The scientific goal of the Hollings Cancer Center (HCC) Developmental Cancer Therapeutics (DCT) Program is to discover and characterize unique agents and pathways that will impact the development of more effective cancer therapies and to translate these discoveries into clinical applications by using proof-of principle, early phase clinical and correlative science studies. The DCT Program is co-led by Kenneth D. Tew, PhD and Carolyn D. Britten, MD. The DCT Program is organized around three themes of scientific investigation: ? Elucidation of Cellular Signaling Pathways. ? Modulation of Redox and Cellular Stress Response. ? Development of Small Molecule Chemotherapeutic Agents. The 46 members of the DCT Program, representing 12 departments within the College of Medicine and the College of Pharmacy, have 87 active grants/contracts totaling $11.7M in cancer research funding ($7.7 in peer-reviewed funding and $3.7M from the NCI). In 2012 the DCT Program implemented 65 early phase (pilot. Phase I, Phase l/ll, and Phase II) interventional treatment clinical trials, of which 25 were invesfigator initiated;224 patients were enrolled onto all DCT Program interventional treatment studies. In the past five years, DCT Program members produced 305 cancer-focused publications with 17% of these representing inter-programmatic and 35% intra-programmatic collaborations and 48% from mulfi-insfitutional collaborations.
Members of the Developmental Cancer Therapeutics Program are linked by synergistic research interests with a focus on drug discovery and development. Collaborations between this program's clinical and laboratory investigators are leading to development of new clinical cancer trials.
|Barton, Virginia; Armeson, Kent; Hampras, Shalaka et al. (2017) Nonmelanoma skin cancer and risk of all-cause and cancer-related mortality: a systematic review. Arch Dermatol Res 309:243-251|
|Alexander-Bryant, Angela A; Zhang, Haiwen; Attaway, Christopher C et al. (2017) Dual peptide-mediated targeted delivery of bioactive siRNAs to oral cancer cells in vivo. Oral Oncol 72:123-131|
|Kim, Sungjin; Alsaidan, Omar Awad; Goodwin, Octavia et al. (2017) Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression. Cancer Res 77:6950-6962|
|Yang, Aimin; Qin, Shenghui; Schulte, Bradley A et al. (2017) MYC Inhibition Depletes Cancer Stem-like Cells in Triple-Negative Breast Cancer. Cancer Res 77:6641-6650|
|Karam, Joseph A; Parikh, Rasesh Y; Nayak, Dhananjaya et al. (2017) Co-chaperone Hsp70/Hsp90-organizing protein (Hop) is required for transposon silencing and Piwi-interacting RNA (piRNA) biogenesis. J Biol Chem 292:6039-6046|
|Mehrotra, Shikhar; Britten, Carolyn D; Chin, Steve et al. (2017) Vaccination with poly(IC:LC) and peptide-pulsed autologous dendritic cells in patients with pancreatic cancer. J Hematol Oncol 10:82|
|Sagar, Amin; Arif, Ehtesham; Solanki, Ashish Kumar et al. (2017) Targeting Neph1 and ZO-1 protein-protein interaction in podocytes prevents podocyte injury and preserves glomerular filtration function. Sci Rep 7:12047|
|Liu, Qinlong; Rehman, Hasibur; Krishnasamy, Yasodha et al. (2017) 8-pCPT-cGMP prevents mitochondrial depolarization and improves the outcome of steatotic partial liver transplantation. Int J Physiol Pathophysiol Pharmacol 9:69-83|
|Ghatak, Shibnath; Hascall, Vincent C; Markwald, Roger R et al. (2017) Transforming growth factor ?1 (TGF?1)-induced CD44V6-NOX4 signaling in pathogenesis of idiopathic pulmonary fibrosis. J Biol Chem 292:10490-10519|
|Lemasters, John J (2017) Evolution of Voltage-Dependent Anion Channel Function: From Molecular Sieve to Governator to Actuator of Ferroptosis. Front Oncol 7:303|
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