Major Strengths Of The JAXCC The major focus of the JAXCC is to understand the complex genomics of cancer that leads to primary resistance to therapy, that enables cancer cell adaptation and evolution, and that pushes progenitor cell transformation. Our ability to address these topics comes from our capabilities in developing technologies and analytics for interrogating the cancer cell genome combined with the exceptional ability ofthe JAXCC to query the function of single genes and large-scale genomic changes using a diverse range of genetically defined mouse strains, reference populations, and unique heterogeneous stocks. Collaboration and programmatic integration are deeply embedded in the scientific culture of The Jackson Laboratory. The limited size of our faculty demands such an operating principle. The JAXCC provides a leadership and administrative structure, and is organized as one research program to further enhance transdisciplinary collaboration and integration within our three-campus structure. Throughout the previous grant cycle, this emphasis on collaboration has been shown in both the number and breadth of joint publications and grants from JAXCC members. Figure 2 depicts the network of interactions among current JAXCC members, based on the number of joint authored publications from the JAXCC as well as funded and pending joint grant submissions in which JAXCC members are co-PIs or named as key personnel. The external collaborative network is also robust, as evidenced by the 58% of publications in the last grant cycle co-authored with external investigators.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA034196-29
Application #
8699307
Study Section
Subcommittee G - Education (NCI)
Project Start
1997-08-01
Project End
2019-06-30
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
29
Fiscal Year
2014
Total Cost
$175,068
Indirect Cost
$75,029
Name
Jackson Laboratory
Department
Type
DUNS #
042140483
City
Bar Harbor
State
ME
Country
United States
Zip Code
04609
Song, Delu; Grieco, Steve; Li, Yafeng et al. (2014) A murine RP1 missense mutation causes protein mislocalization and slowly progressive photoreceptor degeneration. Am J Pathol 184:2721-9
Chow, Kin-Hoe; Shin, Dong-Mi; Jenkins, Molly H et al. (2014) Epigenetic states of cells of origin and tumor evolution drive tumor-initiating cell phenotype and tumor heterogeneity. Cancer Res 74:4864-74
King Jr, Lloyd E; Silva, Kathleen A; Kennedy, Victoria E et al. (2014) Lack of response to laser comb in spontaneous and graft-induced alopecia areata in C3H/HeJ mice. J Invest Dermatol 134:264-6
Low, Benjamin E; Krebs, Mark P; Joung, J Keith et al. (2014) Correction of the Crb1rd8 allele and retinal phenotype in C57BL/6N mice via TALEN-mediated homology-directed repair. Invest Ophthalmol Vis Sci 55:387-95
Potter, Christopher S; Wang, Zhe; Silva, Kathleen A et al. (2014) Chronic proliferative dermatitis in Sharpin null mice: development of an autoinflammatory disease in the absence of B and T lymphocytes and IL4/IL13 signaling. PLoS One 9:e85666
Hosur, Vishnu; Johnson, Kenneth R; Burzenski, Lisa M et al. (2014) Rhbdf2 mutations increase its protein stability and drive EGFR hyperactivation through enhanced secretion of amphiregulin. Proc Natl Acad Sci U S A 111:E2200-9
Roderick, Justine E; Tesell, Jessica; Shultz, Leonard D et al. (2014) c-Myc inhibition prevents leukemia initiation in mice and impairs the growth of relapsed and induction failure pediatric T-ALL cells. Blood 123:1040-50
Korstanje, Ron; Caputo, Christina R; Doty, Rosalinda A et al. (2014) A mouse Col4a4 mutation causing Alport glomerulosclerosis with abnormal collagen ?3?4?5(IV) trimers. Kidney Int 85:1461-8
Grubb, Stephen C; Bult, Carol J; Bogue, Molly A (2014) Mouse phenome database. Nucleic Acids Res 42:D825-34
Inaki, Koichiro; Menghi, Francesca; Woo, Xing Yi et al. (2014) Systems consequences of amplicon formation in human breast cancer. Genome Res 24:1559-71

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