The main objectives of the Administrative Core (Core A) are to develop overarching collaborative initiatives and to provide the necessary coordination and prioritization of the available resources among the participating Research Projects and Reagent/Service Core (Core B). Core A will provide a forum through which the Project Directors and Core Leaders communicate openly and regularly. Activities that Core A will be coordinating include monthly Project Directors'meetings, monthly research conferences, annual research retreat, annual reports to the Advisory Committee, preparation, submission, renewal and monitoring of research protocols (animal, human and biosafety), and communication with internal and external funding agencies regarding budgetary matters. In close consultation with the Advisory Committee, Core A will play a central role in assessing the progress and productivity of this Program, resolve potential barriers and ensure that the entire program and each of its components are on the right track. Through these activities, the Core will serve to ensure cost-effectiveness, enhance program integration, accelerate scientific productivity, and maximize translational output.

Public Health Relevance

The Administrative Core will play a central role in coordinating all the collaborative, administrative, budgetary, and compliance matters for this Program Project grant and in ensuring synergy. Integration and productivity. This will in turn contribute directly to the goals of this Program to understand the molecular tumorigenesis and discover novel therapies for bladder cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA165980-02
Application #
8765243
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2014-09-01
Budget End
2015-08-31
Support Year
2
Fiscal Year
2014
Total Cost
Indirect Cost
Name
New York University
Department
Type
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016
Jin, Honglei; Sun, Wenrui; Zhang, Yuanmei et al. (2018) MicroRNA-411 Downregulation Enhances Tumor Growth by Upregulating MLLT11 Expression in Human Bladder Cancer. Mol Ther Nucleic Acids 11:312-322
Hua, Xiaohui; Xu, Jiheng; Deng, Xu et al. (2018) New compound ChlA-F induces autophagy-dependent anti-cancer effect via upregulating Sestrin-2 in human bladder cancer. Cancer Lett 436:38-51
Peng, Minggang; Wang, Jingjing; Zhang, Dongyun et al. (2018) PHLPP2 stabilization by p27 mediates its inhibition of bladder cancer invasion by promoting autophagic degradation of MMP2 protein. Oncogene :
Li, Xin; Tian, Zhongxian; Jin, Honglei et al. (2018) Decreased c-Myc mRNA Stability via the MicroRNA 141-3p/AUF1 Axis Is Crucial for p63? Inhibition of Cyclin D1 Gene Transcription and Bladder Cancer Cell Tumorigenicity. Mol Cell Biol 38:
Guo, Xirui; Huang, Haishan; Jin, Honglei et al. (2018) ISO, via Upregulating MiR-137 Transcription, Inhibits GSK3?-HSP70-MMP-2 Axis, Resulting in Attenuating Urothelial Cancer Invasion. Mol Ther Nucleic Acids 12:337-349
Weng, Mao-Wen; Lee, Hyun-Wook; Park, Sung-Hyun et al. (2018) Aldehydes are the predominant forces inducing DNA damage and inhibiting DNA repair in tobacco smoke carcinogenesis. Proc Natl Acad Sci U S A 115:E6152-E6161
Yu, Yonghui; Jin, Honglei; Xu, Jiheng et al. (2018) XIAP overexpression promotes bladder cancer invasion in vitro and lung metastasis in vivo via enhancing nucleolin-mediated Rho-GDI? mRNA stability. Int J Cancer 142:2040-2055
Lee, Hyun-Wook; Park, Sung-Hyun; Weng, Mao-Wen et al. (2018) E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells. Proc Natl Acad Sci U S A 115:E1560-E1569
Zhu, Junlan; Li, Yang; Tian, Zhongxian et al. (2017) ATG7 Overexpression Is Crucial for Tumorigenic Growth of Bladder Cancer In Vitro and In Vivo by Targeting the ETS2/miRNA196b/FOXO1/p27 Axis. Mol Ther Nucleic Acids 7:299-313
Weng, Mao-Wen; Lee, Hyun-Wook; Choi, Bongkun et al. (2017) AFB1 hepatocarcinogenesis is via lipid peroxidation that inhibits DNA repair, sensitizes mutation susceptibility and induces aldehyde-DNA adducts at p53 mutational hotspot codon 249. Oncotarget 8:18213-18226

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