Conclusion
It would seem that distinct genetic changes in different genes, the protein products of which interact in particular growth control mechanism may lead to the same cellular abnormality. This is exemplified in the case of the gliomas by the ways in which p53 and the Rb1 phosphorylation mechanisms may be rendered impotent. It seems likely that many further genetic abnormalities affecting genes coding for proteins, either involved in the cellular mechanisms identified or in new growth control mechanisms, will be found in the future. In total our results indicate both differences and similarities between the molecular genetic alterations in tumors with oligodendroglial and astrocytic differentiation. The loss of genetic information from 19q and 1p as well as the rareness ofTP53 mutations in oligodendroglial tumors suggests that the early events in their oncogenesis are distinct from those associated with astrocytic tumors. However, similarities are indicated by the allelic losses on 9p and 10 in the anaplastic tumors, suggesting the utilization of common pathways of progression.
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References
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Collins, V.P. Genetic alterations in gliomas. J Neuro-Oncol 24, 37–38 (1995). https://doi.org/10.1007/BF01052656
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DOI: https://doi.org/10.1007/BF01052656