• Title/Summary/Keyword: mucoepidermoid

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Postoperative Radiotherapy in Malignant Tumors of the Parotid Gland (이하선 악성종양의 수술 후 방사선 치료)

  • Chung Woong-Ki;Ahn Sung Ja;Nam Taek Ken;Chung Kyung-Ae;Nah Byung Sik
    • Radiation Oncology Journal
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    • v.16 no.3
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    • pp.251-258
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    • 1998
  • Purpose : This study was performed to analyze the factors affecting local control in malignant tumors of the parotid gland treated with surgery and postoperative radiation. Materials and methods : Twenty-six patients were treated for malignant tumors of the parotid gland from 1986 to 1995 at Department of Therapeutic Radiology, Chonnam University Hospital. Age of the patients ranged from 14 to 72 years (median : 55 years). Histologically 10 patients of mucoepidermoid carcinoma, 7 of squamous cell carcinoma, 4 of acinic cell carcinoma, 4 of adenoid cystic carcinoma and 1 of adenocarcinoma were treated. Total parotidectomy was performd in 15 of 26 patients, superficial in 7, subtotal in 4. Facial nerve was sacrificed in 5 patients. Postoperatively 4 patients had residual disease, 4 had positive resection margin. Radiation was delivered through an ipsilateral wedged pair of photon in 11 patients. High energy electron beam was mixed with photon in 15 patients. Electron beam dose ranged from 900 cGy to 3800 cGy (median 1700 cGy). Total radiation dose ranged from 5000 cGy to 7560 cGy (median : 6020 cGy). Minimum follow-up period was 2 years. Local control and survival rate were calculated using Kaplan-Meier method. Generalized Wilcoxon test and Cox proportional hazard model were used to test factors affecting local control. Results : Five (19$\%$) of 26 patients had local recurrence. Five year local control rate was 77$\%$. Overall five year survival rate was 70$\%$. Sex, age, tumor size, surgical involvement of cervical lymph node, involvement of resection margin, surgical invasion of nerve, and total dose were analyzed as suggested factors affecting local control rate. Among them patients with tumor size less than 4 cm (p=0.002) and negative resection margin (p=0.011) were associated with better local control rates in univariate analysis. Multivariate analysis showed only tumor size factor is associated with local control rate (p=0.022). Conclusion : This study suggested that tumor size is important in local control of malignant tumors of parotid gland.

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IP-10 Decreases TNF-α Induced MUC5AC Expression in Human Airway Epithelial Cells: a Possible Relation with Little Sputum Production in Idiopathic Pulmonary Fibrosis (IP-10에 의한 기도상피세포에서의 TNF-α 유도 MUC5AC발현 억제: 특발성폐섬유증 환자의 적은 객담과의 연관성)

  • Kim, Seung Joon;Kang, Chun Mi;You, Moon Bin;Yoon, Hyung Kyu;Kim, Young Kyoon;Kim, Kwan Hyoung;Moon, Hwa Sik;Park, Sung Hak;Song, Jeong Sup
    • Tuberculosis and Respiratory Diseases
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    • v.64 no.5
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    • pp.347-355
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    • 2008
  • Background: IPF is characterized by chronic, fibrosing inflammatory lung disease of unknown etiology. Typical symptoms of IPF are exertional dyspnea with nonproductive cough. Why patients with typical IPF have dry cough rather than productive cough, is unknown. IP-10 plays an important regulatory role in leukocyte trafficking into the lung. The present study investigated the effect of IP-10 in the pathogenesis of dry cough rather than productive cough in IPF patients. Methods: IP-10 concentration was measured by ELISA from BALF of IPF patients. To evaluate the role of IP-10 in mucin expression, the expression of the MUC5AC mucin gene was measured in NCI-H292 cells, a human pulmonary mucoepidermoid carcinoma cell line, after stimulation by TNF-${\alpha}$ with or without IP-10 pretreatment. EGFR-MAPK expression was also examined as a possible mechanism. Results: IP-10 levels were significantly higher in the BALF of IPF patients compared to healthy controls. IP-10 pretreatment reduced TNF-${\alpha}$ induced MUC5AC mucin expression by inhibiting the EGFR-MAPK signal transduction pathway in NCI-H292 cells. Conclusion: These findings suggest that little mucus production in IPF patients might be attributable to IP-10 overproduction, which inhibits the EGFR-MAPK signal transduction pathway required for MUC5AC mucin gene expression.