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
Jung, Seung-Hyun; Kim, Min Sung; Lee, Sung-Hak et al. (2016) Whole-exome sequencing identifies recurrent AKT1 mutations in sclerosing hemangioma of lung. Proc Natl Acad Sci U S A 113:10672-7
Qin, Wenning; Kutny, Peter M; Maser, Richard S et al. (2016) Generating Mouse Models Using CRISPR-Cas9-Mediated Genome Editing. Curr Protoc Mouse Biol 6:39-66
Tai, Derek J C; Ragavendran, Ashok; Manavalan, Poornima et al. (2016) Engineering microdeletions and microduplications by targeting segmental duplications with CRISPR. Nat Neurosci 19:517-22
Sundberg, John P; Pratt, C Herbert; Silva, Kathleen A et al. (2016) Dermal lymphatic dilation in a mouse model of alopecia areata. Exp Mol Pathol 100:332-6
Parvanov, Emil D; Tian, Hui; Billings, Timothy et al. (2016) PRDM9 interactions with other proteins provide a link between recombination hotspots and the chromosomal axis in meiosis. Mol Biol Cell :
Ali, Riyasat; Babad, Jeffrey; Follenzi, Antonia et al. (2016) Genetically modified human CD4(+) T cells can be evaluated in vivo without lethal graft-versus-host disease. Immunology 148:339-51
Ishimura, Ryuta; Nagy, Gabor; Dotu, Ivan et al. (2016) Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation. Elife 5:
Jangalwe, Sonal; Shultz, Leonard D; Mathew, Anuja et al. (2016) Improved B cell development in humanized NOD-scid IL2Rγ(null) mice transgenically expressing human stem cell factor, granulocyte-macrophage colony-stimulating factor and interleukin-3. Immun Inflamm Dis 4:427-440
Korstanje, Ron; Deutsch, Konstantin; Bolanos-Palmieri, Patricia et al. (2016) Loss of Kynurenine 3-Mono-oxygenase Causes Proteinuria. J Am Soc Nephrol 27:3271-3277
Samanta, S; Sun, H; Goel, H L et al. (2016) IMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG. Oncogene 35:1111-21

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