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
Lee, Hyeong-Min; Clark, Ellen P; Kuijer, M Bram et al. (2018) Characterization and structure-activity relationships of indenoisoquinoline-derived topoisomerase I inhibitors in unsilencing the dormant Ube3a gene associated with Angelman syndrome. Mol Autism 9:45
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Hall, Hana; Ma, Jingqun; Shekhar, Sudhanshu et al. (2018) Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors. BMC Neurosci 19:43
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Huang, Xinxin; Guo, Bin; Liu, Sheng et al. (2018) Neutralizing negative epigenetic regulation by HDAC5 enhances human haematopoietic stem cell homing and engraftment. Nat Commun 9:2741
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Shinde, Aparna; Wilmanski, Tomasz; Chen, Hao et al. (2018) Pyruvate carboxylase supports the pulmonary tropism of metastatic breast cancer. Breast Cancer Res 20:76
Nenortas, Nathaniel P; Cinelli, Maris A; Morrell, Andrew E et al. (2018) Activity of Aromathecins against African Trypanosomes. Antimicrob Agents Chemother 62:
Norvil, Allison B; Petell, Christopher J; Alabdi, Lama et al. (2018) Dnmt3b Methylates DNA by a Noncooperative Mechanism, and Its Activity Is Unaffected by Manipulations at the Predicted Dimer Interface. Biochemistry 57:4312-4324
Chambers, Andrea M; Wang, Jiao; Lupo, Kyle B et al. (2018) Adenosinergic Signaling Alters Natural Killer Cell Functional Responses. Front Immunol 9:2533

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