Combined Dusp4 and p53 loss with Dbf4 amplification drives tumorigenesis via cell cycle restriction and replication stress escape in breast cancer
Abstract
Deregulated signaling pathways are a hallmark feature of oncogenesis and driver of tumor progression. Dual specificity protein phosphatase 4 (DUSP4) is a critical negative regulator of the mitogen-activated protein kinase (MAPK) pathway and is often deleted or epigenetically silenced in tumors. DUSP4 alterations lead to hyperactivation of MAPK signaling in many cancers, including breast cancer, which often harbor mutations in cell cycle checkpoint genes, particularly in TP53.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jul 18, 2022
- Source ID
- 10.1186/s13058-022-01542-y
Entities
People
- Abigail L. Toren
- Ann Hanna
- Carlos L Arteaga
- Frank M. Mason
- Joshua Bauer
- Justin M. Balko
- M. Valeria Estrada
- Melinda E. Sanders
- Mellissa J. Nixon
- Phillip Owens
- Quanhu Sheng
- Rebecca S. Cook
- Susan R. Opalenik
- Violeta Sanchez
Organizations
- National Cancer Institute
- Susan G. Komen for the Cure
- United States Department of Defense
- Vanderbilt-Ingram Cancer Center