Publications by authors named "Shekha Tahsin"

Article Synopsis
  • Androgen Receptor (AR) activity in the prostate stroma is essential for maintaining a healthy prostate by promoting epithelial cell differentiation via morphogenic factors.
  • In aggressive prostate cancer, there is a loss of AR expression in the stroma, linked to tumor-secreted factors TGFβ1 and TNFα, which suppress AR mRNA and protein levels through the NF-κB signaling pathway, as well as p38-MAPK pathways.
  • Furthermore, the absence of AR leads to decreased production of key morphogens (FGF10 and Wnt16), disrupting normal prostate cell survival and epithelial homeostasis.
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Lack of adequate models significantly hinders advances in prostate cancer treatment, where resistance to androgen-deprivation therapies and bone metastasis remain as major challenges. Current models fail to faithfully mimic the complex prostate physiology. animal models can shed light on the oncogenes involved in prostate cancer development and progression; however, the animal prostate gland is fundamentally different from that of human, and the underlying genetic mechanisms are different.

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Autoantibodies play a major pathogenic role in rheumatoid arthritis. T follicular helper (Tfh) cells promote germinal center B cell and Ab responses. Excessive Tfh cell responses lead to autoimmunity, and therefore, counterregulation is crucial.

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An urgent need exists for the development of more efficacious molecular strategies targeting nonmelanoma skin cancer (NMSC), the most common malignancy worldwide. Inflammatory signaling downstream of Toll-like receptor 4 (TLR4) has been implicated in several forms of tumorigenesis, yet its role in solar UV-induced skin carcinogenesis remains undefined. We have previously shown in keratinocyte cell culture and SKH-1 mouse epidermis that topical application of the specific TLR4 antagonist resatorvid (TAK-242) blocks acute UV-induced AP-1 and NF-κB signaling, associated with downregulation of inflammatory mediators and MAP kinase phosphorylation.

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To maintain health, the immune system must maintain a delicate balance between eliminating invading pathogens and avoiding immune disorders such as autoimmunity and allergies. The gut microbiota provide essential health benefits to the host, particularly by regulating immune homeostasis. Dysbiosis, an alteration and imbalance of the gut microbiota, is associated with the development of several autoimmune diseases in both mice and humans.

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