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Background and Objectives@#A recent study revealed that calcitonin gene-related protein (CGRP) plays an important role in inflammatory airway diseases. However, the influence of CGRP on chronic rhinosinusitis (CRS) has not been studied. This study investigated the expression, activity, and potential pathogenic role of CGRP in patients with CRS with nasal polyposis (CRSwNP).Subjects and Method Patients with CRSwNP and control subjects were enrolled. The CRSwNP group was divided according to the presence of eosinophilic polyps and non-eosinophilic polyps. Nasal polyps (NPs) and uncinate tissues (UTs) from patients with CRSwNP and UTs from control subjects were obtained to investigate the expression of α-/β-CGRP and chromogranin A. In addition, the expression patterns of cytokines following exposure to exogenous CGRP were analyzed in dispersed nasal polyp cells (DNPCs) from patients with eosinophilic or non-eosinophilic CRSwNP. The effects of CGRP on lipopolysaccharide (LPS)-induced nuclear factor-kappa light chain enhancer of activated B cells (NF-κB) signaling change were evaluated in THP-1 cells. @*Results@#The expression of α-/β-CGRP and number of CGRP-producing cells were significantly higher in NPs from patients with CRSwNP than in UTs from controls. Exogenous CGRP decreased the expression of inflammatory cytokines and increased that of the anti-inflammatory cytokines in DNPCs from patients with eosinophilic nasal polyps (EPs) and also increased the expression of tissue remodeling-related and anti-inflammatory cytokines in DNPCs from patients with non-eosinophilic nasal polyps (N-EPs). CGRP inhibited the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (IκB) phosphorylation and NF-κB translocation in LPS-stimulated M1 macrophages. @*Conclusion@#CGRP expression in NPs may play a significant role in nasal polypogenesis through inflammatory modulation, and it could be a future target to modulate certain aspects of CRSwNP.
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With increasing prevalence of thyroid nodules, clinicians are increasingly impelled to identify the optimal predictor of thyroid cancer, with the goal of guiding management based on assessed risk. Fine-needle aspiration cytology is the gold standard diagnostic method for thyroid nodules. However, fine-needle aspiration cytology is not perfect and adjuncts which might complement its predictive value are being investigated from several innovative perspectives. For these vigorous efforts, remarkable advances have been achieved in understanding several major biologic areas of thyroid cancer, including the molecular alterations for loss of radioiodine avidity of thyroid cancer, the pathogenic role of the MAP kinase and PI3K/Akt pathways and their related genetic alterations in thyroid tumorigenesis and pathogenesis. These exciting advances provide unprecedented opportunities for development of molecular-based novel diagnostic and therapeutic strategies for thyroid cancer. The common somatic genetic changes in thyroid cancer of follicular cell origin (RET/PTC, NTRK, RAS, BRAF, PAX8-PPARgamma) are generally mutually exclusive, with distinct genotype-histologic subtype associations of thyroid cancer. Mutation analysis in fine needle aspiration samples has been applied to improve the diagnostic accuracy. In studies regarding gene expression profiling, aberrant gene methylation and miRNA have shown significant progress toward identification of biomarkers that could improve the accuracy of fine needle aspiration cytology in the evaluation of patients with thyroid nodule and prediction of disease aggressiveness. Future clinical trials evaluating the accuracy and cost-effectiveness of applying these biomarkers in the management of thyroid neoplasm should be considered.