論文名稱:

台灣地區口腔鱗狀上皮癌之p53抑癌基因突變

 

THE MUTATION OF p53 TUMOR SUPPRESSOR GENE IN ORAL SQUAMOUS CELL CARCINOMA OF TAIWAN

研究生:

葉政憲  Cheng-Hsien Yeh

 

(以作者名查詢陽明大學館藏系統)

 

(以作者名查詢全國圖書書目資訊網)

指導教授:

張國威  Kuo-Wei Chang

        學位類別:

碩士

        學校名稱:

國立陽明大學

系所名稱:

口腔生物研究所

          學年度:

84

          語文別:

中文

          出版年:

85

關鍵字:

牙醫  DENTIST

 

牙醫學  DENTISTRY

 

口腔  ORAL-HEALTH

 

口腔鱗狀上皮癌 

 

p53抑癌基因 

        論文頁數:

42

摘要:

近年來,p53抑癌基因之突變在癌化過程所扮演之角色日趨明朗。口腔鱗狀上皮癌為 我國極重要之癌症之一,其年發生率居男性癌症之第五位,與嚼檳榔及抽煙有關。研究顯示不同地域之口腔鱗狀上皮癌有其不同之分子病理變異,可能是病因不同之反映。國人之口腔鱗狀上皮癌之p53抑癌基因是否有特殊性至今仍無報導,本研究探討台北及台中榮總牙科50例之口腔鱗狀上皮癌病患標本之p53變異;以基因擴大術/單鏈構形/分析/殖株/讀序(PCR/SSCP/CLONING/SEQUENCING)作基因分析,並以免疫組織化學染色(IMMUNOHISTOCHEMISTRY)探討基因產物之表現,結果發現國人口腔鱗狀上皮癌之p53變異之特性:ぇ台灣地區口腔鱗狀上皮癌患者p53之突變率為26.0%,但只抽煙不吃檳榔與既抽煙又吃檳榔兩群患者之p53突變發生率並無統計上之差異:え密碼子277282為國人口腔鱗狀上皮癌p53突變之好發位置;ぉ本研究度確定p53變與過度表現之相關性,然而亦有高比例p53免疫組織化學染色呈陽性之病性並非導因於此基因之突變。

   
 

In the past years, the role that the mutation of p53 tumor suppressor gene  involved during turnorigenesis became clear. Oral squamous cell carcinoma (OSCC) is the fifth common malignancy in male population in Taiwan. Researches  on gene alteration in OSCC that associated with different oral habits revealed  difference of pathogenesis, which might be the reflections of different  causes. There is no report on the status of p53 tumor suppressor gene in the  OSCC of Taiwan. The purpose of this research is to analyze the p53 status in  fifty OSCC from Taipei and Taichnug Veteran's General Hospital (VGH). We used  polyrnerase chain reaction (PCR)/single strand conformation polymorphism (SSCP)/Cloning/Sequencing to do gene analysis, and immunohistochemistry to  detect the presence of gene product. We concluded that: (1) the p53 mutation  rate in the OSCC of Taiwanese is 26.0%; there is no difference in p53 mutation  between the betel nut chewer and smoker versus smoker only subpopulation. (2)  Codons 277 & 282 tend to be a preferred site for p53 mutation. (3) This study  reassured the fact that p53 missense mutation can cause overexpression,  however, over-expression is not essentially caused by mutation.