Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/5859
DC FieldValueLanguage
dc.contributor林伯雄zh_TW
dc.contributorPo-Hsiung Linen_US
dc.contributor.author阮常新zh_TW
dc.contributor.authorJuan, Chamg-Hsinen_US
dc.contributor.other環境工程學系所zh_TW
dc.date2012en_US
dc.date.accessioned2014-06-06T06:35:53Z-
dc.date.available2014-06-06T06:35:53Z-
dc.identifierU0005-1607201216371400en_US
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dc.identifier.urihttp://hdl.handle.net/11455/5859-
dc.description.abstract本研究主要目的為探討台灣女性乳癌患者之乳癌風險因子,包括年齡、身體質量指數 (body mass index, BMI) 、去氧核醣核酸核酸修復 (DNA repair genes)及雌性激素代謝基因 (estrogen bioactivation genes)之多型性與去鹼基核酸背景值(abasic sites, AP sites)之相關性。研究結果顯示,67位乳癌患者AP sites背景值為 25.1 ± 16.1/106核苷酸 (平均 ± 標準偏差)。 乳癌患者之對偶基因變異 (variant alleles) 頻率,包括雌性激素代謝基因之基因多型性CYP1A1 T3801C、CYP1B1 Leu432Val與去鹼基核酸內切酵素(APE1 Asp148Glu)分別為29.9%、8.21% 與 46.3% 。綜合本實驗室先前所研究之81乳癌患者樣本共148位發現,在BMI < 27之乳癌患者其AP sites背景值較BMI ≧ 27之患者高約1.5倍(ρ<0.05),而此趨勢在年齡小於50歲且BMI小於27研究族群內更為明顯(高約三倍,ρ<0.05)。雌性激素代謝基因之基因多型性(CYP1A1、CYP1B1) 與AP sites背景值結果並無明顯之關聯性,但去氧核醣核酸修復基因之基因多型性(AP endonuclease 1, APE1 Asp148Glu)與AP sites背景值則發現Asp/Glu+Glu/Glu之變異基因型較Asp/Asp基因型高約兩倍(p<0.05)。利用多元線性迴歸可得知,當加入乳癌風險因子BMI與年齡時,AP sites之背景值於APE1變異基因型之患者較無變異患者高出1.63倍(p<0.05)。綜合上述研究結果可獲得之結論,乳癌風險因子年齡乳癌患者之AP sites背景值呈現負相關; 雌性激素代謝基因(CYP1A1、CYP1B1)之基因多型性與AP site無明顯關聯性; 去氧核醣核酸修復基因(APE1)之對偶基因變異型 (Asp/Glu + Glu/Glu)與乳癌患者AP sites背景值呈現正相關。zh_TW
dc.description.abstractThe objectives of this research were to investigate the associations of the risk factors of breast cancer, including body mass index (BMI), age, polymorphisms of genes involved in DNA repair and estrogen metabolism with the background levels of abasic sites (AP sites) in Taiwanese women with breast cancer. Results indicated that the background levels of AP sites (mean � SD) in breast cancer patients (n=67) were estimated to be 25.1 � 16.1 per 106 nucleotides. The frequencies of variant alleles of estrogen bio-activation genes, including CYP1A1 T3801C , CYP1B1 Leu432Val, and AP endonuclease (APE1 Asp148Glu) were estimated to be 29.9% , 8.21%, and 46.3%. We have found total of 148 breast cancer patients that participated in the 81 samples lab study. We noticed that a 1.5-fold increase in the number of AP sites was detected in patients with BMI<27 when compared to those with BMI>27. The tendency was more obvious in subjects with age<50 and BMI<27 (~3 fold). The genotypic polymorphisms of estrogen bioactivation genes (CYP1A1 and CYP1B1) did not correlate with the background levels of AP sites whereas the genotypic polymorphisms of DNA repair gene (APE1) was ~2 fold greater in patients with APE1 (Asp/Glu+Glu/Glu) genotype than in those with Asp/Asp genotype. Results from multiple linear regression indicated that a 1.63-fold increase in the number of AP sites was detected in patients with variant alleles Asp/Glu and Glu/Glu genotypes when compared to those with Asp/Asp genotype. In summary, we concluded that the risk factors of breast cancer, including BMI and age, were negatively correlated with the background levels of AP sites. Additionally, the genotypic polymorphisms of estrogen bio-activation gene (CYP1A1 and CYP1B1) were not correlate with the background levels of AP sites whereas the genotypic polymorphisms of DNA repair gene (APE1 Asp/Glu+Glu/Glu) with breast cancer positively correlated with level of AP sites in breast cancer patients of Taiwanese women.en_US
dc.description.tableofcontents目錄 摘要 I AbstractII 縮寫表 IV 目錄 VII 表目錄 IX 圖目錄 X 第一章 前言 1 第二章 文獻回顧 2 2.1 乳癌風險(Breast Cancer Risk)與乳癌風險因子(Breast Cancer Risk factors) 2 2.1.1 年齡(Age) 3 2.1.2 種族(Race) 3 2.1.3 身體質量指數(BMI) 4 2.1.4 家族乳癌病史(Family History ) 4 2.1.5 抽菸 5 2.2 雌性激素與其代謝途徑 5 2.3 雌性激素與乳癌風險 8 2.4 氧化DNA損害反應 8 2.5 去鹼基核酸((Apurinic/Apyrimidinic Sites,AP sites) 10 2.6 去氧核糖核酸之修復(DNA Repairs)機制 15 2.6.1 鹼基切除修復(Base excision repair,BER): 15 2.6.2 核苷酸切除修復(nucleotide excision repair,NER): 18 2.7 基因多型性(Genetic Polymorphism) 19 2.7.1 CYP1A1之功能及其基因多型性 19 2.7.2 CYP1B1之功能及其基因多型性 20 2.7.3 APE1之功能及其基因多型性 22 2.7.4 XRCC1之功能及其基因多型性 25 2.7.5 OGG1之功能及其基因多型性 26 第三章 實驗架構與設計 28 3-1 實驗架構 28 3-2 實驗設計 30 第四章 實驗材料與方法 31 4.1 實驗設備與材料 31 4.2 研究族群 33 4.3 實驗方法 34 4.3.1 全血分離 34 4.3.2 核酸萃取 35 4.3.3 核酸醛基損害分析方法 (Aldehyde Reactive Probe-Slot-Blot assay, ASB assay) 36 4.3.4 Putrescine-cleavage assay 37 4.4 單一核苷酸基因多型性 (Single Nucleotide Polymorphism, SNP) 38 4.4.1 CYP1A1 T3801C、CYP1B1 Leu432Val與APE1 Asp148Glu 38 4.4.2 聚合酵素鏈鎖反應 (Polymerase Chain Reaction, PCR)產物之定序確認 39 4.5 數據分析 44 第五章 實驗結果 45 5.1 方法偵測極限(method detection limit, MDL)與變異係數(coefficient of variation, C.V.) 45 5.2 Real-Time PCR與DNA之定序結果確認 46 5.3 乳癌患者之AP site背景值之分析結果 48 5.4 雌性激素代謝活化之基因多型性 48 5.5 去氧核醣核酸修復基因之基因多型性 50 5.6 乳癌風險因子: BMI、Age、基因多型性對於AP site之結果比較 50 5.7 氧化壓力對於AP sites背景值之影響 55 第六章 討論 56 6-1 AP sites與年齡 56 6-2 AP sites與BMI 57 6-3 雌性激素代謝基因之基因多型性 60 6-3-1 CYP1A1 T3801C 60 6-3-2 CYP1B1 Leu432Val 63 6-4 去氧核醣核酸修復基因之基因多型性 66 6-4-1 APE1 Asp148Glu 66 6-5 統計分析 70 第七章 結論與建議 73 7-1結論 73 7-2未來研究方向與建議 74 參考文獻 75zh_TW
dc.language.isozh_TWen_US
dc.publisher環境工程學系所zh_TW
dc.relation.urihttp://www.airitilibrary.com/Publication/alDetailedMesh1?DocID=U0005-1607201216371400en_US
dc.subjectDNA損害zh_TW
dc.subjectBiomarkeren_US
dc.subject單一核苷酸基因多型性zh_TW
dc.subjectDNA damageen_US
dc.subjectsingle nucleotide polymorphsimen_US
dc.title探討台灣女性乳癌患者之雌性激素代謝活化基因及去氧核醣核酸修復基因之單一核甘酸多型性與去氧核醣核酸損害之相關性zh_TW
dc.titleInvestigation of the Associations of Single Nucleotide Polymorphisms in Estrogen Bioactivation and DNA Repair Genes with DNA Damage in Taiwanese Women with Breast Canceren_US
dc.typeThesis and Dissertationzh_TW
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