ENDOCRINE MECHANISMS AND HORMONE ACTION IN CANCER PROGRAM The Endocrine Mechanisms and Hormone Action in Cancer (EMHAC) Program is a new cancer center program, initiated in 2006. The overall goal of the program is to discover molecular alterations and signatures of hormone-related cancer and translate these findings into new strategies for effective detection, diagnosis, and cure. The program maintains a focus on translational. research on tumors arising from hormone-responsive tissues, including breast and prostate. Three program areas of focus include: 1) detection and diagnosis, 2) prognosis and progression, and 3) targets and therapy. The main specific Scientific Goals of the program are to: Develop innovative strategies and technologies for early detection of primary cancer and monitoring of therapy response and disease recurrence. Improve diagnostic tumor classification, prognostic and predictive marker analyses, and design of pre-clinical models for drug response prediction to facilitate improved tailored treatment. Exploit mechanisms of hormone action for molecular target identification, improved therapy, and prevention of hormone responsive cancer. Several collaborative initiatives are ongoing between the 15 members from 6 departments, supported by peer-reviewed funding of $4.2 million ($2.7 NCI) per year. An P01 program project grant proposal on breast cancer has been submitted from the program. Although this is a new program, several program members have worked collaboratively over many years, with more than 100 joint publications. Since the program's inception in 2006, there have been more than 20 intra-programmatic publications.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA056036-12
Application #
8302933
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2011-06-01
Budget End
2012-05-31
Support Year
12
Fiscal Year
2011
Total Cost
$31,130
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

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