Reduce the In Vivo Portion of Your Study by 75% vs. a Traditional Two Year Study
Faster Testing Means:
- Lower costs
- Quicker answers on your compounds
- Less compound administration
- Significantly lower risk of spontaneous tumors, reducing the incidence of false-positives
The gold standard carcinogenicity in vivo test
- Approved by the FDA and the International Conference on Harmonisation (ICH) S1B Guideline 1
- A substantial amount of phenotypic background data is available for rasH2 demonstrating low incidences of spontaneous tumors and the robustness of the model in identifying carcinogens
- rasH2 mice are sold with full research use rights and are readily available in typical study quantities
- Carries the human homolog of the Harvey rat sarcoma virus oncogene (c-Ha-ras, now identified as HRAS) with its own promoter region in addition to the endogenous murine Ha-ras oncogene
- Total ras-encoded p21 protein expressed at 2-3 times normal levels, in all tissues, with somatic mutational activation found only in tumor tissue transgenes
- Significantly more rapid onset and higher incidence of more malignant tumors after treatment with genotoxic carcinogens compared to wild type controls
- Very low incidence of spontaneous tumors, with no indication of pre-neoplastic cell stages or tumors at 6 months of age
- Approximately 50% of transgenic rasH2 mice develop spontaneous tumors by 18 months of age, predominantly angiosarcomas and lung adenocarcinomas
- Useful as a rapid, cost-effective, and sensitive carcinogenicity testing model for detection of nongenotoxic and genotoxic carcinogens, as supported by studies conducted by ILSI
- Also useful in the study of oncogene-initiated tumorigenesis and can be used to evaluate tumor treatment compounds
- In Japan, contact CLEA Japan, Inc. for purchase of rasH2 mice
- Please note that the model nomenclature has been updated. The CIEA designation for the rasH2 model, CB6F1/Jic-TgrasH2@Tac was used previously.
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Genetic Background:
BALB/cBy x C57BL/6 F1 Hybrid Background Origin:
The rasH2 mouse was developed in the laboratory of Tatsuji Nomura of the Central Institute for Experimental Animals (CIEA) in Kawaski, Japan. The model was created by microinjecting the human c-Ha-ras gene into C57BL/6 x DBA/2 zygotes. Hybrid transgenes were constructed from two human HRAS (c-Ha-ras) genes isolated from malignant melanoma and bladder carcinoma tumors. The transgene integrated into the murine transgenic genome as 3* copies in tandem array. The resultant mice were backcrossed to C57BL/6J. Taconic received original stock in March 2000 and the line is genetically refreshed at least every five years. Taconic has received original stock for refresh in 2005, 2012, 2016, and 2020. The mice were derived by embryo transfer and are maintained by intercrossing C57BL/6JJic-Tg(HRAS)2Jic hemizygous male mice with BALB/cByJJic female mice, therefore rasH2-Tg and rasH2-Wt are littermates.
Genetics:
Carries Nnt mutation
Color:
Black Agouti Species:
Mouse Initial Publication:
- Saitoh A, Kimura M, Takahashi R, Yokoyama M, Nomura T, Izawa M, Sekiya T, Nishimura S, Katsuki M. (1990) Most tumors in transgenic mice with human c-Ha-ras gene contained somatically activated transgenes. Oncogene, 5(8):1195-1200.
- *Suemizu H, et al. (2004) Exp. Anim. 53 (5) 463-466.
