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Volumn 13, Issue 1, 2003, Pages 20-27

Neurofibromatosis 1: Closing the GAP between mice and men

Author keywords

[No Author keywords available]

Indexed keywords

NEUROFIBROMIN; RAS PROTEIN; TUMOR SUPPRESSOR PROTEIN;

EID: 0037310530     PISSN: 0959437X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-437X(02)00015-1     Document Type: Review
Times cited : (83)

References (42)
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    • Astrocyte-specific inactivation of the neurofibromatosis 1 gene (NF1) is insufficient for astrocytoma formation
    • This report demonstrates that neurofibromin loss in maturing astrocytes is not sufficient for astrocytoma formation in the mouse. In this study, the authors employ multiple approaches to inactivating neurofibromin in astrocytes and find that Nf1 loss in type-1 astrocytes does not confer a neoplastic phenotype. These findings suggest that NF1-associated glioma formation may require additional cellular or genetic changes
    • Bajenaru M.L., Zhu Y., Hedrick N.M., Donahoe J., Parada L.F., Gutmann D.H. Astrocyte-specific inactivation of the neurofibromatosis 1 gene (NF1) is insufficient for astrocytoma formation. Mol. Cell. Biol. 22:2002;5100-5113 This report demonstrates that neurofibromin loss in maturing astrocytes is not sufficient for astrocytoma formation in the mouse. In this study, the authors employ multiple approaches to inactivating neurofibromin in astrocytes and find that Nf1 loss in type-1 astrocytes does not confer a neoplastic phenotype. These findings suggest that NF1-associated glioma formation may require additional cellular or genetic changes.
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  • 40
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    • Nf1; Trp53 mice develop glioblastoma with evidence of strain-specific effects
    • +/- mice maintained on specific genetic backgrounds develop brain tumors whereas in other strains, brain tumor development is uncommon. These findings suggest that additional 'modifier' genes exist that influence tumorigenesis in the mouse
    • +/- mice maintained on specific genetic backgrounds develop brain tumors whereas in other strains, brain tumor development is uncommon. These findings suggest that additional 'modifier' genes exist that influence tumorigenesis in the mouse.
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    • Epidermal growth factor receptor signaling pathways are associated with tumorigenesis in the Nf1:p53 mouse tumor model
    • This report describes the cooperative effect of EGFR expression and activation in Schwann cell tumor proliferation in mice developing MPNST. The authors find that EGFR overexpression is seen in both mouse and human MPNSTs, suggesting that additional signaling abnormalities conferred by the aberrant expression of EGFR impact on the pathogenesis of one of the malignant tumor types in NF1
    • Li H., Velasco-Miguel V., Vass C.W., Parada L.F., DeClue J.E. Epidermal growth factor receptor signaling pathways are associated with tumorigenesis in the Nf1:p53 mouse tumor model. Cancer Res. 62:2002;4507-4513 This report describes the cooperative effect of EGFR expression and activation in Schwann cell tumor proliferation in mice developing MPNST. The authors find that EGFR overexpression is seen in both mouse and human MPNSTs, suggesting that additional signaling abnormalities conferred by the aberrant expression of EGFR impact on the pathogenesis of one of the malignant tumor types in NF1.
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    • Li, H.1    Velasco-Miguel, V.2    Vass, C.W.3    Parada, L.F.4    DeClue, J.E.5
  • 42
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    • Learning deficits, but normal development and tumor predisposition, in mice lacking exon 23a of Nf1
    • +/- mice, but are not prone to tumors. These findings suggest that neurofibromin-containing exon 23a contributes to learning and memory in mice, but has a limited role in tumor formation
    • +/- mice, but are not prone to tumors. These findings suggest that neurofibromin-containing exon 23a contributes to learning and memory in mice, but has a limited role in tumor formation.
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    • Costa, R.M.1    Yang, T.2    Huynh, D.P.3    Pulst, S.M.4    Viskochil, D.H.5    Silva, A.J.6    Brannan, C.I.7


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.