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Intratumoural heterogeneity of 1p deletions andMYCN amplification in neuroblastomas

2001; Alan R. Liss, Inc.; Volume: 36; Issue: 1 Linguagem: Inglês

10.1002/1096-911x(20010101)36

1096-911X

Peter F. Ambros, I.M. Ambros, Reinhold Kerbl, A. Luegmayr, S. Rumpler, Ruth Ladenstein, Gabriele Amann, Heinrich Kovar, Ernst Horcher, Bruno De Bernardi, Jean Michon, Helmut Gadner,

Ion channel regulation and function

At least three genetic hallmarks identify aggressive tumour behaviour in neuroblastomas; amplification of the oncogene MYCN; deletion (loss of heterozygosity [LOH]) at the short arm of chromosome 1 (del1p36), seen in approximately 28% of the cases; and di-tetraploidy. The MYCN oncogene is amplified in approximately 23% of all neuroblastomas and becomes important for the stratification of therapy in localised and 4s tumours. Up to now, it has been believed that the genetic constellation of neuroblastic tumours is stable and does not alter during tumour evolution or during tumour progression.Using fluorescence in situ hybridisation techniques (FISH) to investigate different tumour areas on touch preparations and histological sections, we show that genetic heterogeneity can be detected in neuroblastomas, especially in tumours detected by urinary mass screening.The identification of such cell clones is important, because the MYCN amplification and/or the deletion at 1p36 appear to be responsible for aggressive local growth and development of metastases.