Understanding the Role of Wnt Signaling in Schwann Cell Tumors

Loading...
Thumbnail Image

View/Download File

Persistent link to this item

Statistics
View Statistics

Journal Title

Journal ISSN

Volume Title

Title

Understanding the Role of Wnt Signaling in Schwann Cell Tumors

Published Date

2012-04-18

Publisher

Type

Presentation

Abstract

Malignant Peripheral Nerve Sheath Tumors (MPNSTs) originate in the Schwann cell and often occur in patients with Neurofibromatosis Type 1 (NF1), but can also form spontaneously (3). NF1 is a genetic disease that occurs in 1 in 3,000 live births, and predisposes patients to benign neurofibromas. 10% of NF1 patients will have one of their benign neurofibromas undergo malignant transformation into an MPNST, the leading cause of death in NF1 patients (3). The average survival rate with patients with MPNSTs is 21 months and due to the lack of complete understanding of the genetic basis for MPNST development, the common treatments for these MPNSTs are surgery and non-specific chemotherapy (3). A current goal in the field is to understand which signaling pathways drive MPNST development and progression, with the hopes of discovering novel targeted therapies to improve the treatment these patients.

Description

Faculty Advisor: David Largaespada

Related to

Replaces

License

Series/Report Number

Funding information

This research was supported by the Undergraduate Research Opportunities Program (UROP).

Isbn identifier

Doi identifier

Previously Published Citation

Suggested citation

Halfond, Amanda. (2012). Understanding the Role of Wnt Signaling in Schwann Cell Tumors. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/141258.

Content distributed via the University Digital Conservancy may be subject to additional license and use restrictions applied by the depositor. By using these files, users agree to the Terms of Use. Materials in the UDC may contain content that is disturbing and/or harmful. For more information, please see our statement on harmful content in digital repositories.