ABSTRACT
Sinonasal Undifferentiated Carcinoma (SNUC) is a very rare, highly aggressive malignant tumor of the nasal cavity and paranasal sinuses. SNUC tends to present with advanced-stage disease, often with intracranial invasion. It requires an aggressive multimodality therapy that includes surgical resection. A cure rate of less than 20% is generally reported in the literature, with most patients dying within 1 year of onset of the disease. Three patients diagnosed as SNUC were treated at the Yeungnam University Medical Center between the years 2000 and 2003 were analyzed retrospectively. All patients presented with the disease very advanced. The three cases were given chemotherapy or chemotherapy with radiotherapy. Two patients died of the disease, surviving only 6 and 11 months following treatment, respectively. We did a follow-up on just the one remaining case with incomplete controlled disease for 27 months. The overall prognosis of SNUC is very poor. We consider that more intensive multimodality therapies are recommended for all patients with SNUC.
Subject(s)
Humans , Academic Medical Centers , Carcinoma , Drug Therapy , Follow-Up Studies , Nasal Cavity , Paranasal Sinuses , Prognosis , Radiotherapy , Retrospective StudiesABSTRACT
BACKGROUND AND OBJECTIVES: Cyclooxygenase-2 (COX-2) is a key molecule in the biosynthesis of prostaglandins, which are important inflammatory mediators in human airway inflammatory diseases. This study was designed to investigate the effects of several COX inhibitors on the interleukin-1beta (IL-1beta)-mediated COX-2 expression in human airway epithelial cells. MATERIALS AND METHOD: We observed the effects of anti-inflammatory drugs such as budesonide, triamcinolone, dexamethasone, NS-398, indomethacin, salicylate and resveratrol on the IL-1beta-induced COX-2 expression in cultured human airway NCI-H292 epithelial cells. The levels of COX-2 mRNA and COX-2 protein were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: NS398, reveratrol and three corticosteroids strongly suppressed the IL-1beta-mediated COX-2 expression. However, indomethacin and salicylate did not inhibit or inhibited only weakly. CONCLUSION: The extent of IL-1beta-induced supression of COX-2 expression in the cultured human airway NCI-H292 epithelial cells depended on the kinds of anti-inflammatory drugs.
Subject(s)
Humans , Adrenal Cortex Hormones , Blotting, Western , Budesonide , Cyclooxygenase 2 , Dexamethasone , Epithelial Cells , Indomethacin , Interleukin-1 , Interleukin-1beta , Prostaglandin-Endoperoxide Synthases , Prostaglandins , RNA, Messenger , TriamcinoloneABSTRACT
BACKGROUND AND OBJECTIVES: Mucin gene expression and mucin production are highly increased during inflammatory airway disorders such as, asthma, chronic bronchitis and sinusitis. Cytokines, lipopolysaccharides and other inflammatory mediators are related with secretion and production of mucin. However, among of inflammatory mediators, the relation of leukotrienes and mucin genes expression is not clear. The aim of this study is to evaluate MUC2/5AC genes expression and mucin secretion through leukotriene receptor in human airway epithelial cells. SUBJECTS AND METHOD: The effect of Leukotriene D4 and leukotriene receptor antagonist, pranlukast hydrate (ONO-1078) on the regulation of MUC2/5AC gene expression and mucin secretion was observed in the human airway NCI-H292 epithelial cells. The mRNA levels of MUC2/5AC and the amount of mucin protein were determined by reverse transcription-polymerase chain reaction (RT-PCR) and immunoassay. RESULTS: Leukotriene D4 upregulated MUC2/5AC gene expression and mucin secretion on a dose dependent pattern. Pranlukast hydrate (ONO-1078, 100 micrometer) downregulated the leukotriene D4-mediated MUC2/5AC gene expression and mucin secretion. CONCLUSION: These results suggest that the leukotriene receptor system is one of the expression mechanisms of MUC2/5AC genes and mucin secretion.