The Pharmacokinetics (PK) Core is a new core in the University of Michigan Comprehensive Cancer Center (UMCCC). PK core has four objectives to support UMCCC strategic goals for next five years: Objective 1: To support preclinical pharmacokinetics (PK) for lead compound selection and dose regimen optimization, which enhances anticancer drug discovery &development for Experimental Therapeutics Program of UMCCC. Objective 2: To support clinical pharmacokinetics (PK) and optimize dose regimen of anticancer drugs In clinical studies, which supports and increase investigator-initiated clinical trials (phase I and phase II) for Translational and Clinical Research Programs of UMCCC. Objective 3: To increase grants, publications, and patent applications with UMCCC members, Objective 4;To enhance Interactions among UMCCC members for preclinical experimental and clinical developmental therapeutics. PK Core has 3000 sq ft lab space, 3.5 FTE, four LC-MS end three HPLC systems. The PK core is operated under Core Director and Advisory Committee. In the last two years during its establishment, the PK core has supported preclinical and clinical pharmacokinetics in animal models and clinical trials of 341 compounds (97% from UMCCC) from 31 investigators (76% are UMCCC members). For instance, the PK core has supported IAP Inhibitor (AT-406) development to advance lo phase I clinical studies at UMCCC. The PK core also significantly contributed Mdm2 inhibitor development with joint patents together with UMCCC members, which was licensed by Sanofl-Aventis for $360M. The pharmacokinetic studies In PK core has resulted in 20 joint grant applications, 20 manuscripts, 7 meeting abstracts, and three patents with UMCCC members in the last two years. The PK core provides significant cost effectiveness with 50% discount to UMCCC members and enhances scientific Interactions with UMCCC members. The PK core expects to spend 60% effort (compounds and required effort) for preclinical pharmacokinetics in animal models and 40% effort (compounds and required efforts) for clinical pharmacokinetics in clinical trials.
Pharmacokinetics (PK) core supports preclinical pharmacokinetics for lead compound selection in anticancer drug discovery and development, and supports clinical pharmacokinetics for clinical trials of anticancer drugs in UMCCC.
|Mathewson, Nathan D; Jenq, Robert; Mathew, Anna V et al. (2016) Gut microbiome-derived metabolites modulate intestinal epithelial cell damage and mitigate graft-versus-host disease. Nat Immunol 17:505-13|
|Owen, John Henry; Graham, Martin P; Chinn, Steven B et al. (2016) Novel method of cell line establishment utilizing fluorescence-activated cell sorting resulting in 6 new head and neck squamous cell carcinoma lines. Head Neck 38 Suppl 1:E459-67|
|Lee, Alice W; Ness, Roberta B; Roman, Lynda D et al. (2016) Association Between Menopausal Estrogen-Only Therapy and Ovarian Carcinoma Risk. Obstet Gynecol 127:828-36|
|Kadakia, Kunal C; Snyder, Claire F; Kidwell, Kelley M et al. (2016) Patient-Reported Outcomes and Early Discontinuation in Aromatase Inhibitor-Treated Postmenopausal Women With Early Stage Breast Cancer. Oncologist 21:539-46|
|Boonstra, Philip S; Mukherjee, Bhramar; Gruber, Stephen B et al. (2016) Tests for Gene-Environment Interactions and Joint Effects With Exposure Misclassification. Am J Epidemiol 183:237-47|
|Peng, Dongjun; Tanikawa, Takashi; Li, Wei et al. (2016) Myeloid-Derived Suppressor Cells Endow Stem-like Qualities to Breast Cancer Cells through IL6/STAT3 and NO/NOTCH Cross-talk Signaling. Cancer Res 76:3156-65|
|Hardiman, Karin M; Ulintz, Peter J; Kuick, Rork D et al. (2016) Intra-tumor genetic heterogeneity in rectal cancer. Lab Invest 96:4-15|
|Boonstra, Philip S; Taylor, Jeremy M G; Smolska-Ciszewska, Beata et al. (2016) Alpha/beta (Î±/Î²) ratio for prostate cancer derived from external beam radiotherapy and brachytherapy boost. Br J Radiol 89:20150957|
|Amin, Nisar A; Malek, Sami N (2016) Gene mutations in chronic lymphocytic leukemia. Semin Oncol 43:215-21|
|Zhao, Ende; Maj, Tomasz; Kryczek, Ilona et al. (2016) Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction. Nat Immunol 17:95-103|
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