexistent for desmoplastic fibroma, periosteal desmoid tumor, osteofibrous dysplasia, and fibrous dysplasia. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] To determine the frequency of trisomy 8 and trisomy 20 in additional desmoid tumor cases and to examine their presence in related fibrous lesions of bone, both standard karyotypic analysis and molecular cytogenetic analysis were performed on 22 representative specimens. Materials and Methods Cytogenetic AnalysisTwenty-two specimens (to include three desmoplastic fibromas, two periosteal desmoid tumors, nine desmoid tumors, four osteofibrous dysplasias, and four fibrous dysplasias) from 19 different patients were examined by traditional cytogenetic and molecular cytogenetic methodologies. A 0.5-to 1.0-cm 3 sample of each specimen was received for cytogenetic analysis. Standard culture and harvesting procedures were used that have been described previously. 4 Briefly, the tissues were disaggregated mechanically and enzymatically and then cultured in RPMI 1640 medium supplemented with 20% fetal bovine serum and 1% penicillin/streptomycin-L-glutamine (Irvine Scientific, Santa Ana, CA) for 3 to 5 days. Two to four hours before harvest, cells were exposed to Colcemid (0.02 g/ml). After hypotonic treatment (0.074 mol/L KCl for 30 minutes for flasks and 0.8% sodium citrate for 25 minutes for coverslips), the preparations were fixed three times with methanol/glacial acetic acid (3:1). Metaphase cells were banded with Giemsa trypsin. The karyotypes were expressed according to the International System for Human Cytogenetic Nomenclature 1995. 18

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Biologic and clinical significance of cytogenetic and molecular cytogenetic abnormalities in benign and malignant cartilaginous lesions

Cited by 102 publications

References 57 publications

Chromosome rearrangements in synovial chondromatous lesions

Chromosome rearrangements in synovial chondromatous lesions

Extraskeletal myxoid chondrosarcoma of the thigh with a t(9;17) translocation

Trisomies 8 and 20 Characterize a Subgroup of Benign Fibrous Lesions Arising in Both Soft Tissue and Bone

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