During the past decade, genetically modified mice have increasingly been a source of many new cancer models that have helped elucidate pathways contributing to tumor development and progression. With the completion of the human and mouse genome sequences and the initiation of large-scale efforts to functionally annotate these genomes, this trend continues to accelerate. Production of genetically modified mice requires highly specialized instrumentation and expertise not available in most labs. The mission of the Gene Targeting and Transgenic Shared Resource (GTTR) is to ensure that investigators have access to state-of-the-art transgenic mouse technologies, methods and animal models. The Resource Director and Assistant Director provide guidance to investigators from the earliest planning stages of the project when constructs are designed to advanced stages of the project during phenotype analysis. Resource technicians perform the specialized ES cell and embryo manipulation methods to generate the genetically modified mice. During the past fourteen years, the Facility has provided over 700 new genetically modified lines. Shared Resource staff have generated mutant mice on multiple strain backgrounds, generated 200 knockouts and 520 transgenics (including BACs) from 165 constructs for the six CCSG Programs. GTTR has also assisted in the development of unique mouse models that contribute to understanding imprinting and its role in cancer, regulation of important genes and two transgenic models that mimic chromosome rearrangements associated with specific human cancers. Use of the Resource has continued to increase with the ongoing recruitment into the Genetics, Cell Stress and Biophysical Therapies, Genitourinary Cancers and Experimental Therapeutics Programs. Projects requiring the development of transgenic mouse models are becoming increasingly relevant to validate in vitro findings, especially in light of high-throughput clinical-based findings. As such, the GTTR has been seeing an increasing trend in the use of the Resource by clinical researchers as well as basic scientists. First priority for use is given to peer-review-funded CCSG members;second to non-peer-review-funded CCSG members;third to non-members and academic collaborators;and last priority to external users. During the reporting period, the Gene Targeting and Transgenic Shared Resource has served 28 members from 5 research programs, with 15% utilization by CCSG members with peer reviewed funding. The CCSG support provides 11% of the overall proposed budget.
Genetically modified mice are critical to elucidate pathways contributing to tumor development and progression and validate in vitro findings. The Gene Targeting and Transgenic Shared Resource provides access to specialized technologies, services, and expertise that enhance scientific interaction and productivity.
|Wilton, John; Kurenova, Elena; Pitzonka, Laura et al. (2016) Pharmacokinetic analysis of the FAK scaffold inhibitor C4 in dogs. Eur J Drug Metab Pharmacokinet 41:55-67|
|Zhao, Zhiguo; Wen, Wanqing; Michailidou, Kyriaki et al. (2016) Association of genetic susceptibility variants for type 2 diabetes with breast cancer risk in women of European ancestry. Cancer Causes Control 27:679-93|
|Goossens, Maria E; Isa, Fatima; Brinkman, Maree et al. (2016) International pooled study on diet and bladder cancer: the bladder cancer, epidemiology and nutritional determinants (BLEND) study: design and baseline characteristics. Arch Public Health 74:30|
|Clyde, Merlise A; Palmieri Weber, Rachel; Iversen, Edwin S et al. (2016) Risk Prediction for Epithelial Ovarian Cancer in 11 United States-Based Case-Control Studies: Incorporation of Epidemiologic Risk Factors and 17 Confirmed Genetic Loci. Am J Epidemiol 184:579-589|
|Austin, David C; Strand, Douglas W; Love, Harold L et al. (2016) NF-ÎºB and androgen receptor variant 7 induce expression of SRD5A isoforms and confer 5ARI resistance. Prostate 76:1004-18|
|Sexton, Sandra; Tulowitzki, Ryan; Jones, Craig A et al. (2016) Involvement of the renin-angiotensin system in the development of nephrogenic systemic fibrosis-like lesions in the RenTag mouse model. Clin Exp Nephrol 20:162-8|
|Shafirstein, Gal; Battoo, Athar; Harris, Kassem et al. (2016) Photodynamic Therapy of Non-Small Cell Lung Cancer. Narrative Review and Future Directions. Ann Am Thorac Soc 13:265-75|
|Pharoah, Paul D P; Song, Honglin; Dicks, Ed et al. (2016) PPM1D Mosaic Truncating Variants in Ovarian Cancer Cases May Be Treatment-Related Somatic Mutations. J Natl Cancer Inst 108:|
|Bistulfi, Gaia; Affronti, Hayley C; Foster, Barbara A et al. (2016) The essential role of methylthioadenosine phosphorylase in prostate cancer. Oncotarget 7:14380-93|
|Rohrbach, Daniel J; Rigual, Nestor; Arshad, Hassan et al. (2016) Intraoperative optical assessment of photodynamic therapy response of superficial oral squamous cell carcinoma. J Biomed Opt 21:18002|
Showing the most recent 10 out of 1099 publications