The Chemical Library Screening Shared Resource (CLS) offers Cancer Center scientists the ability to develop and conduct large-scale chemical library screens for the generation of selective probes of biochemical processes of tumor biology and for the discovery of compounds that can be developed further as drug leads for therapeutic applications. High-throughput screening is not widely available at academic institutions;thus, this resource provides our Cancer Center with rare access to technology, expertise and infrastructure resources that will enable them to develop novel means for characterizing cellular targets involved in tumor pathogenesis and tumor onset that will advance the development of new lead molecules for anti-tumor therapies. The CLS consists of 4 specialized but highly integrated facilities: 1) the High Throughput Assay Development Facility supports the development, miniaturization, optimization, and validation of biochemical and cell-based high throughput assays, as well as supports follow-up analysis of screens, including IC50 determination, structure-activity-relationship (SAR) and mechanism-of-action studies;2) the Compound Management and HT Screening Facility, that curates the Institute's compound collections and performs the large-scale automated screening;3) the High Content Screening (HCS) Facility that supports imagebased high content assays utilizing high throughput microscopy, as well as automated microscopy for nonscreening applications - This facility also supports the image-based screening efforts of the Functional Genomics Shared Resource;and 4) the Medicinal Chemistry Facility provides both technical and scientific assistance in medicinal chemistry, synthesis, structure-activity relationship development, and generates optimized compounds for preclinical studies. CLS supported over half (34) of the Cancer Center laboratories in the last year. Chemical genomics has become a major focus of the Burnham Cancer Center, and has many opportunities for providing insight into potential therapeutic targets and strategies. CCSG funding of CLS leverages a substantial Institutional and NIH MLPCN investment in the Center for Chemical Genomics infrastructure, and is critical to bringing this cutting edge technology to Cancer Center researchers by funding facility personnel that conduct their projects. Overall, $189,798 in CCSG support is requested in the first year, representing 10.5% of the total projected annual CLS Shared Resource operating budget.

Public Health Relevance

Chemical biology can both elucidate the function of proteins involved in tumor development and progression, and identify novel targets and lead compounds with therapeutic potential in treating human cancers. The unique combination of basic cancer biology studies supported by extensive resources and expertise to perform high throughput screening and medicinal chemistry will lead to important new findings.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
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Subcommittee G - Education (NCI)
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Sanford-Burnham Medical Research Institute
La Jolla
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Gong, Xiao-Min; Ding, Yi; Yu, Jinghua et al. (2015) Structure of the Na,K-ATPase regulatory protein FXYD2b in micelles: implications for membrane-water interfacial arginines. Biochim Biophys Acta 1848:299-306
Brun, S N; Markant, S L; Esparza, L A et al. (2015) Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma. Oncogene 34:3770-9
You, Weon-Kyoo; Yotsumoto, Fusanori; Sakimura, Kenji et al. (2014) NG2 proteoglycan promotes tumor vascularization via integrin-dependent effects on pericyte function. Angiogenesis 17:61-76
Vargas, Lina M; Leal, Nancy; Estrada, Lisbell D et al. (2014) EphA4 activation of c-Abl mediates synaptic loss and LTP blockade caused by amyloid-? oligomers. PLoS One 9:e92309
Volkmann, Niels; Page, Christopher; Li, Rong et al. (2014) Three-dimensional reconstructions of actin filaments capped by Arp2/3 complex. Eur J Cell Biol 93:179-83
Bailey, Ann M; Zhan, Le; Maru, Dipen et al. (2014) FXR silencing in human colon cancer by DNA methylation and KRAS signaling. Am J Physiol Gastrointest Liver Physiol 306:G48-58
Valencia, Tania; Kim, Ji Young; Abu-Baker, Shadi et al. (2014) Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis. Cancer Cell 26:121-35
Northcott, Paul A; Lee, Catherine; Zichner, Thomas et al. (2014) Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma. Nature 511:428-34
Kim, H; Claps, G; Moller, A et al. (2014) Siah2 regulates tight junction integrity and cell polarity through control of ASPP2 stability. Oncogene 33:2004-10
Finlay, Darren; Vamos, Mitchell; Gonzalez-Lopez, Marcos et al. (2014) Small-molecule IAP antagonists sensitize cancer cells to TRAIL-induced apoptosis: roles of XIAP and cIAPs. Mol Cancer Ther 13:5-15

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