The Solid Tumor Therapeutics Program, which evolved from the Experimental Therapeutics Program, is a new program within the re-organized Duke Cancer Institute. The Solid Tumor Therapeutics Program focuses disease specific drug development and testing in the following disease groups: gastrointestinal cancers (esophageal, gastric, small intestine, colorectal, anal, hepatobiliary and pancreatic, genitourinary cancers (kidney, bladder, prostate, testicular), thoracic cancers (lung), sarcoma, melanoma and head and neck cancers. Most solid tumors share common alterations in the major signaling pathways regulating development and homeostasis, including the EGF, TGF-?, PDGF, VEGF, IGF, Hh, Wnt, Src and c-Met pathways. In addition, solid tumor share conserved roles for the tumor microenvironment (immune system, angiogenesis). Further, gaining insight into the cancer cell autonomous and tumor microenvironment alterations that will result in improvements in clinical practice requires the development of more relevant pre-clinical or concurrent models. Accordingly, a major goal of the Solid Tumor Therapeutics Research Program is to align the research efforts across these disease sites along these themes (signal transduction, tumor microenvironment, preclinical modeling), promoting synergy across research groups at Duke as we capitalize on early stage drug discovery and lead development efforts of the Developmental Therapeutics Program, and increase disease specific drug development and testing with investigator initiated trials, including Phase I experimental therapeutics. Opportunities for translational and clinical trial development will occur through the NCI Experimental Therapeutics Clinical Trials Network with Phase I emphasis (ET-CTN) grant and the National Clinical Trials Network (NCTN) lead academic site grant, both of which are led by investigators in this program. The program is comprised of 45 primary members and 29 secondary members from a wide spectrum of 12 different departments within the School of Medicine. Total funding (Direct + Indirect) for primary program members is $21.2M, of which $7.6M is peer reviewed. Of the $7.6M in peer reviewed funding, $2.9M is from the NCI and $4.7M is from the NIH and other peer-reviewed organizations, demonstrating the cancer focus of this program, as well as the balance between peer reviewed and industry funding for this translational research program. From 2009-2013, program members published 833 papers in peer-reviewed journals cited in PubMed. Of these publications, 184 (22%) are the result of intra-programmatic collaborations and 157 (19%) are due to inter-programmatic collaborations.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
Project #
Application #
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Duke University
United States
Zip Code
Galaz-Montoya, Monica; Wright, Sara J; Rodriguez, Gustavo J et al. (2017) ?2-Adrenergic receptor activation mobilizes intracellular calcium via a non-canonical cAMP-independent signaling pathway. J Biol Chem 292:9967-9974
Lanier, Megan L; Park, Hyeri; Mukherjee, Paramita et al. (2017) Formal Synthesis of (+)-Laurencin by Gold(I)-Catalyzed Intramolecular Dehydrative Alkoxylation. Chemistry 23:7180-7184
Shi, Qiong; Liu, Hongliang; Han, Peng et al. (2017) Genetic Variants in WNT2B and BTRC Predict Melanoma Survival. J Invest Dermatol 137:1749-1756
Woyach, Jennifer A; Ruppert, Amy S; Guinn, Daphne et al. (2017) BTKC481S-Mediated Resistance to Ibrutinib in Chronic Lymphocytic Leukemia. J Clin Oncol 35:1437-1443
Wang, Yanru; Freedman, Jennifer A; Liu, Hongliang et al. (2017) Associations between RNA splicing regulatory variants of stemness-related genes and racial disparities in susceptibility to prostate cancer. Int J Cancer 141:731-743
Fayanju, Oluwadamilola M; Hall, Carolyn S; Bauldry, Jessica Bowman et al. (2017) Body mass index mediates the prognostic significance of circulating tumor cells in inflammatory breast cancer. Am J Surg 214:666-671
Leu, David; Spasojevic, Ivan; Nguyen, Huy et al. (2017) CNS bioavailability and radiation protection of normal hippocampal neurogenesis by a lipophilic Mn porphyrin-based superoxide dismutase mimic, MnTnBuOE-2-PyP5. Redox Biol 12:864-871
Sauer, Scott J; Tarpley, Michael; Shah, Imran et al. (2017) Bisphenol A activates EGFR and ERK promoting proliferation, tumor spheroid formation and resistance to EGFR pathway inhibition in estrogen receptor-negative inflammatory breast cancer cells. Carcinogenesis 38:252-260
Pan, Yongchu; Liu, Hongliang; Wang, Yanru et al. (2017) Associations between genetic variants in mRNA splicing-related genes and risk of lung cancer: a pathway-based analysis from published GWASs. Sci Rep 7:44634
Yin, Jieyun; Liu, Hongliang; Liu, Zhensheng et al. (2017) Pathway-analysis of published genome-wide association studies of lung cancer: A potential role for the CYP4F3 locus. Mol Carcinog 56:1663-1672

Showing the most recent 10 out of 480 publications