This study explores the oncogenic effects of the human RRAS2 Q72L mutation. Using a Rosa26 Knockin mouse with FLEx-controlled expression of the human RRAS2^Q72L gene, activated by tamoxifen-inducible Cre-ERT2, researchers observed the development of multiple tumor types. Tumors were dependent on mTORC1 signaling, but independent of PI3K and MEK, identifying selective vulnerabilities in RRAS2-driven cancers.
Human RRAS2 Q72L mutation is a strong oncogenic driver that induces a spectrum of tumors and signals predominantly through mTORC1, offering specific therapeutic targets.
Human RRAS2^Q72L Knockin mouse model using FLEx technology inserted at the Rosa26 locus; tamoxifen-inducible expression via Cre-ERT2 system.
Oncology, Tumorigenesis, mTORC1 pathway, RAS signaling, T-cell leukemia
Knockin, Human gene, Rosa26 locus, FLEx switch, Tamoxifen-inducible Cre-ERT2
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
