Administrative Core. This administrative Core will have both scientific and organizational responsibilities. The scientific aspects will be carried out by Dr. Kwiatkowski. He will advise investigators on strategic and technical issues, promote collaboration and contact among projects, monitor the functions and effectiveness of the core facilities, and assess the scientific quality and progress of the work. This will require active interactions with all groups on a regular basis. Any scientific problems or organizational issues that arise will be discussed first with the co-PI, Dr. Cantley. There will also be an Internal Advisory Board composed of senior scientists in the Boston area, who will meet on an ad hoc basis to assist with any scientific or organizational issues. There will also be an External Advisory Board composed of senior scientists from outside Boston. There will be annual all-day meetings at which Project and Core Investigators will present research progress and plans to members of the Internal and External Advisory Board. Organizational aspects of the PPG will be handled by Dr. Kwiatkowski and the Administrative Coordinator, Robyn Naigles. She will organize all interactions among the projects and the cores, including arranging the annual meeting, and deal with all other administrative aspects including preparations of all progress reports and applications related to this PPG.
The overall goal of this program project application is to find treatments forthe hamartoma syndromes, and the common cancers in which these same genes (TSCl, TSC2, LKBI, PTEN) are involved. This administrative core sen/es a critical function in the administration and facilitation of this overall research program.
|Akbay, Esra A; Koyama, Shohei; Liu, Yan et al. (2017) Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade. J Thorac Oncol 12:1268-1279|
|Li, Xinghui; Zhang, Zhibin; Li, Lupeng et al. (2017) Myeloid-derived cullin 3 promotes STAT3 phosphorylation by inhibiting OGT expression and protects against intestinal inflammation. J Exp Med 214:1093-1109|
|Housden, Benjamin E; Muhar, Matthias; Gemberling, Matthew et al. (2017) Loss-of-function genetic tools for animal models: cross-species and cross-platform differences. Nat Rev Genet 18:24-40|
|Lobbardi, Riadh; Pinder, Jordan; Martinez-Pastor, Barbara et al. (2017) TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia. Cancer Discov 7:1336-1353|
|Howell, Jessica J; Hellberg, Kristina; Turner, Marc et al. (2017) Metformin Inhibits Hepatic mTORC1 Signaling via Dose-Dependent Mechanisms Involving AMPK and the TSC Complex. Cell Metab 25:463-471|
|Breitkopf, Susanne B; Taveira, Mateus De Oliveira; Yuan, Min et al. (2017) Serial-omics of P53-/-, Brca1-/- Mouse Breast Tumor and Normal Mammary Gland. Sci Rep 7:14503|
|Bowden, John A; Heckert, Alan; Ulmer, Candice Z et al. (2017) Harmonizing lipidomics: NIST interlaboratory comparison exercise for lipidomics using SRM 1950-Metabolites in Frozen Human Plasma. J Lipid Res 58:2275-2288|
|Cao, Juxiang; Tyburczy, Magdalena E; Moss, Joel et al. (2017) Tuberous sclerosis complex inactivation disrupts melanogenesis via mTORC1 activation. J Clin Invest 127:349-364|
|Manning, Brendan D; Toker, Alex (2017) AKT/PKB Signaling: Navigating the Network. Cell 169:381-405|
|Lam, Hilaire C; Liu, Heng-Jia; Baglini, Christian V et al. (2017) Rapamycin-induced miR-21 promotes mitochondrial homeostasis and adaptation in mTORC1 activated cells. Oncotarget 8:64714-64727|
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