This study investigates the role of wild-type RRAS2 overexpression in the development of chronic lymphocytic leukemia (CLL). Researchers generated a conditional Knockin mouse model with human RRAS2 inserted into the Rosa26 locus, controlled by a loxP-flanked STOP cassette and an IRES-EGFP reporter. Upon Cre-mediated recombination, RRAS2 is overexpressed in B cells, leading to the development of CLL characterized by CD5+IgM+ B cell expansion, splenomegaly, and reduced survival. The model mirrors human CLL features and is valuable for preclinical testing of therapies.
Overexpression of wild-type RRAS2 in B cells induces CLL-like disease in mice, demonstrating its oncogenic potential without activating mutations and providing a model for therapeutic research.
Conditional Knockin mouse model with human RRAS2 inserted into the Rosa26 locus, featuring a loxP-flanked STOP cassette and an IRES-EGFP reporter; Cre recombinase under the mb1 promoter ensures B cell-specific expression.
Chronic lymphocytic leukemia, B cell malignancy, Oncogene overexpression, Preclinical model
Knockin model, Rosa26 locus, loxP-flanked STOP cassette, IRES-EGFP reporter, B cell-specific Cre expression
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
