Cell Identity and Signaling (CIS) Research Program Project Summary The key scientific goals of the Cell Identity and Signaling (CIS) Research Program are to advance discovery of novel molecular mechanisms of cell identity and cell signaling, to apply this knowledge towards understanding cancer pathogenesis, and to use this knowledge to develop novel, mechanism-based approaches to prevent or interfere with cancer cell growth, aiming for cancer solutions. It is well-established that cancer cells hijack normal regulation of cell growth, differentiation, and embryonic development, via genetic and epigenetic mechanisms. The CIS Program aims to understand these fundamental mechanisms and shepherd them toward cancer solutions. The CIS Program has 27 members, $5.5 million in cancer-focused, peer-reviewed extramural funding, with 38% of the total funding from the NCI. CIS research themes span a spectrum from basic discovery, using simple model organisms and cellular and animal cancer models, to cancer solutions. CIS members are highly productive with 202 cancer-related publications since July 2015, and highly interactive with a 70% increase in collaborative publications. Importantly, 73% of all cancer-relevant CIS publications are collaborative. In the previous funding cycle, the CIS Program, supported by competitive pilot grants from the Purdue Center for Cancer Research (PCCR), successfully fostered highly collaborative, cancer-relevant studies linking CIS Program themes (intra- programmatic) with other PCCR programs (inter-programmatic), and also with external partners (inter- institutional). For the next funding period, the goal of the CIS Program is to advance the breadth and depth of our understanding of cancer-relevant mechanisms and to maximize their transition to cancer solutions. The approach towards this goal is to enable and foster collaborative and transdisciplinary studies by providing competitive PCCR pilot grants, and access to state-of-the-art, PCCR-supported Shared Resources, and modern technology in structural biology, drug discovery, cancer genomics, bioinformatics and computational biology.
Three specific aims are proposed.
Aim 1 : To further enhance discovery of basic and cancer-relevant mechanisms by strengthening the integration of computational genomics and bioinformatics and increasing expertise and training in computational biology.
Aim 2 : To enhance discovery of cancer-relevant mechanisms of signal transduction, gene expression and epigenetics by supporting collaborative, transdisciplinary approaches and modern technologies.
Aim 3 : To accelerate transition of newly discovered cancer-relevant mechanisms towards cancer solutions, by developing essential mechanisms as therapy targets, and by employing transdisciplinary approaches.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA023168-40
Application #
10024917
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
Project End
Budget Start
2020-08-01
Budget End
2021-06-30
Support Year
40
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Purdue University
Department
Type
DUNS #
072051394
City
West Lafayette
State
IN
Country
United States
Zip Code
47907
Lin, Clement; Wu, Guanhui; Wang, Kaibo et al. (2018) Molecular Recognition of the Hybrid-2 Human Telomeric G-Quadruplex by Epiberberine: Insights into Conversion of Telomeric G-Quadruplex Structures. Angew Chem Int Ed Engl 57:10888-10893
Hsu, Alan Y; Gurol, Theodore; Sobreira, Tiago J P et al. (2018) Development and Characterization of an Endotoxemia Model in Zebra Fish. Front Immunol 9:607
Li, Zhiguo; Kong, Yifan; Song, Longzhen et al. (2018) Plk1-Mediated Phosphorylation of TSC1 Enhances the Efficacy of Rapamycin. Cancer Res 78:2864-2875
Xiong, Yan; Yue, Feng; Jia, Zhihao et al. (2018) A novel brown adipocyte-enriched long non-coding RNA that is required for brown adipocyte differentiation and sufficient to drive thermogenic gene program in white adipocytes. Biochim Biophys Acta Mol Cell Biol Lipids 1863:409-419
Mani, Saravana Kumar Kailasam; Andrisani, Ourania (2018) Hepatitis B Virus-Associated Hepatocellular Carcinoma and Hepatic Cancer Stem Cells. Genes (Basel) 9:
Zhou, Wenqing; Pal, Arpita S; Hsu, Alan Yi-Hui et al. (2018) MicroRNA-223 Suppresses the Canonical NF-?B Pathway in Basal Keratinocytes to Dampen Neutrophilic Inflammation. Cell Rep 22:1810-1823
Dayal, Neetu; Opoku-Temeng, Clement; Hernandez, Delmis E et al. (2018) Dual FLT3/TOPK inhibitor with activity against FLT3-ITD secondary mutations potently inhibits acute myeloid leukemia cell lines. Future Med Chem 10:823-835
Onel, Buket; Carver, Megan; Agrawal, Prashansa et al. (2018) The 3'-end region of the human PDGFR-? core promoter nuclease hypersensitive element forms a mixture of two unique end-insertion G-quadruplexes. Biochim Biophys Acta Gen Subj 1862:846-854
Sorlien, Erin L; Witucki, Mary A; Ogas, Joseph (2018) Efficient Production and Identification of CRISPR/Cas9-generated Gene Knockouts in the Model System Danio rerio. J Vis Exp :
Mani, Saravana Kumar Kailasam; Andrisani, Ourania (2018) Interferon signaling during Hepatitis B Virus (HBV) infection and HBV-associated hepatocellular carcinoma. Cytokine :

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