2001
DOI: 10.1038/sj.onc.1205024
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Neural precursor cell apoptosis and glial tumorigenesis following transplacental ethyl-nitrosourea exposure

Abstract: Neural precursor cells (NPCs) populate the embryonic ventricular zone and persist in the subependymal zone of the adult brain. We hypothesized that hereditary and/or acquired mutations in apoptosis-associated genes, such as p53 and caspases, may protect NPCs from DNA damage-induced death and predispose them to subsequent neoplastic transformation. To test this hypothesis, we exposed NPCs from wild-type and targeted gene-disrupted mouse embryos (p53, caspase-9, caspase-3, and bax mutants) to ethyl-nitrosourea (… Show more

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Cited by 34 publications
(32 citation statements)
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“…They also resemble the previously described hyperplastic areas observed after intraventricular grafting of astrocytes-like stem cells (Zheng et al, 2002). The increased number of cells in the SVZ of p53 Ϫ/Ϫ mice is not attributable to decreased apoptosis, as predicted by the well known proapoptotic function of p53 (D'Sa-Eipper et al, 2001;Leonard et al, 2001;Katayama et al, 2005). Our results clearly indicate an increase in compensatory apoptosis in p53 Ϫ/Ϫ mice.…”
Section: Discussionsupporting
confidence: 73%
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“…They also resemble the previously described hyperplastic areas observed after intraventricular grafting of astrocytes-like stem cells (Zheng et al, 2002). The increased number of cells in the SVZ of p53 Ϫ/Ϫ mice is not attributable to decreased apoptosis, as predicted by the well known proapoptotic function of p53 (D'Sa-Eipper et al, 2001;Leonard et al, 2001;Katayama et al, 2005). Our results clearly indicate an increase in compensatory apoptosis in p53 Ϫ/Ϫ mice.…”
Section: Discussionsupporting
confidence: 73%
“…The concept that glioblastoma formation involves the synergism between distinct pathways is supported by several other studies demonstrating tumor formation in p53 Ϫ/Ϫ mice after increased PDGF signaling (Hesselager et al, 2003), prenatal exposure to ENU (Oda et al, 1997;Leonard et al, 2001), or Ras activation (Reilly et al, 2000).…”
Section: Discussionsupporting
confidence: 54%
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“…Animals are more vulnerable with prenatal exposure to ENU (when there is more neural precursor activity) and the preneoplastic lesions that occur are identified in the SVZ (Schiffer et al 1978;Pilkington & Lantos 1979). In mice, ENU-induced brain tumorigenesis occurs only in the context of p53 homozygous deletion and, in these animals, preneoplastic/early neoplastic lesions are also identified in the SVZ (Oda et al 1997;Leonard et al 2001;Wilhelmsson et al 2003). p53K/K Mice have increased proliferative activity in the SVZ and more neurospheres can be isolated from this region, suggesting an expansion of the NSC pool, which may make it more susceptible to neoplastic transformation (Gil-Perotin et al 2006;Meletis et al 2006).…”
Section: Cells Of Origin For Brain Cancermentioning
confidence: 99%