論文名稱:

抽煙對口腔鱗狀上皮細胞癌之P53P16抑癌基因之影響

 

Alterations of p53 and p16 Tumor Suppressor Genes by Tobacco Smoking in Oral Squamous Cell Carcinoma

研究生:

李佩倫  Pei-Lun Li

 

(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

 

抽煙 

 

口腔鱗狀上皮細胞癌 

 

P53抑癌基因 

        論文頁數:

63

摘要:

p53抑癌基因對於癌生成的過程扮演重要角色,特別是在與抽煙有關的癌症上發現高 度的p53突變及過度表現發生。流行病學的證據顯示出,吸煙為口腔鱗狀上皮細胞癌最主要的危險因子之一,而p53突變極可能是口腔癌癌化之重要病因,為了探討抽煙是否即為p53突變之主因,本研究由藉由聚合%鏈反應/單股構行多行性及DNA讀序法,分析比較口腔鱗狀上皮細胞癌中與抽煙有關的次族群以及與抽煙無關的次族群其p53突變差異,以了解抽煙對p53基因的影響。本研究亦探討這兩個族群的患者之p16/MTS1/CDKN2的變化,以了解抽煙是否亦為此一抑癌基因變異的重要因子。結果顯示,21%(7/33)的口腔鱗狀上皮細胞癌有p53突變發生在表現子5-9之保留結構區內。與抽煙有關的口腔鱗狀上皮細胞癌次族群有較高比例p53突變(6/16),以G←→A轉同作用佔大部分:與抽煙無關的次族群P53突變較不明顯(1/17),卻集在表現子6內。p16/MTS1/CDKN2的突變率佔口腔鱗狀上皮細胞癌之12%(4/33),顯示在癌化的過程中,p16/MTS1/CDKN2所扮演的角色較p53不明顯。本研究結論,p53在口腔鱗狀上皮癌的癌化過程扮演重要角色,而抽煙為p53突變之重要原因之一。

   
 

It is known that p53 tumor suppressor gene play a significat role in the  process of carcinogenesis. In particular, a high incidence of p53 mutation and  protein overexpression has been shown in tabacco-related cancers. According to  epidemiological survey, cigarette smoking is one of the most risky factors for  the development of oral squamous cell carcinoma (OSCCs). To determine whether  smoking results in p53 alterations, this study analyze the difference of p53  mutaion between tabacco-related population and non-smoker's population in OSCC  by polyrnerase chain reaction/single strand conformation polymorphism  (PCR/SSCP). To determine whether smoking is also critical for pl6/MTS1/CDKN2  mutation, similar method was used to detect the pl6/MTS1/CDKN2 mutaion in 

these two subgroups. Twenty-one percent (7/33) of the OSCCs exhibited a  mutation in exon 5-9 of the p53 conserved region. A higher incidence (6/16) of  p53 mutations in tobacco-related OSCCs compared to those who had never used  tabacco (1/17) is noted. G to A or A to G transitions were the dominant  mutation in OSCCs from smoker population. There were only twelve percent (4/33) mutation rate of pl6/MTS1/CDKN2 in OSCCs indicating that a less importance  of pl6/MTS1/CDKN2 during carcinogenesis of OSCC. In conclusion, p53 plays  significant role in oral carcinogenesis, and tabacco use induces a specific  p53 mutation in OSCCs.