Journal
CANCER CELL
Volume 7, Issue 1, Pages 65-75Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2004.10.016
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Funding
- NCI NIH HHS [T32 CA059268] Funding Source: Medline
- NINDS NIH HHS [R01 NS028840-09, NS28840, R01 NS028840] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [T32CA059268] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS028840] Funding Source: NIH RePORTER
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Benign neurofibromas and malignant peripheral nerve sheath tumors are serious complications of neurofibromatosis type 1. The epidermal growth factor receptor is not expressed by normal Schwann cells, yet is overexpressed in subpopulations of Nf1 mutant Schwann cells. We evaluated the role of EGFR in Schwann cell tumorigenesis. Expression of EGFR in transgenic mouse Schwann cells elicited features of neurofibromas: Schwann cell hyperplasia, excess collagen, mast cell accumulation, and progressive dissociation of non-myelin-forming Schwann cells from axons. Mating EGFR transgenic mice to Nf1 hemizygotes did not enhance this phenotype. Genetic reduction of EGFR in Nf1(+/-);p53(+/-) mice that develop sarcomas significantly improved survival. Thus, gain- and loss-of-function experiments support the relevance of EGFR to peripheral nerve tumor formation.
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