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.
|Xu, Yang; Taylor, Paul; Andrade, Joshua et al. (2018) Pathologic Oxidation of PTPN12 Underlies ABL1 Phosphorylation in Hereditary Leiomyomatosis and Renal Cell Carcinoma. Cancer Res 78:6539-6548|
|Gagner, Jean-Pierre; Zagzag, David (2018) Probing Glioblastoma Tissue Heterogeneity with Laser Capture Microdissection. Methods Mol Biol 1741:209-220|
|Tsay, Jun-Chieh J; Wu, Benjamin G; Badri, Michelle H et al. (2018) Airway Microbiota Is Associated with Upregulation of the PI3K Pathway in Lung Cancer. Am J Respir Crit Care Med 198:1188-1198|
|Martin, Patricia K; Marchiando, Amanda; Xu, Ruliang et al. (2018) Autophagy proteins suppress protective type I interferon signalling in response to the murine gut microbiota. Nat Microbiol 3:1131-1141|
|de la Parra, Columba; Ernlund, Amanda; Alard, Amandine et al. (2018) A widespread alternate form of cap-dependent mRNA translation initiation. Nat Commun 9:3068|
|Coux, Rémi-Xavier; Teixeira, Felipe Karam; Lehmann, Ruth (2018) L(3)mbt and the LINT complex safeguard cellular identity in the Drosophila ovary. Development 145:|
|Patibandla, Jay R; Fehniger, Julia E; Levine, Douglas A et al. (2018) Small cell cancers of the female genital tract: Molecular and clinical aspects. Gynecol Oncol 149:420-427|
|Fanok, Melania H; Sun, Amy; Fogli, Laura K et al. (2018) Role of Dysregulated Cytokine Signaling and Bacterial Triggers in the Pathogenesis of Cutaneous T-Cell Lymphoma. J Invest Dermatol 138:1116-1125|
|Berger, Ashton C; Korkut, Anil; Kanchi, Rupa S et al. (2018) A Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers. Cancer Cell 33:690-705.e9|
|Harper, Lamia; Balasubramanian, Divya; Ohneck, Elizabeth A et al. (2018) Staphylococcus aureus Responds to the Central Metabolite Pyruvate To Regulate Virulence. MBio 9:|
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