Affordable Access

Access to the full text

Advancement in research and therapy of NF1 mutant malignant tumors

Authors
  • Tao, Junyan1
  • Sun, Dantong1
  • Dong, Lina1
  • Zhu, Hua1
  • Hou, Helei1
  • 1 the Affiliated Hospital of Qingdao University, No. 59 Haier Road, Qingdao, Shandong, 266000, China , Qingdao (China)
Type
Published Article
Journal
Cancer Cell International
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Oct 09, 2020
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12935-020-01570-8
Source
Springer Nature
Keywords
License
Green

Abstract

The NF1 gene encodes neurofibromin, which is one of the primary negative regulatory factors of the Ras protein. Neurofibromin stimulates the GTPase activity of Ras to convert it from an active GTP-bound form to its inactive GDP-bound form through its GTPase activating protein-related domain (GRD). Therefore, neurofibromin serves as a shutdown signal for all vertebrate RAS GTPases. NF1 mutations cause a resultant decrease in neurofibromin expression, which has been detected in many human malignancies, including NSCLC, breast cancer and so on. NF1 mutations are associated with the underlying mechanisms of treatment resistance discovered in multiple malignancies. This paper reviews the possible mechanisms of NF1 mutation-induced therapeutic resistance to chemotherapy, endocrine therapy and targeted therapy in malignancies. Then, we further discuss advancements in targeted therapy for NF1-mutated malignant tumors. In addition, therapies targeting the downstream molecules of NF1 might be potential novel strategies for the treatment of advanced malignancies.

Report this publication

Statistics

Seen <100 times