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MDM2 gene amplification correlates with ring chromosomes in soft tissue tumors
Author(s) -
Nilbert Mef,
Mitelman Felix,
Mandahl Nils,
Rydholm Anders,
Willén Helena
Publication year - 1994
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870090406
Subject(s) - gene duplication , mdm2 , ring chromosome , biology , chromosome , sarcoma , liposarcoma , gene , comparative genomic hybridization , microbiology and biotechnology , cancer research , karyotype , pathology , genetics , medicine
The human homolog of the murine double minute type 2 gene ( MDM2 ) has been cloned and mapped to 12q 13‐14. The gene presumably functions as a cellular regulator and mediator of TP53 function. Amplification of the MDM2 gene has recently been observed in soft tissue sarcoma and in osteosarcoma. We studied MDM2 amplification in a series of 94 mesenchymal tumors and found 3‐20‐fold amplification in 20 tumors: in 10 of 49 malignant fibrous histiocytomas (MFH), in 1 of 2 pleomorphic liposarcomas, in 6 of 7 atypical lipomas, and in 3 of 12 typical lipomas. Normal hybridization patterns were detected in all 16 myxoid liposarcomas, in all 3 leiomyosarcomas, and in all 5 leiomyomas studied. The MDM2 amplification correlated with the presence of marker ring chromosomes; of the 10 MFH with MDM2 amplification, 5 had ring chromosomes, compared to 4 of 39 without MDM2 amplification, and all 9 lipomas with MDM2 amplification had ring chromosomes, in 5 of the tumors as the sole karyotypic anomaly. The correlation between ring chromosomes and MDM2 gene amplification indicates that the marker rings of MFH and of atypical lipoma often harbor genetic material derived from chromosome 12. Genes Chrom Cancer 9:26 1‐265 (1994). © 1994 Wiley‐Liss, Inc.