Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/2960
Title: Centrosome amplification as a possible mechanism for numerical chromosome aberrations in cerebral primitive neuroectodermal tumors with TP53 mutations
Authors: Weber, RG
Bridger, JM
Benner, A
Weisenberger, D
Ehemann, V
Reifenberger, G
Lichter, P
Issue Date: 1998
Publisher: Karger
Citation: Cytogenet Cell Genet. 83: 266-269
Abstract: Although alterations in chromosome number have frequently been detected in human tumor cells and associated with tumor initiation and progression, the causal mechanisms are still not understood. One protein known to be involved in maintaining genetic stability is tumor suppressor p53. In mice, p53 has been implicated in the maintenance of diploidy (Cross et al., 1995) and the regulation of centrosome duplication (Fukasawa et al., 1996). Here we report on cerebral primitive neuroectodermal tumors that lacked the wild-type p53 gene (TP53) and showed multiple numerical chromosome aberrations, as detected by comparative genomic hybridization. In these tumors, the centrosome number was significantly higher than in a control tumor without a detected TP53 mutation and with few chromosomal imbalances. These findings indicate that abnormal centrosome amplification can occur in human tumors lacking wild-type TP53 and may be a mechanism by which numerical chromosome aberrations are generated.
URI: http://bura.brunel.ac.uk/handle/2438/2960
DOI: http://dx.doi.org/10.1159/000015168
Appears in Collections:Community Health and Public Health
Dept of Clinical Sciences Research Papers

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