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題名 | Lack of Correlation of Betel Nut Chewing, Tobacco Smoking, and Alcohol Consumption with Telomerase Activity and the Severity of Oral Cancer=口腔癌症病患之檳榔、煙、酒的食用習性與端粒脢活性及與臨床癌期缺乏相關性 |
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作 者 | 廖俊達; 陳一豪; 張東杰; 王宏銘; 謝玲玲; 鄭恩加; | 書刊名 | 長庚醫學 |
卷期 | 26:9 2003.09[民92.09] |
頁次 | 頁637-645 |
分類號 | 416.94 |
關鍵詞 | 口腔癌; 端粒脢; 檳榔; 癌症分期; Oral cancer; Telomerase activity; Betel nut; Cancer stage; |
語文 | 英文(English) |
中文摘要 | 背景:口腔癌是臺灣十大癌症之一,流行病學的研究顯示,口腔癌的發生率與檳榔、煙、酒的食用習性有關。近年來,研究又顯示端糖脢在癌化的過程中扮演一個重要角色,因此在本研究中,我們探應在口腔癌症病患中,檳榔、煙、酒的食用習性與臨床癌期及與端粒脢是否且有相關性。 方法:本研究中共有154位口腔癌症病患收錄參與,每位病患均取一小塊的正常口腔黏膜與癌化組織檢體來研究。端粒脢活性的檢測是以PCR-EIA的方法,而以Pearson chisquare的統計學方法來分析檳榔、煙、酒與臨床癌期或與端粒脢之相關性。 結果:病患中分別有86.4%要61.0%和83.3%有嚼食檳榔、喝酒及吸煙的習慣。在所有檢測的檢體中,80.5%的癌組織及3.2%的正常黏膜細胞程現陽性的端粒脢活性,但是統計學的研究顯示,臨床癌症或端粒脢活性的高低均與檳榔、煙、酒的食用習性(不論個別或結合習用)無關。 結論:過去的許多報告顯示,檳榔、煙及酒與口腔癌的發生率有密切相關,但本研究中卻顯示這些食用習性,與癌化程度或與端粒脢活性無統計相關,這些結果引申隱喻,這些食用習性也許只在口腔癌的癌化初期扮演某些角色,然而癌組織形成後期的繼續惡化,他許與環環因素較無相關,反之,更端賴於細胞分子本身。 |
英文摘要 | Backgorund: Oral cancer is one of most frequent cancers. A strong association has been found between oral cancer incidence and the use of betel nut, alcohol, and tobacco. Telomerase activity (TA) has also been shown to play a role in carcinogenesis. We therefore surveyed the consumption habits of betel nut chewing, alcohol drinking, and tobacco smoking in oral cancer patients and evaluated the association of these habits with TA level and clinical stage. Methods: In total, 154 oral cancer patients were recruited. TA was measured in paired (grossly normal and cancerous) tissues using a polymerase chain reactionbased enzyme immunoassay. Associations of these factors with clinical stage and TA level were analyzed using the Pearson chi-square test. Results: In these patients, 86.4%, 61.0% and 83.3% used betel nut, alcohol, and tobacco, respectively. For all tissue assayed, 80.5% of cancerous and 3.2% of grossly normal mucosae were positive for TA. However, neither clinical stage nor TA level in cancerous tissues had a statistical association with the use of individual substances (betel nut, alcohol, and tobacco) or their combined use. Conclusion: Even thought the habitual uses of these substances have been preciously reported to be associated with oral cancer incidence, we found a lack of correlation with TA level or with disease severity in our study. These results imply that these consumption habits might only be associated with the early stages of oral cancer development, while the later stages of cancer progression may be more associated with other external factors or dependent on host cellular factors, all of which require confirmation through further investigations. |
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