The Cellular Products Laboratory (CPL) is dedicated to generation and preparation of quality products for tumor vaccines and for cellular and gene therapy of cancer. This laboratory has assumed an increasingly important role in supporting the conduct of novel immunotherapy clinical trials and gene therapy clinical trials at the UPCI. It performs 3,464 procedures annually and these vary in complexity from large-scale cell production to smaller cultures for research and development purposes. The main users are members of the Biological Therapeutics Program and the Head and Neck Cancer Program. In FY 2002, the CPL services were utilized to support 14 clinical or research protocols. Its responsibilities include cell culture of hematopoietic or non-hematopoietic cells, vaccine preparation, genetic modification of human cells, tissue procurement, processing and distribution for clinical trials, sterility and safety evaluation of each product prior to its administration to patients, and development of new products and procedures for use in future clinical protocols. The CPL pilots preparation of new cellular products, and assists in preparation of INDs. Once IRB and FDA approvals are obtained, the CPL produces and delivers to the bedside therapeutic-grade cells. Recently, generation of dendritic cell (DC)-based vaccines and research associated with therapeutic DC generation have been the major effort, representing nearly 80% of CPL activities. The CPL is operated according to FDA criteria for good manufacturing practice (GMP). The CPL has established a fee-for-service price schedule. The Laboratory has established an excellent record of accomplishments and its unique expertise has enabled rapid translation of novel technologies to clinical trials.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA047904-17
Application #
6989560
Study Section
Subcommittee G - Education (NCI)
Project Start
2004-09-22
Project End
2009-07-31
Budget Start
2004-09-22
Budget End
2005-07-31
Support Year
17
Fiscal Year
2004
Total Cost
$126,654
Indirect Cost
Name
University of Pittsburgh
Department
Type
DUNS #
004514360
City
Pittsburgh
State
PA
Country
United States
Zip Code
15213
Samuelsson, Laura B; Bovbjerg, Dana H; Roecklein, Kathryn A et al. (2018) Sleep and circadian disruption and incident breast cancer risk: An evidence-based and theoretical review. Neurosci Biobehav Rev 84:35-48
Chen, Dongshi; Ni, Hong-Min; Wang, Lei et al. (2018) PUMA induction mediates acetaminophen-induced necrosis and liver injury. Hepatology :
Tahata, Shawn; Singh, Shivendra V; Lin, Yan et al. (2018) Evaluation of Biodistribution of Sulforaphane after Administration of Oral Broccoli Sprout Extract in Melanoma Patients with Multiple Atypical Nevi. Cancer Prev Res (Phila) 11:429-438
Moravcikova, Erika; Meyer, E Michael; Corselli, Mirko et al. (2018) Proteomic Profiling of Native Unpassaged and Culture-Expanded Mesenchymal Stromal Cells (MSC). Cytometry A 93:894-904
Beumer, Jan H; Inker, Lesley A; Levey, Andrew S (2018) Improving Carboplatin Dosing Based on EstimatedĀ GFR. Am J Kidney Dis 71:163-165
Shiffman, Saul; Mao, Jason M; Kurland, Brenda F et al. (2018) Do non-daily smokers compensate for reduced cigarette consumption when smoking very-low-nicotine-content cigarettes? Psychopharmacology (Berl) 235:3435-3441
Cao, Chunyu; Wu, Hao; Vasilatos, Shauna N et al. (2018) HDAC5-LSD1 axis regulates antineoplastic effect of natural HDAC inhibitor sulforaphane in human breast cancer cells. Int J Cancer 143:1388-1401
Yochum, Zachary A; Cades, Jessica; Wang, Hailun et al. (2018) Targeting the EMT transcription factor TWIST1 overcomes resistance to EGFR inhibitors in EGFR-mutant non-small-cell lung cancer. Oncogene :
Lee, Young-Sun; Lee, Dae-Hee; Choudry, Haroon A et al. (2018) Ferroptosis-Induced Endoplasmic Reticulum Stress: Cross-talk between Ferroptosis and Apoptosis. Mol Cancer Res 16:1073-1076
Tong, Jingshan; Zheng, Xingnan; Tan, Xiao et al. (2018) Mcl-1 Phosphorylation without Degradation Mediates Sensitivity to HDAC Inhibitors by Liberating BH3-Only Proteins. Cancer Res 78:4704-4715

Showing the most recent 10 out of 1187 publications