The Case CCC Protocol Review and Monitoring System (PRMS) is responsible for scientific evaluation, prioritization, and monitoring of all cancer clinical trials conducted at consortium institutions. The PRMS is independent of and complements the activities of the Institutional Review Boards (IRBs) and Data Safety and Toxicity Committee (DSTC). The Case CCC PRMS is operationalized through the Protocol Review and Monitoring Committee (PRMC). The PRMC resides within the Case CCC Clinical Research Office, which oversees and coordinates the activities of the Clinical Trials Core Facility (CTCF), Protocol Review and Monitoring System, Data and Safety Monitoring, and Protocol Specific Research Support. The PRMC supports the clinical research programs of the Case CCC by providing scientific review (and associated feedback to assist in protocol development), establishing priority ranking for protocols within a given disease category and by monitoring the progress and patient accrual. The PRMC membership is selected to ensure diverse expertise relevant to cancer clinical research and is composed of pharmacists, nurses, clinical investigators, biostatisticians, translational PhD scientists and patient advocates from consortium member institutions. The PRMC operates as a single committee across the consortium and has authority to review all new clinical research protocols, including those sponsored by the Cancer Center, NCI, other NIH, industry, foundations, or other sources. These include therapeutic, behavioral, and observational studies. The PRMC has authority for closure of ongoing studies that are accruing slowly and are unlikely to accomplish their scientific goals, and a structured process for accrual evaluation is followed. New protocols, continuing reviews and amendments are evaluated by the PRMC. In 2011, PRMC reviewed 185 new protocols.
The Case Comprehensive Cancer Center is Northeast Ohio's only NCI designated comprehensive cancer center providing bench-to-bedside medical research involving partnerships between basic, clinical and population scientists to speed translation of laboratory discoveries into new prevention/intervention and cancer treatments.
|Zhao, S; Sedwick, D; Wang, Z (2015) Genetic alterations of protein tyrosine phosphatases in human cancers. Oncogene 34:3885-94|
|Dermawan, Josephine Kam Tai; Gurova, Katerina; Pink, John et al. (2014) Quinacrine overcomes resistance to erlotinib by inhibiting FACT, NF-?B, and cell-cycle progression in non-small cell lung cancer. Mol Cancer Ther 13:2203-14|
|Brubaker, Douglas; Difeo, Analisa; Chen, Yanwen et al. (2014) Drug Intervention Response Predictions with PARADIGM (DIRPP) identifies drug resistant cancer cell lines and pathway mechanisms of resistance. Pac Symp Biocomput :125-35|
|Yori, Jennifer L; Lozada, Kristen L; Seachrist, Darcie D et al. (2014) Combined SFK/mTOR inhibition prevents rapamycin-induced feedback activation of AKT and elicits efficient tumor regression. Cancer Res 74:4762-71|
|Dabir, Snehal; Kluge, Amy; McColl, Karen et al. (2014) PIAS3 activates the intrinsic apoptotic pathway in non-small cell lung cancer cells independent of p53 status. Int J Cancer 134:1045-54|
|Zapanta Rinonos, Serendipity; Rai, Urvashi; Vereb, Sydney et al. (2014) Sequential logic of polarity determination during the haploid-to-diploid transition in Saccharomyces cerevisiae. Eukaryot Cell 13:1393-402|
|Sizemore, Gina M; Sizemore, Steven T; Seachrist, Darcie D et al. (2014) GABA(A) receptor pi (GABRP) stimulates basal-like breast cancer cell migration through activation of extracellular-regulated kinase 1/2 (ERK1/2). J Biol Chem 289:24102-13|
|Sossey-Alaoui, Khalid; Pluskota, Elzbieta; Davuluri, Gangarao et al. (2014) Kindlin-3 enhances breast cancer progression and metastasis by activating Twist-mediated angiogenesis. FASEB J 28:2260-71|
|Dotan, Efrat; Devarajan, Karthik; D'Silva, A James et al. (2014) Patterns of use and tolerance of anti-epidermal growth factor receptor antibodies in older adults with metastatic colorectal cancer. Clin Colorectal Cancer 13:192-8|
|Arachiche, Amal; de la Fuente, María; Nieman, Marvin T (2014) Platelet specific promoters are insufficient to express protease activated receptor 1 (PAR1) transgene in mouse platelets. PLoS One 9:e97724|
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