This study investigates the cooperative role of Dusp4 loss, p53 deletion, and Dbf4 amplification in promoting breast cancer tumorigenesis. Using a genetically engineered mouse model with mammary-specific deletion of Dusp4, researchers demonstrated that Dusp4 loss alone is insufficient to drive tumorigenesis. However, when combined with Trp53 loss and MYC amplification, there is a significant increase in tumor formation, characterized by replication stress escape and cell cycle deregulation. The study highlights the amplification of Dbf4 as a key event facilitating these oncogenic processes.
The combination of Dusp4 and p53 loss, along with Dbf4 amplification, synergistically drives breast cancer tumorigenesis by enabling cells to overcome replication stress and bypass cell cycle checkpoints.
Conditional Dusp4 floxed mouse model developed by genOway, enabling mammary-specific deletion of Dusp4 to study its role in breast cancer development.
Breast cancer, Tumorigenesis, Cell cycle regulation, Replication stress, DUSP4, p53, Dbf4
Conditional Knockout model, Cre-loxP system, Mammary-specific gene deletion, Gene amplification studies
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
