IMMUNOLOGICAL MECHANISMS IN CANCER PROGRAM The Immunological Mechanisms in Cancer Program comprises nineteen investigators from six academic departments. The primary objectives of the IMC Program are 1) to create a strong, intellectual and highly interactive scientific environment in which the functioning of the immune system as it relates to the cancer problem can be imaginatively and efficiently investigated;and 2) to foster, through intra- and inter-programmatic collaboration, the translation of the knowledge gained from these studies to the development of approaches for the prevention, diagnosis and treatment of cancer. The interests of the faculty are varied but the program is unified by four main themes: 1) to improve our understanding of the molecular and cellular basis for the development hematopoietic malignancies;2) to elucidate the nature of tumor antigen recognition and response to tumors by the immune system, thereby supporting development of immunotherapeutic approaches to cancer;3) to investigate the role of viruses in the development of cancer and cancer therapies;and 4) to create improvements in bone marrow transplantation approaches for the treatment of hematopoietic malignancies. Of the nineteen program members, eighteen have been funded through peer-reviewed awards. Current NCI and total peer review support for this program total approximately 1.8 and 8.2 million dollars, respectively. In the previous funding period, program members published 150 cancer-relevant papers, 14 and 20 percent of which resulted from intra, and inter-programmatic collaborations, respectively. Collaborations between members of this and other programs in the Kimmel Cancer Center have contributed to the production of reagents and analysis of preclinical models for testing novel therapies that have resulted in clinical trials. The expertise and the insight provided by members of the program is of increasing importance to the center for the definition of both functional and molecular aspects of the host-tumor interaction. Further development of the program is planned in the areas of tumor immunology and the immunobiology of dendritic cells.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA056036-11
Application #
8084090
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2010-06-01
Budget End
2011-05-31
Support Year
11
Fiscal Year
2010
Total Cost
$27,849
Indirect Cost
Name
Thomas Jefferson University
Department
Type
DUNS #
053284659
City
Philadelphia
State
PA
Country
United States
Zip Code
19107
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
Sullivan-Reed, Katherine; Bolton-Gillespie, Elisabeth; Dasgupta, Yashodhara et al. (2018) Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Tumor Cells. Cell Rep 23:3127-3136
Lu, Huimin; Bowler, Nicholas; Harshyne, Larry A et al. (2018) Exosomal ?v?6 integrin is required for monocyte M2 polarization in prostate cancer. Matrix Biol 70:20-35
Lapadula, Dominic; Farias, Eduardo; Randolph, Clinita E et al. (2018) Effects of Oncogenic G?q and G?11 Inhibition by FR900359 in Uveal Melanoma. Mol Cancer Res :
Vite, Alexia; Zhang, Caimei; Yi, Roslyn et al. (2018) ?-Catenin-dependent cytoskeletal tension controls Yap activity in the heart. Development 145:
McNair, Christopher; Xu, Kexin; Mandigo, Amy C et al. (2018) Differential impact of RB status on E2F1 reprogramming in human cancer. J Clin Invest 128:341-358
Garcia, Samantha A; Lebrun, Aurore; Kean, Rhonda B et al. (2018) Clearance of attenuated rabies virus from brain tissues is required for long-term protection against CNS challenge with a pathogenic variant. J Neurovirol 24:606-615
Vido, Michael J; Le, Kaitlyn; Hartsough, Edward J et al. (2018) BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association. Cell Rep 25:1501-1510.e3
Brody, Jonathan R; Dixon, Dan A (2018) Complex HuR function in pancreatic cancer cells. Wiley Interdiscip Rev RNA 9:e1469

Showing the most recent 10 out of 807 publications