Publications by authors named "O C Chen"

The current opioid crisis urgently calls for developing non-addictive pain medications. Progress has been slow, highlighting the need to uncover targets with unique mechanisms of action. Extracellular adenosine alleviates pain by activating the adenosine A1 receptor (A1R).

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Primary hypoalphalipoproteinemia is typically caused by genetic disorders and is characterized by low high-density-lipoprotein cholesterol (HDL-C). Low HDL-C has been proposed to confer an increased risk of atherosclerotic cardiovascular disease; however, a causal relationship has not been determined. We describe the case of an otherwise healthy and asymptomatic 37-year-old woman with severely low HDL-C who was found to have significant coronary artery disease in whom genetic testing supported a diagnosis of Tangier disease.

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Article Synopsis
  • - Drug resistance in EGFR-mutant non-small cell lung cancer (NSCLC) is complicated by mechanisms like pathway reactivation and fusion of receptor tyrosine kinases (RTKs), leading to challenges in treatment with tyrosine kinase inhibitors (TKIs).
  • - A study involving multiple institutions analyzed 27 patients with RTK fusions identified through genetic testing, focusing on their response to dual TKI therapy, with results showing a 24% objective response rate and an 80% disease control rate overall.
  • - The majority of patients had ALK or RET fusions, and those who received dual TKI treatment had a slightly lower response rate (21.4%) but no new side effects were reported, suggesting this approach
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A critical host response against viral infections entails the activation of innate immune signaling that culminates in the production of antiviral proteins. DNA viruses are sensed by the cytosolic pattern recognition receptor cyclic GMP-AMP synthase (cGAS), which initiates a signaling pathway that results in production of proinflammatory cytokines such as Interferon-β (IFN-β) and activation of the antiviral response. Precise regulation of the antiviral innate immune response is required to avoid deleterious effects of its overactivation.

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