Publications by authors named "Colby Shad Thaxton"

PIK-75 (F7) is a potent multikinase inhibitor that targets p110α, DNA-PK, and p38γ. PIK-75 has shown potential as a therapy in preclinical cancer models, but it has not been used in the clinic, at least in part, due to limited solubility. We therefore developed a nanoparticle to encapsulate PIK-75 and enable targeted cellular delivery.

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CpG oligodeoxynucleotides (CpGs) can induce an anti-tumor immune response, but also uniquely cause direct lymphoma cytotoxicity. To improve the delivery and efficacy of CpGs, we utilized a tri-ethylene modified CpG conjugated gold nanoparticle (tmCpG NP) platform that is compatible with both class B and class C CpGs, to treat various types of lymphoma, including diffuse large B cell lymphoma, high-grade lymphoma, Burkitt's lymphoma, and mantle cell lymphoma. Both classes of tmCpG NPs reduced viability of human and murine lymphoma cells via apoptosis compared with free CpGs, while having no toxic effects on dendritic cells.

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High-density lipoproteins (HDLs) are a diverse group of natural nanoparticles that are most well known for their role in cholesterol transport. However, HDLs have diverse functions that provide significant opportunities for cancer therapy. Presented is a focused review of the ways that synthetic versions of HDL have been used as targeted therapies for cancer, and as vehicles for the delivery of diverse therapeutic cargo to cancer cells.

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Introduction: RNA interference (RNAi) is a powerful mechanism for gene silencing with the potential to greatly impact the development of new therapies for many human diseases. Short interfering RNAs (siRNAs) may be the ideal molecules for therapeutic RNAi. However, therapeutic siRNAs face significant challenges that must be overcome prior to widespread clinical use.

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Objectives: Patients with rheumatoid arthritis (RA) have a reduced life expectancy due to increased cardiovascular disease. The lack of a suitable animal model resembling both RA and atherosclerosis has hindered studies demonstrating a direct link between systemic inflammation in RA and the development of atherosclerosis. Our objective was to overcome this barrier by generating an animal model (K/BxA(g7)) that spontaneously develops both RA-like disease and atherosclerosis.

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