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Mol Path 55:389-393 doi:10.1136/mp.55.6.389
  • Short report

Evaluation of paediatric osteosarcomas by classic cytogenetic and CGH analyses

  1. J R Batanian1,
  2. L R Cavalli2,
  3. N M Aldosari2,
  4. E Ma1,
  5. C Sotelo-Avila1,
  6. M B Ramos3,
  7. J D Rone2,
  8. C M Thorpe3,
  9. B R Haddad2
  1. 1Departments of Pediatrics and Pathology, St Louis University School of Medicine, Pediatric Research Institute, Cytogenetics Laboratory, Cardinal Glennon Children’s Hospital, St Louis, Missouri MO 63104, USA
  2. 2Institute for Molecular and Human Genetics, Lombardi Cancer Center and Departments of Oncology and Obstetrics and Gynecology, Georgetown University Medical Center, Main 4000, Washington, DC, 20007, USA
  3. 3Department of Pathology, St Louis University School of Medicine, St Louis, Missouri, USA
  1. Correspondence to:
 Dr B R Haddad, Institute for Molecular and Human Genetics, Georgetown University Medical Center, 3800 Reservoir Road NW, Main 4000, Washington, DC, 20007, USA; haddadb1{at}georgetown.edu
  • Accepted 30 August 2002

Abstract

Classic cytogenetic and comparative genomic hybridisation (CGH) data on osteosarcomas have been reported extensively in the literature. However, the number of paediatric osteosarcoma cases studied below the age of 14 years remains relatively small. This study reports four new cases of paediatric osteosarcoma in patients aged 3 to 13 years, evaluated by classic cytogenetics and CGH analyses. Clonal chromosomal alterations were detected in all the cases and included structural rearrangements at 1p11–13, 1q11, 4q27–33, 6p23–25, 6q16–25, 7p13–22, 7q11–36, 11p10–15, 11q23, 17p11.2–13, 21p11, and 21q11–22. The CGH analysis revealed recurrent gains at 1p, 4q, 17p, and 21q and losses at 3q and 16p. Five amplification sites were observed at 1q11–23, 6p21, 8q13, 8q21.3–24.2, and 17p. The data are discussed and compared with other cytogenetic reports in the literature.

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