The Tumor Microenvironment and Metastasis (TMM) Program was launched in 2012 to bring together a multidisciplinary team of cutting-edge immunologists and cancer biologists under a synergistic and collaborative scientific umbrella. This initiative provides for the natural evolution of the former Immunology Program that was dissolved at the end of 2011 as part of the strategic reorganization of the Cancer Center. The TMM Program comprises ten investigators with experimental interests aligned along three major flagship themes: Immunoregulation ofthe tumor microenvironment (i);Pathophysiology of metastasis (ii);and Bi-directional interaction between tumor and non-cancerous cells and their products (iii). The overarching goal of the TMM Program is to merge basic mechanistic understanding of multidisciplinary pathways of host-tumor interactions and metastatic dissemination with novel translational opportunities for disease diagnosis and (immuno)therapy. Despite the Program's recent inception, its integrated research platform has produced successful faculty recruitment, opened new opportunities for graduate education in cancer biology, considerably enhanced cancer focus, and developed extensive inter-programmatic and collaborative advances in the biology of metastasis, host-tumor cell crosstalk and immune modulation of tumor onset and progression. In terms of disease-relevance, TMM Program members are leading the development of a newly launched Ovarian Cancer Research Continuum Signature, a disease site-specific inter-programmatic initiative designed to merge basic, translational and patient oriented cancer research in a single scientific continuum. As of 2013, the TMM Program is expected to leverage a strong NCI funding base of $2.3 million, a total cancer-related peer-reviewed funding of $3.4 million (all direct costs), and currently lists 83 cancer-relevant publications, of which 29% are intra- and inter-programmatic collaborations, and 89% are inter-institutional collaborations. Building on these accomplishments, the TMM Program is on a steep, upward trajectory of research impact, scientific collaboration, and translational opportunities that leverage successful inter-institutional outreach partnerships as well as technological advances in key Shared Resources. During the next budget period, the TMM Program is ideally poised to significantly contribute to the Cancer Center's overarching mission in the continuum of cancer research by expanding scientific themes in the areas of metastatic competency and translational tumor immunology.

Public Health Relevance

The ability of tumor cells to thrive in vivo largely depends on the exploitation of cells and tissues that surround them, referred to as the microenvironment. Understanding how this immunosuppressive, proangiogenic, and pro-metastatic microenvironment is orchestrated to drive malignant progression may open new therapeutic prospects for patients with advanced and disseminated disease.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA010815-45
Application #
8690264
Study Section
Subcommittee G - Education (NCI)
Project Start
2014-03-01
Project End
2019-02-28
Budget Start
2014-03-01
Budget End
2015-02-28
Support Year
45
Fiscal Year
2014
Total Cost
$31,554
Indirect Cost
$12,576
Name
Wistar Institute
Department
Type
DUNS #
075524595
City
Philadelphia
State
PA
Country
United States
Zip Code
19104
Tempera, Italo; De Leo, Alessandra; Kossenkov, Andrew V et al. (2016) Identification of MEF2B, EBF1, and IL6R as Direct Gene Targets of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Critical for EBV-Infected B-Lymphocyte Survival. J Virol 90:345-55
Nelson, David M; Jaber-Hijazi, Farah; Cole, John J et al. (2016) Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability. Genome Biol 17:158
Seo, Jae Ho; Rivadeneira, Dayana B; Caino, M Cecilia et al. (2016) The Mitochondrial Unfoldase-Peptidase Complex ClpXP Controls Bioenergetics Stress and Metastasis. PLoS Biol 14:e1002507
Haut, Larissa H; Gill, Amanda L; Kurupati, Raj K et al. (2016) A Partial E3 Deletion in Replication-Defective Adenoviral Vectors Allows for Stable Expression of Potentially Toxic Transgene Products. Hum Gene Ther Methods :
Peck, Barrie; Schug, Zachary T; Zhang, Qifeng et al. (2016) Inhibition of fatty acid desaturation is detrimental to cancer cell survival in metabolically compromised environments. Cancer Metab 4:6
Chae, Young Chan; Vaira, Valentina; Caino, M Cecilia et al. (2016) Mitochondrial Akt Regulation of Hypoxic Tumor Reprogramming. Cancer Cell 30:257-72
Vazquez, Alexei; Kamphorst, Jurre J; Markert, Elke K et al. (2016) Cancer metabolism at a glance. J Cell Sci 129:3367-73
Kumar, Vinit; Patel, Sima; Tcyganov, Evgenii et al. (2016) The Nature of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment. Trends Immunol 37:208-20
Kung, Che-Pei; Murphy, Maureen E (2016) The role of the p53 tumor suppressor in metabolism and diabetes. J Endocrinol 231:R61-R75
Patro, Sean C; Azzoni, Livio; Joseph, Jocelin et al. (2016) Antiretroviral therapy in HIV-1-infected individuals with CD4 count below 100 cells/mm3 results in differential recovery of monocyte activation. J Leukoc Biol 100:223-31

Showing the most recent 10 out of 582 publications