The Role of Cumulative Genetic Defects in NF1 Tumorigenesis
Abstract
This project studied the genetic basis of tumor pathogenesis in neurofibromatosis 1 (NF1). This work tested the two-hit hypothesis in NF1 tumors (neurofibromas and MPNSTs), and involvement of other loci such as TP53. Human tumor samples were collected, with development of cell cultures from some. Discoveries: the two-hit mechanism operates in at least a large proportion of neurofibromas (which may include methylation as a mechanism); there is a genetically abnormal clonal Schwann cell component in these tumors; somatic isodisomy may be present in loss of heterozygosity cases; the TP53 gene (and RB1 and P73) is implicated only in MPNSTs; and the ErbB2 gene may be a modifier of NF1.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2002
- Accession Number
- ADA412154
Entities
People
- Margaret R. Wallace
Organizations
- University of Florida