This study examines how overexpression of human HMMR modifies breast cancer risk in BRCA1-deficient contexts. Using a mouse model with human HMMR inserted into Rosa26 under Blg-Cre control, the authors show that HMMR enhances tumorigenesis through mitotic instability, AURKA activation, NF-κB pathway activation, and macrophage recruitment.
Human HMMR overexpression accelerates tumor development in BRCA1-deficient tissue via genomic instability and inflammatory signaling, identifying it as a breast cancer risk modifier.
Rosa26 Knockin of human HMMR gene with loxP-STOP-loxP cassette; Cre-inducible expression driven by Blg-Cre in mammary epithelial cells, combined with Brca1 and Trp53 mutations.
BRCA1-associated breast cancer, Inflammation, Tumor progression, Risk modifier genes
Human gene Knockin, Rosa26 locus, Cre-loxP, Conditional overexpression, Mammary-specific Blg-Cre
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
