Publications by authors named "Jonah R Riddell"

Article Synopsis
  • - Chronic inflammation contributes to a tumor-friendly environment, specifically in prostate cancer, by enhancing angiogenesis which is the formation of new blood vessels necessary for tumor growth.
  • - Peroxiredoxin 1 (Prx1) acts as a signaling molecule in prostate cancer, promoting inflammation and angiogenesis through its interaction with Toll-like receptor 4 (TLR4) and influencing the expression of vascular endothelial growth factor (VEGF).
  • - The study indicates a feedback loop where Prx1 increases the activity of both hypoxia-inducible factor-1 (HIF-1) and NF-κB, leading to higher VEGF expression, suggesting that targeting Prx1 could potentially slow tumor growth by disrupting this pro-angiogenic
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In recent years a number of studies have implicated chronic inflammation in prostate carcinogenesis. However, mitigating factors of inflammation in the prostate are virtually unknown. Toll-like receptor 4 (TLR4) activity is associated with inflammation and is correlated with progression risk in prostate cancer (CaP).

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Peroxiredoxin 1 (Prx1) is an antioxidant and molecular chaperone that can be secreted from tumor cells. Prx1 is overexpressed in many cancers, and elevation of Prx1 is associated with poor clinical outcome. In the current study, we demonstrate that incubation of Prx1 with thioglycollate-elicited murine macrophages or immature bone marrow-derived dendritic cells resulted in TLR4-dependent secretion of TNF-alpha and IL-6 and dendritic cell maturation.

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