Abstract
The aim of this study was to investigate genetic changes occurring in Ewing Tumors (ETs) and Neuroblastomas (NBs). We analyzed whether the same genetic alteration, i.e. the deletion of genetic material at chromosomal region 1p36, occurs in both tumor types at a comparable rate and whether these aberrations are acquired during tumor progression. Consecutive tumor samples from the same patients at different stages of the disease and topographically different samples from single tumors were studied. Furthermore, we focused on the detection of the status of the MYCN oncogene in NBs. Deletions at 1p36 are found in ETs and NBs at a comparable frequency (approx. 20%) and account for an unfavorable prognosis in localized disease.1,2,3 In ETs, the loss of 1p36 material was frequently observable in a sub-population of cells and is therefore regarded as a later event in the tumor development. In NBs, it seemed more likely that the aberrations found in a subgroup of tumors (i.e. dellp, MYCN amplification, and gain of 17q) are very early on initial events as virtually all tumor cells within an individual tumor were thought to bear the respective genetic aberra- tion. This view is supported by the results obtained so far.4 However, recent data indicate that deletions at 1p36 and also MYCN amplifications can be acquired during tumor progression (Ambros et al. in press), because sub-populations of cells showing these aberrations interspersed between cells not showing these aberrations exist in evolutionary early tumors.
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Ambros, P.F. et al. (1999). Genetic Heterogeneity in Ewing Tumors and Neuroblastomas. In: Abraham, N.G., Tabilio, A., Martelli, M., Asano, S., Donfrancesco, A. (eds) Molecular Biology of Hematopoiesis 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4797-6_17
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DOI: https://doi.org/10.1007/978-1-4615-4797-6_17
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