The Growth Control Program is composed of 38 investigators (34 Full and 4 Associate members) from 15 Departments with a common interest in understanding the cellular and molecular mechanisms by which eukaryotic cells regulate survival proliferation, and/or division. Moreover, members of this Program are committed to integrating basic research with an understanding of malignant transformation and the identification of targets for cancer therapeutics. The overall goal of the Program is to actively promote research collaborations amongst its members and facilitate the application of a wide range of cutting-edge research tools and approaches to better understand basic regulatory mechanisms that suppress malignant transformation in human cells. The Program has the following Specific Aims: 1) To study transcriptional and epigenetic machineries that regulate cell proliferation and differentiation;2) To elucidate intracellular cell signaling networks regulating cell survival and growth;3) To determine how cells control their division and checkpoints;4) To understand the mechanisms of action of oncogenes and tumor suppressors;and 5) To translate the knowledge generated from basic studies into tools to fight cancer. Wei Dai and Michele Pagano are the Co-Leaders for this Program. Total funding increased from $16,079,153 to $16,483,886 since the last competitive application. Membership has decreased from 45 to 38. Publications for the period total 477, of which 7.5% are intra-programmatic, 19.3% are inter-programmatic, and 2.7% are both intra- and interprogrammatic collaborations.
Cancer is a collection of diseases characterized by uncontrolled cell growth. Deregulated cellular and molecular processes that govern cell survival, division, and/or death play key roles in the development of cancer. The Program functions to promote research collaborations among its members to better understand basic mechanisms that curb cancer development.
|Huang, Chao; Zeng, Xingruo; Jiang, Guosong et al. (2017) XIAP BIR domain suppresses miR-200a expression and subsequently promotes EGFR protein translation and anchorage-independent growth of bladder cancer cell. J Hematol Oncol 10:6|
|Silvera, Deborah; Ernlund, Amanda; Arju, Rezina et al. (2017) mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells. Mol Cell Biol 37:|
|Koh, Hyunwook; Blaser, Martin J; Li, Huilin (2017) A powerful microbiome-based association test and a microbial taxa discovery framework for comprehensive association mapping. Microbiome 5:45|
|Ma, Lijie; Liu, Yan; Landry, Nichole K et al. (2017) Point mutation in D8C domain of Tamm-Horsfall protein/uromodulin in transgenic mice causes progressive renal damage and hyperuricemia. PLoS One 12:e0186769|
|Morabito, Michael V; Ravussin, Yann; Mueller, Bridget R et al. (2017) Weight Perturbation Alters Leptin Signal Transduction in a Region-Specific Manner throughout the Brain. PLoS One 12:e0168226|
|Koetz-Ploch, Lisa; Hanniford, Douglas; Dolgalev, Igor et al. (2017) MicroRNA-125a promotes resistance to BRAF inhibitors through suppression of the intrinsic apoptotic pathway. Pigment Cell Melanoma Res 30:328-338|
|Feig, Jessica L; Mediero, Aranzazu; Corciulo, Carmen et al. (2017) The antiviral drug tenofovir, an inhibitor of Pannexin-1-mediated ATP release, prevents liver and skin fibrosis by downregulating adenosine levels in the liver and skin. PLoS One 12:e0188135|
|Ono, Kentaro; Viet, Chi T; Ye, Yi et al. (2017) Cutaneous pigmentation modulates skin sensitivity via tyrosinase-dependent dopaminergic signalling. Sci Rep 7:9181|
|Wang, Xing; Zhang, Fenglin; Wu, Xue-Ru (2017) Inhibition of Pyruvate Kinase M2 Markedly Reduces Chemoresistance of Advanced Bladder Cancer to Cisplatin. Sci Rep 7:45983|
|Garré, Juan Mauricio; Silva, Hernandez Moura; Lafaille, Juan J et al. (2017) CX3CR1+ monocytes modulate learning and learning-dependent dendritic spine remodeling via TNF-?. Nat Med 23:714-722|
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