Comparative Medicine Signature Program Funding
Through a competitive process, the Office of the Associate Dean for Research in partnership with the Comparative Medicine Signature Program steering committee
Targeting energy metabolism in bulk tumor and CSC populations in human and feline oral cancer
Principal Investigator: Erin Dickerson, Dept.of Veterinary Clinical Sciences
Co-Investigators: Lester R. Drewes, Medical School, UMD, Timothy O'Brien, Veterinary Population Medicine, Michael S. Henson, Veterinary Clinical Sciences
Abstract: Oral squamous cell carcinoma (OSCC) is a devastating disease, which affects humans as well as companion animals. In humans, the high mortality and morbidity is primarily due to the anatomy of the disease site, which is close to vital blood vessels and nerves, diagnosis at an advanced stage of the disease, and tumor relapse due to drug resistance, which remains one of the most significant hurdles to treatment. Treatment resistance also is a problem in cats since the majority of OSCCs are poorly sensitive to radiation and chemotherapies. An improved understanding of the treatment resistance mechanisms used by OSCC is needed in both species in order to improve patient outcomes. In this proposal we will test the hypothesis that CSCs and non-CSCs from human and feline OSCCs display unique metabolic properties that allow their identification, and that targeting MCT1 will reduce the viability of CSCs, providing a more efficacious approach to therapy.
Cold atmospheric pressure plasma therapy for antibiotic-resistant chronic wound infections
Principal Investigator: Jennifer Granick, Dept. of Veterinary Clinical Sciences
Co-Investigators: Peter Bruggeman, Mechanical Engineering, Ryan Hunter, Microbiology
Abstract: Two percent of the US population has chronic non-healing wounds and their care exceeds $50 billion annually. Antibiotic-resistant wound infections are difficult to treat and can progress to more severe illness. The ideal therapy for chronic, infected wounds would be non-painful, bactericidal without risk of bacterial resistance, able to break-up biofilms and enhance wound healing. Cold atmospheric pressure plasma (CAP) is one such novel technology. It generates reactive oxygen and nitrogen species, which contribute to bacterial killing, cell proliferation and wound healing, and can be applied topically and controlled in time. Plasma is the fourth state of matter, and cold plasma can operate at room temperature and is non-painful to touch. The outcome of this study is expected to lead to a treatment procedure and design of an up-scaled version of a plasma-wound healing device for future large animal studies and clinical trials in humans. CAP has the potential to combine antiseptic and wound healing capabilities in a single treatment procedure and could eliminate the risk of cytotoxicity present in many current treatment methodologies.
TUDCA in the treatment of prion disease
Principal Investigator: Davis Seelig, Veterinary Clinical Sciences
Co-Investigators: Clifford Steer, Medicine, Gastroenterology, Susanta Hui, Medicine, Radiation Oncology, Chi Chen, College of Food, Agriculture, and Natural Re
Abstract:The prion diseases are a family of progressive and uniformly fatal neurodegenerative diseases that affect both humans and animals. In humans, the most common prion disease in Creutzfeldt-Jakob disease (CJD), which can be genetic, sporadic, or infectious in origin. There is currently no effective therapy for human prion disease and nearly all patients with CJD die within 14 months of their diagnosis. Similar to other neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases (AD and PD), the prion diseases are the result of the progressive accumulation of misfolded, insoluble protein within the brain. This accumulation of protein then initiates a cascade of destructive neuropathology culminating in terminal neurocognitive decline and dementia. While the mechanisms that link protein misfolding in the brain and a fatal neurodegenerative disease are not completely known, there is increasing evidence that the unabated activation of a cell stress response mechanism, denoted the unfolded protein response (UPR), plays an important role. We, and others, have shown that the therapeutic bile acid TUDCA (Tauroursodeoxycholic acid) protects cells against injury in a variety of neurodegenerative disorders, including mouse models of both AD and PD. The objective of the proposed work is to determine the efficacy of TUDCA as a prion disease therapeutic using a well-characterized mouse model that recapitulates all of the features of human prion disease.
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