Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment consisting of surgery and/or radiation therapy for patients with squamous cell carcinoma of the head and neck has frequently been successful in earlier stages of disease. Advanced and non-resectable tumor stages have a very poor cure rate. We initiated this trail to assess the role of the potentiation between cis-PDD and radiation previously reported in advanced head and neck tumors. Eighteen patients were investigated in this study. The treatment consisted of cis-PDD and hyperfractionated radiotherapy. Seventeen (94%) of the patients responded to the treatment regimen with either a complete regression (5/18 = 33%) or a partial regression (11/18 = 61%) of the tumor. Median survival was short and lasted 12+ months among complete responders and 8+ months among partial responders. However all patients did experience an increased and not tolerable incidence of delayed radiation toxicity such as mucositis combined with necrotic stomatitis. Both complications limited the compliance to the therapy. Because of these complications we had to stop the ongoing study.
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PMID:Radiosensitizing with cis-platin in advanced head and neck cancer. Results and problems. 269 49

Plasmacytoid dendritic cells (pDCs) secrete large amounts of IFN-alpha upon exposure to virus, subsequently promoting and regulating innate and adaptive immune responses. However, little is known about the functional regulation of virus-activated pDCs after they exert functions in secondary lymph organs. Our previous studies show that splenic stromal microenvironment can down-regulate the T cell response by inducing generation of regulatory myeloid dendritic cells; therefore, we wondered whether the splenic stromal microenvironment can regulate the function of virus-activated pDCs. In this study, we provide evidences that the splenic stromal microenvironment can chemoattract vesicular stomatitis virus (VSV)-activated pDCs via stromal cell-derived factor 1 (SDF-1), inhibit the secretion of IFN-alpha, IL-12, TNF-alpha, and expression of I-Ab, CD86, CD80, and CD40 by VSV-activated pDCs, and subsequently inhibit VSV-infected pDCs to activate NK cell IFN-gamma production and cytotoxicity. Stroma-derived TGF-beta participates in the negative regulation of VSV-activated pDCs. Therefore, we demonstrate that splenic stromal microenvironment negatively regulates the virus-activated pDCs through TGF-beta, outlining an additional mechanistic explanation for maintenance of immune homeostasis.
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PMID:Splenic stromal microenvironment negatively regulates virus-activated plasmacytoid dendritic cells through TGF-beta. 1829 17