The Wistar Institute Cancer Center presents four Type II Shared Resources in this application: Bioinformatics, Genomics, Molecular Screening, and Proteomics. During the past project period the Cancer Center made substantial investments in the Type II Shared Resources, utilizing over $5.5 million in capital funds and equipment grants for equipment upgrades and facility improvements. These Resources function as engines, integrated components ofthe research being conducted by Cancer Center members. The Type II Resources have demonstrated a significant impact to the scientific objectives of the Cancer Center, contributing to 153 of 382 (40%) of the unique cancer-related publications reported by the three scientific Programs. Following a comprehensive realignment of all of its Shared Resources by the appointment of dedicated leadership as described in the Cancer Center Administration section of this application. Shared Resources were grouped as Type I or Type II, reflecting the intensity of collaborative input of their services. Type II Shared Resources provide a higher intensity of collaboration and impact on service, requiring an initial consultation to define the scope of service and remain consultative throughout the service delivery. For many projects. Type II Shared Resources participate in experiment design for sample preparation, services often need to be adapted to address specific scientific problems, and frequently the resulting complex datasets need to be reviewed with the user followed by further data analysis. Regular correspondence and method modifications are required throughout the delivery ofthe service in order to determine the appropriate course of action. Therefore, a distinctive feature of Type II Resources is a substantial amount of individualized, project-driven consultative time and effort provided by Resource staff to users. Accordingly, it is usually impractical for such services to achieve full recovery of operating costs through chargebacks. Clear benchmarks and objective review criteria were introduced in order to enable timely oversight, scientific impact, quality of service, and financial strength for each Shared Resource. Regular evaluations of scientific impact for the Cancer Center (i) and sustainability of services (ii) for each Resource, guide the decision-making process for the Shared Resources. Overall Type II Shared Resources represent clear engines for research as their impact on innovation and discovery is inherent to the individualized nature of their services.
The multidisciplinary nature and extraordinary complexity of modern cancer research require technologically advanced approaches that support refinement of the experimental question, customization of the most appropriate research tool and consultative review of data analysis and interpretation. Type II Shared Resources offer these services to Cancer Center investigators as an integrated and scientifically-driven extension of their research laboratories.
|Qin, Jie; Rajaratnam, Rajathees; Feng, Li et al. (2015) Development of organometallic S6K1 inhibitors. J Med Chem 58:305-14|
|Tomescu, Costin; Seaton, Kelly E; Smith, Peter et al. (2015) Innate activation of MDC and NK cells in high-risk HIV-1-exposed seronegative IV-drug users who share needles when compared with low-risk nonsharing IV-drug user controls. J Acquir Immune Defic Syndr 68:264-73|
|Gekonge, Bethsebah; Bardin, Matthew C; Montaner, Luis J (2015) Short communication: Nitazoxanide inhibits HIV viral replication in monocyte-derived macrophages. AIDS Res Hum Retroviruses 31:237-41|
|Webster, Marie R; Xu, Mai; Kinzler, Kathryn A et al. (2015) Wnt5A promotes an adaptive, senescent-like stress response, while continuing to drive invasion in melanoma cells. Pigment Cell Melanoma Res 28:184-95|
|Zhang, Xuhui; Akech, Jacqueline; Browne, Gillian et al. (2015) Runx2-Smad signaling impacts the progression of tumor-induced bone disease. Int J Cancer 136:1321-32|
|Kung, Che-Pei; Khaku, Sakina; Jennis, Matthew et al. (2015) Identification of TRIML2, a novel p53 target, that enhances p53 SUMOylation and regulates the transactivation of proapoptotic genes. Mol Cancer Res 13:250-62|
|Wolf, Amaya I; Strauman, Maura C; Mozdzanowska, Krystyna et al. (2014) Pneumolysin expression by streptococcus pneumoniae protects colonized mice from influenza virus-induced disease. Virology 462-463:254-65|
|Gumireddy, Kiranmai; Li, Anping; Kossenkov, Andrew V et al. (2014) ID1 promotes breast cancer metastasis by S100A9 regulation. Mol Cancer Res 12:1334-43|
|Budina-Kolomets, Anna; Balaburski, Gregor M; Bondar, Anastasia et al. (2014) Comparison of the activity of three different HSP70 inhibitors on apoptosis, cell cycle arrest, autophagy inhibition, and HSP90 inhibition. Cancer Biol Ther 15:194-9|
|Newhart, Alyshia; Janicki, Susan M (2014) Seeing is believing: visualizing transcriptional dynamics in single cells. J Cell Physiol 229:259-65|
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