The mission of the Cancer Cell Biology and Signaling (CCBS) Program is to elucidate the role of cell signaling in regulating cell growth, differentiation, apoptosis and migration, and to assist Cancer Center members in their efforts to harness this understanding into approaches to cancer detection, prognosis and treatment. Program members focus on three major areas of research: 1) understanding the molecular mechanisms involved in the regulation of cell growth and differentiation with an emphasis on the role of tyrosine kinase and G protein-coupled receptor signaling pathways;2) elucidating the molecular mechanisms regulating cell apoptosis;and 3) addressing the role of the extracellular matrix in regulating cell growth and migration. The Program is led by Drs. Jeffrey Benovic and George Prendergast, both of whom have extensive administrative experience and established research programs focused on cell signaling and cancer. The Program is comprised of twenty-three members and one associate member from nine departments and three Institutions (Jefferson, Lankenau Institute for Medical Research and Drexel). Program members currently have $3.4 million of NCI support and $12.0 million of total, peer-reviewed support and have published a total of 650 manuscripts (11% intra-programmatic and 26% inter-programmatic) during the last funding period.

Public Health Relevance

An important scientific goal of the CCBS Program is to integrate fundamental studies on the mechanisms that regulate cell growth, differentiation, apoptosis and migration with the translational research efforts at the KCC. This should result in a better understanding of the biology of cancer and also in translation of basic research into novel therapeutic strategies for the treatment of cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA056036-15
Application #
8753657
Study Section
Subcommittee B - Comprehensiveness (NCI)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
15
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Thomas Jefferson University
Department
Type
DUNS #
City
Philadelphia
State
PA
Country
United States
Zip Code
19107
Hussain, Maha; Daignault-Newton, Stephanie; Twardowski, Przemyslaw W et al. (2018) Targeting Androgen Receptor and DNA Repair in Metastatic Castration-Resistant Prostate Cancer: Results From NCI 9012. J Clin Oncol 36:991-999
Shafi, Ayesha A; Schiewer, Matthew J; de Leeuw, Renée et al. (2018) Patient-derived Models Reveal Impact of the Tumor Microenvironment on Therapeutic Response. Eur Urol Oncol 1:325-337
Meyer, Sara E; Muench, David E; Rogers, Andrew M et al. (2018) miR-196b target screen reveals mechanisms maintaining leukemia stemness with therapeutic potential. J Exp Med 215:2115-2136
Mazina, Olga M; Mazin, Alexander V (2018) Reconstituting the 4-Strand DNA Strand Exchange. Methods Enzymol 600:285-305
Magee, Michael S; Abraham, Tara S; Baybutt, Trevor R et al. (2018) Human GUCY2C-Targeted Chimeric Antigen Receptor (CAR)-Expressing T Cells Eliminate Colorectal Cancer Metastases. Cancer Immunol Res 6:509-516
Chervoneva, Inna; Freydin, Boris; Hyslop, Terry et al. (2018) Modeling qRT-PCR dynamics with application to cancer biomarker quantification. Stat Methods Med Res 27:2581-2595
Capparelli, Claudia; Purwin, Timothy J; Heilman, Shea A et al. (2018) ErbB3 Targeting Enhances the Effects of MEK Inhibitor in Wild-Type BRAF/NRAS Melanoma. Cancer Res 78:5680-5693
Nevler, Avinoam; Muller, Alexander J; Cozzitorto, Joseph A et al. (2018) A Sub-Type of Familial Pancreatic Cancer: Evidence and Implications of Loss-of-Function Polymorphisms in Indoleamine-2,3-Dioxygenase-2. J Am Coll Surg 226:596-603
Peng, Weidan; Furuuchi, Narumi; Aslanukova, Ludmila et al. (2018) Elevated HuR in Pancreas Promotes a Pancreatitis-Like Inflammatory Microenvironment That Facilitates Tumor Development. Mol Cell Biol 38:
Waldman, Scott A; Camilleri, Michael (2018) Guanylate cyclase-C as a therapeutic target in gastrointestinal disorders. Gut 67:1543-1552

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