Publications by authors named "E O Major"
Dysregulation of the expression levels and the activity of kinases/phosphatases is an intrinsic hallmark of tumor transformation and progression, as either as a primary cause or consequence. The myosin phosphatase (MP)/protein arginine methyltransferase 5 (PRMT5)/histone (H4) pathway is an oncogenic signaling pathway downregulating the gene expression of tumor suppressors. However, the upstream regulators of the pathway are unknown.
View Article and Find Full Text PDFObjective: To investigate the benefits of topical 8% capsaicin patches for the decrease of postsurgical neuropathic pain level and area.
Methods: A systematic review with pooled analysis was conducted utilizing the PRISMA 2020 guidelines. Five commonly used databases were employed utilizing a search string made from MeSH terms and boolean operators.
As tumor-associated macrophages (TAM) exercise a plethora of protumor and immune evasive functions, novel strategies targeting TAMs to inhibit tumor progression have emerged within the current arena of cancer immunotherapy. Activation of the mannose receptor 1 (CD206) is a recent approach that recognizes immunosuppressive CD206high M2-like TAMs as a drug target. Ligation of CD206 both induces reprogramming of CD206high TAMs toward a proinflammatory phenotype and selectively triggers apoptosis in these cells.
View Article and Find Full Text PDFArticle Synopsis
- Immune checkpoint inhibitors (ICIs) are effective for treating metastatic melanoma, but about 50% of patients show poor responses, often linked to low HLA-DR levels in tumors.
- The study highlights how lysophosphatidic acid (LPA), abundant in melanoma, increases IL-10 release and negatively impacts HLA-DR expression through the LPAR1-DR6 pathway.
- A significant correlation was found between the expression of LPAR1, DR6, and IL-10 in melanoma tissues, suggesting this pathway may contribute to tumor cells' ability to evade immune detection and compromise ICI therapy effectiveness.
Progressive multifocal leukoencephalopathy is a rare but devastating demyelinating disease caused by the JC virus (JCV), for which no therapeutics are approved. To make progress towards addressing this unmet medical need, innovations in clinical trial design are needed. Quantitative JCV DNA in CSF has the potential to serve as a valuable biomarker of progressive multifocal leukoencephalopathy disease and treatment response in clinical trials to expedite therapeutic development, as do neuroimaging and other fluid biomarkers such as neurofilament light chain.
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