Allelic Losses from Chromosome 17 in Human Osteosarcomas

Marianna SZTÁN1, Zsuzsa PÁPAI2, Miklós SZENDRŐI3, Marco VAN DER LOOIJ1, Edit OLÁH1

1Department of Molecular Biology, National Institute of Oncology, Budapest, Hungary
2Department of Internal Medicine, National Institute of Oncology, Budapest, Hungary
3Institute of Orthopedics, Semmelweis Medical University, Budapest, Hungary


Genetic alterations of chromosome 17 have been reported to occur frequently both in human sporadic and familial malignancies. The present study was undertaken to explore the possible involvement of chromosome 17 genes including TP53 and the breast cancer susceptibility BRCA1 tumor suppressor genes in the development of sporadic osteogenic sarcoma. Fifteen patients were screened by polymerase chain reaction (PCR) for loss of heterozygosity (LOH) using four highly polymorphic markers. Loss of heterozygosity at the TP53 locus was detected in 40% (6/15) of informative cases while it was 14% (2/14) at the locus of thyroid hormone receptor alpha (THRA1), 21% (3/14) at the D17S855 locus intragenic to BRCA1 and 27% (4/15) at the D17S579 locus. In 53% of the cases studied at least one locus on chromosome 17 was affected by LOH. In our panel, the overall LOH frequency on 17p and 17q was observed to be 40% (6/15) and 27% (4/15), respectively. Comparison of LOH frequencies with clinical and prognostic features revealed significant correlation only with tumor recurrence. Our results confirm that the role of the TP53 tumor suppressor gene is important in the pathogenesis of sporadic osteosarcoma and suggest that 17q12-21 region abnormalities may be involved in the development and/or progression of this tumor. Pathology & Oncology Research, Vol 3, Nr 2, 115-120, 1997

Key words: chromosome 17; TP53; tumor suppressor gene; loss of heterozygosity; osteosarcoma

Received: Apr 28, 1997; accepted: Jun 4, 1997
Correspondence: Edit OLÁH, Department of Molecular Biology, National Institute of Oncology, Ráth György u. 7-9. Budapest H-1525, Hungary, Fax: +36-1-1562402; E-mail:

Click here to get the full-text version in PDF!