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研究生:廖國盟
研究生(外文):Liao Kuo Meng
論文名稱:台灣地區女性肺腺癌分子流行病學研究
論文名稱(外文):Molecular epidemiology of female lung adenocarcinoma in Taiwan
指導教授:陳建仁陳建仁引用關係
指導教授(外文):Chen Chien Jen
學位類別:博士
校院名稱:國立臺灣大學
系所名稱:流行病學研究所
學門:醫藥衛生學門
學類:公共衛生學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:英文
論文頁數:261
中文關鍵詞:肺癌病例對照研究吸菸台灣地區女性危險因子基因多形性油煙
外文關鍵詞:lung cancercase-control studycigarette smokingTaiwanfemalerisk factorgenetic polymorphismcooking fume
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背景: 肺癌是台灣女性之首要癌症死因。近三十年來,台灣男女性肺癌幾乎都增加八倍,是世界上增加最快的地區。性比例約保持在1.6-2.3,屬於世界最低的地區。女性肺癌病人只有9-10%吸菸,而族群中女性吸菸率僅3-4%。這些流行病學特徵都顯示除了主動吸菸外,應該還有其他危險因子扮演重要角色。烹飪油煙,二手菸,女性荷爾蒙,及遺傳易罹癌性都是可能的危險因子。
材料及方法:第一個研究是世代追蹤研究,其目的在於探討吸菸對台灣各種主要疾病之相對危險性及可歸因死亡人數。一共收案14,397名四十歲以上之男女,分別來自台灣的十二個鄉鎮,收案時間是1982-1986。主要收集香菸及其他重要危險因子之暴露狀態。追蹤時間至1994年為止。第二個研究是病例對照研究,主要探討台灣地區女性肺腺癌之可能危險因子。總共收案184名新發女性肺腺癌病例及350名健康對照。研究個案均接受結構式問卷訪談調查,其內容包括吸菸及二手菸暴露、烹飪油煙暴露、月經史、懷孕史、個人病史、及家族病史;並且探討各種易感受基因之多形性和女性肺腺癌之關係。本研究探討之基因多形性包括第一階段異物代謝酵素如細胞色素P4501A1、1A2、1B1、2C19及2E1;第二階段異物代謝酵素如GSTM1、GSTT1、GSTP1,NAT1、NAT2、EH及COMT;及女性荷爾蒙接受器及代謝酵素如CYP1A1、CYP17、CYP19、ESR及COMT。一共有147名新發女性肺腺癌及267名健康對照組接受基因型之鑑定。
結果:世代追蹤研究發現,吸菸會增加男性的全死因(RR=1.3)、所有癌症(RR=1.5)、胃癌(RR=1.9)、肝癌(RR=2.2)、肺癌(RR=3.7)、缺血性心臟病(RR=1.8)、其他心臟病(RR=1.4)及慢性阻塞性肺病(RR=1.9)的死亡危險性。抽菸會增加女性的全死因(RR=1.8)、肺癌(RR=3.6)及消化性潰瘍(RR=17.8)的死亡危險性。估計台灣一年死於吸菸者,男性約有8161人(13.9%),女性約有1216人(3.3%)。
病例對照研究發現,菸煙暴露(OR=2.0)、用動物油煮食 (OR=2.0)、口服避孕藥(OR=0.6)、女性荷爾蒙補充治療(OR=0.2)、身體質量指數BMI(OR=0.5)、及停經狀況(OR=9.8)都與女性肺腺癌有統計顯著相關。在第一階段異物代謝基因的複迴歸模式中,我們發現CYP1A2多形性(GG/GA vs. AA)有統計顯著意義(OR=6.5)。若將CYP1A1、CYP1A2、CYP2E1之危險基因型合併分析,其基因劑量效應也達邊際統計顯著水準(p=0.06)。若將吸菸、烹飪油煙、及危險基因多形性合併分析,則發現危險因子數目越多,女性肺腺癌危險性越高之顯著劑量效應關係。具備有上述三項危險因子者比三項危險因子皆無者,罹患女性肺腺癌的危險性高達20.8倍。在第二階段異物代謝酵素基因多形性的複迴歸分析中,我們發現COMT (Met/Met, Met/Val vs. Val/Val, OR=2.2)、EH (Tyr/Tyr vs. Tyr/His, His/His, OR=2.0) 與女性肺腺癌之相關達統計顯著水準。若將COMT、EH、GSTM1之危險基因型合併分析,發現擁有三項危險基因型者罹患女性肺腺癌的相對危險性高達三項危險基因型皆無者的11.7倍,同時呈現顯著之劑量效應關係(p<0.001)。基因及環境暴露之合併分析,也呈現統計顯著的劑量效應關係。在NAT1及NAT2的合併分析中,具有一或二個快速乙醯化基因型的人比兩者皆屬慢乙醯化基因型的人有較高的風險,其相對危險性高達8.4倍。在女性荷爾蒙接受器及代謝酵素基因多形性複迴歸分析中,我們發現COMT (Met/Met, Met/Val vs. Val/Val, OR=1.7)、CYP17 (A2/A2 vs. A1/A1, OR=2.2)均與女性肺腺癌有統計顯著相關。而COMT和CYP17之危險基因型對於女性肺腺癌具有加成到相乘之交互作用,且其交互作用會受到 BMI 及女性荷爾蒙暴露期間之修飾。
結論:在世代研究中,我們發現在台灣59%的男性肺癌可歸因於吸菸,但僅有10%的女性肺癌可歸因於吸菸,因此可能有其他之危險因子也會導致肺癌之發生。在病例對照研究中,我們發現二手菸及烹飪油煙仍然是重要的外在危險因子。然而本研究卻發現內源性及外源性之女性荷爾蒙濃度也會影響女性肺腺癌之發生。較高的女性荷爾蒙濃度,或較長期的女性荷爾蒙暴露均具有保護女性肺腺癌之作用。我們提出下列假說來解釋:「三十年來台灣女性肺腺癌之增加,主要導因於增加外在暴露(如烹飪油煙及二手菸)和華人較低的女性荷爾蒙濃度所產生之交互作用」。此交互作用之生理機轉有兩種可能性:(1)女性荷爾蒙在不同之濃度具有促進氧化或抗氧化之作用,進而修飾外在環境暴露之致癌作用。(2)環境暴露的許多物質會誘導CYP1A1、CYP1A2、CYP1B1等酵素活性,進而加速女性荷爾蒙之代謝。我們也發現CYP1A2、 NAT1、NAT2和女性肺腺癌之發生有較高的相關性,這結果強烈暗示著中式烹飪之油煙暴露中所產生的多環胺(heterocyclic amines, HAAs)及二手菸中的芳香胺( aromatic amines)是女性肺腺癌之主要致癌物。油煙所含多環胺會誘導CYP1A2在肺臟及肝臟之表現。使得多環胺臟肝臟或肺部經CYP1A2代謝,形成氮- 基多環胺( N-hydroxyl HAAs),然後在於肺部經由NATs 進行氧乙醯化(O-acetylation),最後形成 DNA鍵結物,而產生肺腺癌。我們發現COMT和CYP17對於女性肺腺癌之發生會呈現加成到相乘之交互作用,而且進一步受到 BMI 及女性荷爾蒙暴露時間之修飾。此結果與女性肺腺癌和荷爾蒙相關因子有顯著相關之結果一致,再次肯定女性肺腺癌與女性荷爾蒙有關。大規模的病例對照研究及家族研究可以朝此方向進行。
Background: Lung cancer is the leading cancer death among women in Taiwan since 1986. In Taiwan, the increasing secular trend of lung cancer mortality in past thirty years was highest in the world showing an eight-fold increase. The male-to-female ratio of lung cancer mortality in Taiwan was the lowest (1.6-2.3) compared with other countries. The prevalence of active cigarette smoking for lung cancer patients and general population in Taiwanese women was also the lowest in the world. These epidemiological findings suggest some risk factors other than active smoking may play a major role in the development of female lung adenocarcinoma in Taiwan. Cooking fumes exposure, passive tobacco smoke, hormonal factors, and genetic susceptibility were suspected factors.
Methods: In the first study, we examined the relative risk of dying from various diseases for cigarette smoking and annual mortality attributable to cigarette smoking in Taiwan. A cohort of 14,397 male and female residents aged 40 years or older recruited from 12 townships and precincts in Taiwan from 1982 to 1986. Information on cigarette smoking was collected from each subject at local health centers through a standardized personal interview based on a structured questionnaire. They were followed up regularly to determine their vital status until 1994. In the second study, we investigated the potential risk factors for female lung adenocarcinoma. We recruited a total of 184 incident female patients with lung adenocarcinoma from National Taiwan University Hospital and 350 healthy controls from hospital health examinees from National Taiwan University Hospital. Data on risk factors, including tobacco smoke exposure, cooking fume exposure, hormone-related risk factors, personal medical history and family history of lung cancer were obtained from standardized interview based on a structured questionnaire. In this study, we investigated the association with female lung adenocarcinoma for genetic polymorphisms of xenobiotic metabolism enzymes and estrogen receptor. The included phase I xenobiotic metabolism enzymes including CYP1A1, CYP1A2, CYP1B1, CYP2E1, CYP2C19; phase II xenobiotic metabolism enzymes including GSTM1, GSTT1, GSTP1, NAT1, NAT2, EH, COMT; and estrogen receptor and metabolism enzymes, including CYP1A1, CYP17, CYP19, ESR, and COMT. The genotyping was carried out on 148 incident cases of female lung adenocarcinoma and the 267 healthy controls.
Results: In the cohort study, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (RR= 1.3), cancer of all sites combined (RR = 1.5), stomach cancer (RR = 1.9), liver cancer (RR = 2.2), lung cancer (RR = 3.7), ischaemic heart disease (RR = 1.8), other heart diseases (RR = 1.4), and chronic obstructive pulmonary disease (RR = 1.9) among men. Among women, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (RR = 1.8), lung cancer (RR = 3.6), and peptic ulcer (RR = 17.8). The estimated number of deaths attributable to cigarette smoking in Taiwan was 8161 (13.9% of total deaths) for men and 1216 (3.3% of total deaths) for women.
In the case-control study, cooking with lard (OR=2.0), use of oral contraceptives (OR=0.6), hormone replacement therapy (OR=0.2), body mass index (OR=0.5), tobacco smoke exposure (OR=2.0), and menopause (OR=9.8) were all statistically significantly associated with lung adenocarcinoma in the multiple logistic regression analysis. Among phase I xenobiotic metabolism enzymes, only CYP1A2 was significantly associated with development of female lung adenocarcinoma (GG/GA vs. AA, OR=6.5). In the analysis of combinatory effects of high-risk genotypes of, CYP1A1, CYP1A2, and CYP2E1, a borderline significance was found (p test for trend=0.06) for the dose-response relationship. In further analysis of gene-environment interaction, women who had three putative high-risk environmental and genetic factors were strongly associated with lung adenocarcinoma (OR=20.8) compared with referent group with no high-risk factors. In the multiple logistic regression analysis of association with female lung adenocarcinoma for genetic polymorphisms of phase II xenobiotic metabolism enzymes, COMT (Met/Met, Met/Val vs. Val/Val OR=2.2), EH (Tyr/Tyr vs. Tyr/His, His/His, OR=2.0) were significantly associated with development of female lung adenocarcinoma. Those who had three high-risk genotypes of GSTM1, EH, and COMT had an 11.7-folds increase in risk of developing lung adenocarcinoma. There was a significant trend of female lung adenocarcinoma risk by the number of high-risk genotypes of GSTM1, EH, and COMT. A significant gene-environment interaction was also observed for phase II xenobiotic metabolism enzymes. Analysis of association between female lung adenocarcinoma and genetic polymorphisms of NAT1/NAT2, those who with one or two rapid acetylator genotypes of NAT1 and NAT2 had an 8.4-folds risk of female lung adenocarcinoma, compared with slow acetylator genotypes of both NAT1 and NAT2. In multiple logistic regression analysis of female hormone-related genetic polymorphisms, COMT (Met/Met, Met/Val, vs. Val/Val, OR=1.7), and CYP17 (A2/A2 vs. A1/A1) were significantly associated with female lung adenocarcinoma. There was an additive to multiplicative interaction between genetic polymorphisms of CYP17 and COMT on the development of female lung adenocarcinoma. The interactive effect of CYP17 and COMT was modified by body mass index and duration of female hormone exposure. There was a significant trend (p<0.005) of female lung adenocarcinoma by the number of high-risk genotypes of female hormone-related enzymes.
Conclusion: In the cohort study, we found that 59% of male lung cancers and only 10% of female lung cancers were attributable to cigarette smoking. Some risk factors other than cigarette might play an important role in the development of female lung adenocarcinoma in Taiwan. In the case-control study, we found both cooking fume and passive tobacco smoke were important external exposure associated with female lung adenocarcinoma. Furthermore, endogenous and exogenous hormone could also affect the risk for female lung adenocarcinoma. The high level of estrogen or long duration of estrogen exposure was protective factors for female lung adenocarcinoma. It is hypothesized that the increasing exposure to passive cigarette smoke and cooking fume during past thirty years might interact with endogenous hormonal factors to result in the growing epidemic of female lung adenocarcinoma in Taiwan. The etiological mechanisms of the interaction may include: 1) Estrogen might modify the carcinogenic effect of cooking fume and passive cigarette smoke through its pro-oxidant and anti-oxidant effects. The predominance of effects of lipid peroxidation or free radical scavenger depends on the level of catechol estrogen. 2) Carcinogens from cooking fume and passive cigarette smoke might act as an inducer of CYP1A1, 1A2, and 1B1. The induction might facilitate the metabolism of estrogen. In the analysis of genetic polymorphisms of xenobiotic metabolism enzymes, CYP1A2, NAT1, and NAT2 were associated with the risk of lung adenocarcinoma. The results suggest that heterocyclic amines from cooking fumes or aromatic amines from passive cigarette smoke, which are metabolized by CYP1A2 and NATs, are major carcinogens for lung adenocarcinoma. The heterocyclic amines inhaled from cooking fume may induce CYP1A2 expression in lung tissue. Initially, the heterocyclic amines were metabolized by CYP1A2 to form N-hydroxyl heterocyclic amines in the liver or lung. They may then be O-acetylated by NATs in the lung tissue, and form DNA adducts finally. Genetic polymorphisms of CYP17 and COMT were found to interact additively to multiplicatively in development of female lung adenocarcinoma, and the interactive effect was modified by BMI and hormone exposure period. The findings are compatible with the hypothesis that female lung adenocarcinoma is a hormone-related cancer.
目錄
中文摘要……………………………………………………………1
英文摘要……………………………………………………………5
第一章: 肺癌之流行病學特徵、危險因子及防治策略…………11
中文摘要…………………………………………………12
英文摘要…………………………………………………13
前言………………………………………………………14
世界各國之肺癌流行病學特徵特徵……………………14
台灣之肺癌流行病學特徵………………………………16
肺癌之危險因子…………………………………………17
防治策略…………………………………………………26
總結及展望………………………………………………33
參考文獻…………………………………………………35
圖表………………………………………………………45
第二章: 台灣地區吸菸對各主要疾病可歸因死亡之世代追蹤研究:
12年追蹤結果…………………………………………51
英文摘要…………………………………………………52
前言………………………………………………………54
材料及方法………………………………………………56
結果………………………………………………………61
討論………………………………………………………65
參考文獻…………………………………………………73
圖表………………………………………………………75
第三章: 台灣地區女性肺腺癌之危險因子………………………85
英文摘要…………………………………………………86
前言………………………………………………………89
材料及方法………………………………………………93
結果………………………………………………………98
討論………………………………………………………104
參考文獻…………………………………………………119
圖表………………………………………………………123
第四章: 台灣地區女性肺腺癌之分子流行病學研究: 第一階段異物代謝酵素基因多形性………………137
英文摘要…………………………………………………138
前言………………………………………………………140
材料及方法………………………………………………145
結果………………………………………………………150
討論………………………………………………………154
參考文獻…………………………………………………167
圖表………………………………………………………171
第五章: 台灣地區女性肺腺癌之分子流行病學研究: 第二階段異物代謝酵素基因多形性………………177
英文摘要…………………………………………………178
前言………………………………………………………180
材料及方法………………………………………………186
結果………………………………………………………191
討論………………………………………………………195
參考文獻…………………………………………………208
圖表………………………………………………………214
第六章: 台灣地區女性肺腺癌之分子流行病學研究: 女性荷爾蒙接受器及代謝酵素基因多形性………223
英文摘要…………………………………………………224
前言………………………………………………………226
材料及方法………………………………………………231
結果………………………………………………………236
討論………………………………………………………240
參考文獻…………………………………………………250
圖表………………………………………………………253
1.Kenneth S, Jan S. Lung cancer- a worldwide health problem. Chest, 96 (suppl): 1s-4s, 1988.
2.Parkin DM, Pisani P, Ferlay J. Estimate of the worldwide incidence of eighteen major cancers in 1985. Int J Cancer, 54: 594-606, 1993.
3.World Health Organization. The World Health Organization histological typing of lung tumors. Second Edition. Am J Clin Pathol, 77: 123-136, 1981.
4.Koo LC, Ho JH-C. Worldwide epidemiological patterns of lung cancer in nonsmokers. Int J Epidemiol, 19 (suppl): s14-s23, 1990.
5.Yang SP, Luh KT, Kuo SH, et al. Chronological observation of epidemiological characteristics of lung cancer in Taiwan with etiological consideration- A 30-year consecutive study. Jpn J Clin Oncol, 14(1): 7-19, 1984.
6.陸坤泰, 張登斌. 台灣的肺癌.台灣醫誌, 91卷附冊1: s1-s7, 1992.
7.Higginson J, Muir CS, Munoz N. Human Cancer: Epidemiology and Environmental Causes. Cambridge University Press, 333-345, 1992.
8.Aronchick JM. Lung Cancer: Epidemiology and risk factor. Sem Roetgenol, 25: 5-11, 1990.
9.Parkin DM, Muir CS, Whelon, et al. Cancer incidence in five continents. Vol 6. Lyon: International Agency for Research on Cancer, 1992.
10.Mumford JL, He XZ, Chapman RS, et al. Lung cancer and indoor air pollution in Xuan Wei, China Science, 235: 217-220, 1987.
11.Zang EA, Wynder EL. Differences in lung cancer risk between men and women: Examination of the evidence. J Natl Cancer Inst, 88: 183-92, 1996.
12.Devesa SS, Blot WJ, Fraumeni JF, et al. Declining lung cancer among young men and women in the United States: a cohort analysis. J Natl Cancer Inst, 81: 1568-71, 1991.
13.Tay SC, Tsai SF, Lee SS, et al. Lung cancer in Taiwan. Natl Public Health Assoc (ROC), 8 (3): 189-201, 1988.
14.Lin CC. A study of lung cancer in Taiwan. Jpn J Chest Dis, 7:1593-1603, 1963 (in Japanese).
15.Luh KT, Kuo SW, Lin CC, et al. Primary lung cancer in Taiwan. J Formosan Med Assoc, 73:129-146, 1974.
16.Lee LT, Lee WC, Lin RS, et al. Age-period-cohort analysis of lung cancer mortality in Taiwan, 1966-1990. Anticancer Res, 14: 673-676, 1994.
17.蕭光明.台灣地區肺癌之流行病學特徵. 臨床醫學, 29: 347-352, 1992.
18.Redmond DE. Tobacco and cancer: The first clinical report, 1761. N Eng J Med, 282:18-23, 1970.
19.Ochsner A, DeBakey ME. Primary pulmonary malignancy treatment by total pneumonectomy: Analysis of 79 collected cases and presentation of 7 personal cases. Surg Gynecol Obstet, 68: 435, 1939.
20.Doll R, Hill AB. Mortality in relation to smoking: Ten years of observations of British doctors. Br Med J, 1: 1399-1410, 1460-1467, 1964.
21.Wynder EL, Graham EA. Tobacco smoking as a possible etiologic factor in bronchogenic carcinoma: a study of 654 proved cases. J Am Med Assoc, 143: 329-336, 1950.
22.US Public Health Service. The health consequences of smoking: Cancer. A Report of the Surgeon General, Rockville, Maryland: US DHHS, Public Health Service, Office on Smoking and Health, 1982.
23.International Agency for Research on Cancer. IARC Monographs on the evaluation of carcinogenic risks of chemicals to humans: Tobacco smoking. Vol 38. Lyon: International Agency for Research on Cancer, 1986.
24.Doll R, Peto R. Cigarette smoking and bronchial carcinoma: dose and time relationships among regular smokers and lifelong non-smokers. J Epidemiol Community Health, 32: 303-313, 1987.
25.Chen CJ, Wu HY, Chuang YC, et al. Epidemiological characteristics and multiple risk factors of lung cancer in Taiwan. Anticancer Res, 10: 971-976, 1990.
26.Akiba S, Kato H, Blot WJ. Passive smoking and lung cancer among Japanese women. Cancer Res, 46: 4804-4807, 1986.
27.Wynder EL. Strategies toward the primary prevention of cancer. Arch Surg, 125: 163-169, 1990.
28.Hirayama T. Non-smoking wives of heavy smokers have a higher risk for lung cancer: A study from Japan. Br Med J, 282: 183-185, 1981.
29.Trichopoulos D, Kalandidi A, Sparros L, et al. Lung cancer and passive smoking. Int J Cancer, 27: 1-4, 1981.
30.Garfinkel L. Time trends in lung cancer mortality in non-smokers and a note on passive smoking. J Natl Cancer Inst, 66: 1061-1066, 1981.
31.Correa P, Pickle LW, Fontham E, et al. Passive smoking and lung cancer. Lancet, 2: 595-597, 1983.
32.Wu AH, Henderson BE, Pike MC, et al. Smoking and other risk factors for lung cancer in women. J Natl Cancer Inst, 74: 747-751, 1985.
33.Garfinkel L, Auerbach O, Joubert L. Involuntary smoking and lung cancer: A case-control study. J Natl Cancer Inst, 75: 463-469, 1985.
34.Koo LC, Ho JH, Saw D. Is passive smoking an added risk factor for lung cancer for Chinese women? J Exp Clin Cancer Res, 3: 277-283, 1984.
35.Wynder EL, Muscat JE. The changing epidemiology of smoking and lung cancer histology. Environ Health Perspect, 103 (suppl 8): 143-148, 1995.
36.National Research Council. Environmental tobacco Use: Measuring the exposure and assessing health effects. Report from committee on passive smoking. Washington: National Academy Press, 1986.
37.Ger LP, Hsu WL, Chen KT, et al. Risk factors of lung cancer by histological category in Taiwan. Anticancer Res, 13: 1491-1500, 1993.
38.Liu ZY. Smoking and lung cancer in China combined analysis of eight case-control studies. Int J Epidemiol, 21: 197-201, 1992.
39.Finkelstein M, Kusiak R, Suranyi G. Mortality among miners receiving workwomen‘s compensation for silicosis in Ontario: 1940-1975. J Occup Med, 24: 663-667, 1982.
40.Doll R. Mortality from lung cancer in asbestos workers. Br J Ind Med, 12: 81-86, 1989.
41.Selikoff IJ, Hammond EC. The occurrence of asbestosis among insulation workers in the US. Ann NY Acad Sci, 132: 139-155, 1965.
42.Bogovski P, Gilson JC, Timbrell V, et al. Biological effects of asbestos proceeding of a working conference held at the IARC. Lyon: IARC Scientific Publication No 8, 1972.
43.Selikoff IJ, Hammond EC, Churg J. Asbestos exposure, smoking and neoplasm. J Am Med Assoc, 204: 106-112, 1968.
44.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Man-made Mineral Fibers and Radon. Vol 43. Lyon: International Agency for Research on Cancer, 1988.
45.Wilkinson P, Hansell DM, Janssens J, et al. Is lung cancer associated with asbestos exposure when there are no small opacities on the chest radiograph? Lancet, 345: 1074-1078, 1995.
46.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Overall evaluations of carcinogenicity: an updating of IARC Monographs. Vol 1 to 42, supplement 7. Lyon: International Agency for Research on Cancer, 1987.
47.Chiou HY, Hsueh YM, Liaw KF, et al. Incidence of internal cancers and ingested inorganic arsenic: A seven -year follow-up study in Taiwan. Cancer Res, 55: 1296-1300, 1995.
48.Chen CJ, Wu MM, Lee SS, et al. Atherogenicity and carcinogenicity of high -arsenic artesian well water: multiple risk factors and related malignant neoplasms of blackfoot disease. Arteriosclerosis, 8: 452-460, 1988.
49.Horng SF, Liaw KF, Lin LJ, et al. A cohort study on lung cancer in the endemic area of Blackfoot disease. Chin J Public Health (Taipei), 14 (1): 32-40, 1995.
50.Easton DF, Peto J, Doll R. Cancers of the respiratory tract in mustard gas workers. Br J Ind Med, 45: 652-659, 1988.
51.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Chromium, nickel and molding. Vol 53. Lyon: International Agency for Research on Cancer, 1990.
52.Doll R. Cadmium in the human environment. Lyon: International Agency for Research on Cancer, 459-464, 1982.
53.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Silica and some silicates. Vol 42. Lyon: International Agency for Research on Cancer, 1987b.
54.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Wood dust and formaldehyde. Vol 62. Lyon: International Agency for Research on Cancer, 1995.
55.International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Polycyclic aromatic hydrocarbon. Vol 34. Lyon: International Agency for Research on Cancer, 1988.
56.Axelson D, Andusso K, Desai G, et al. Indoor radon exposure and active and passive smoking in relation to occurrence of lung cancer. Scan J Work Environ Health, 14: 286-292, 1988.
57.UNSCEAR. Sources, effects and risks of ionizing radiation. New York: United Nations, 1988.
58.NRC Committee on the Biological Effects of Ionizing Radiation. Health risks of radon and other internally deposited alpha-emitters. Washington: National Academy Press, 1988.
59.WolBach SB. Effects of vitamin A deficiency and hyper-vitaminosis A in animals. Vol 1, Academic Press, New York, 106-137, 1954.
60.Khanduja KL, Koul IB, Gandhi RB, et al. Effect of combined deficiency of fat and vitamin A on N-nitrosodiethylamine-induced lung carcinogenesis in mice. Cancer Lett, 62: 57-62, 1992.
61.Bjelke E. Dietary vitamin A and human lung cancer. Int J Cancer, 15: 561-565, 1975.
62.Shekelle R, Lepper M, Liu S, et al. Dietary vitamin A and risk of cancer in the western electric study. Lancet, 2: 1185-1190, 1981.
63.Kvale G, Bjelke E, Gart JJ. Dietary habits and lung cancer risk. Int J Cancer, 31: 397-405, 1983.
64.Mettlin C, Graham S, Swanson M. Vitamin A and Lung cancer. J Natl Cancer Inst, 62: 1435-1438, 1979.
65.Kolonel LN, Nomura AMY, Hinds MW, et al. Role of diet in cancer incidence in Hawaii. Cancer Res, 43 (suppl): 2397s-2402s, 1983.
66.Samet JN, Skipper BJ, Humble CG, et al. Lung cancer risk and vitamin A consumption in New Mexico. Am Rev Respir Dis, 131: 198-202, 1985.
67.Ziegler RG, Mason TJ, Stemhagen A, et al. Dietary carotene and vitamin A and the risk of lung cancer among white man in New Jersey. J Natl Cancer Inst, 73: 1429-35, 1984.
68.Wald N, Idle M, Borcham J, et al. Low serum vitamin A and subsequent risk of cancer risk: Preliminary results of a prospective study. Lancet, 2: 813-815, 1980.
69.Nomura AMY, Stemmermann GN, Heilbrun LK, et al. Serum vitamin level and the risk of cancer of specific sites in men of Japan ancestry in Hawaii. Cancer Res, 45: 2369-2372, 1985.
70.Willet WC, Polk BF, Underwood BA, et al. Relation of serum vitamin A and E and carotenoids to the risk of cancer. N Engl J Med, 310: 430-434, 1985.
71.Menkes MS, Comstock GW, Vuilleunier JP, et al. Serum b-carotene, vitamin A and E, selenium, and the risk of lung cancer. New Engl J Med, 315: 1250-1254, 1986.
72.Pastorino U, Pisani P, Berrino, et al. Vitamin A and female lung cancer: A case-control study on plasma and diet. Nutr Cancer, 10: 171-179, 1987.
73.Salonen JT, Salonen R, Lappetelainen R. Risk of cancer in relation to serum concentrations of selenium and vitamin A and E: Matched case-control analysis of prospective data. Br Med J, 290: 417-420, 1985.
74.Kune GA, Kune S, Waston LF, et al. Serum level of b-carotene, vitamin A, and zinc in male lung cancer cases and controls. Nutr Cancer, 12: 169-176, 1989.
75.Byers T, Vena J, Mettlin C, et al. Dietary vitamin A and lung cancer risk: An analysis by histology subtype. Am J Epidemiol, 120: 769-776, 1984.
76.Koo LC. Dietary habits and lung cancer risk among Chinese females in Hong Kong who never smoke. Nutr Cancer, 11: 155-172, 1989.
77.Gonzalae FJ, Jaiswal AK, Nebert DW. P450 genes: Evolution, regulation and relationship to human cancer. In Cold Spring Harbor Symposia on quantitative biology: Molecular Biology of Homo sapiens, 51: 879-890.
78.Shields PG, Sugimura H, Caporaso NE, et al. Polycyclic aromatic hydrocarbon-DNA adducts and the CYP1A1 restriction fragment length polymorphism. Environ Health Perspect, 98: 191-4, 1992.
79.Nakachi K, Imai K, Hayashi S, et al. Genetic susceptibility to squamous cell carcinoma of the lung in relation to cigarette smoking dose. Cancer Res, 51 (19): 5177-80, 1991.
80.Nakachi K, Imai K, Hayashi S, et al. Identification of genetically high risk individuals to lung cancer by DNA polymorphisms of the cytochrome P4501A1 gene. FEBS Lett, 263: 131-133, 1990.
81.Nakachi K, Imai K, Hayashi S, et al. Genetic linkage of lung cancer-associated MspI polymorphisms with amino acid replacement in the heme binding region of the human cytochrome P4501A1 Gene. J Biochem, 110: 407-411, 1990.
82.Alexandrie AK, Sundberg MI, Seidegard J, et al. Genetic susceptibility to lung cancer with special emphasis on CYP1A1 and GSTM1: A study on host factors in relation to age at onset, gender and histological cancer types. Carcinogenesis, 15 (9): 1785-90, 1994.
83.Kawajiri K, Nakachi K, Imai K, et al. Germ line polymorphisms of p53 and CYP 1A1 genes involved in human lung cancer. Carcinogenesis, 14 (6): 1085-9, 1993.
84.Nakachi K, Imai K, Hayashi S, et al. Polymorphisms of the CYP1A1 and glutathione S-transferase genes associated with susceptibility to lung cancer in relation to cigarette dose on a Japanese population. Cancer Res, 53 (13): 2994-9, 1993.
85.Anttila S, Hietanen E, Vainio H, et al. Smoking and peripheral type of cancer are related to high levels of pulmonary cytochrome P450Ia in lung cancer patients. Int J Cancer, 47: 681-685, 1991.
86.McLemore TL, Adelberg S, Liu MC, et al. Expression of CYP1A1 Gene in patients with lung cancer: Evidence for cigarette smoke-induced gene expression in normal lung tissue and for altered gene regulation in primary pulmonary carcinoma. J Natl Cancer Inst, 82: 1333-1339, 1990.
87.Taioli E, Crofts F, Trachman J, et al. A specific African-American CYP1A1 polymorphisms is associated with adenocarcinoma of the lung. Cancer Res, 55: 472-473, 1995.
88.Ayesh R, Idle JR, Ritchie JC, et al. Metabolic oxidation phenotypes as markers for susceptibility to lung cancer. Nature, 312: 109-110, 1984.
89.Hayashi S, Watanabe J, Kawajiri K, et al. Genetic polymorphisms in 5’-flanking region change transcriptional regulation of the human cytochrome P450 2E1 gene. J Biochem, 110: 559-565, 1991.
90.Hackl H. Ungtuberkulose und Bronchuskarinom. Tuberkuloscarzt, 13: 643, 1959.
91.Bobrowitz ID, Elkin M, Evans JC, et al. Effect of direct irradiation on the course of pulmonary tuberculosis using cancerocidal doses. Dis Chest, 40: 397, 1961.
92.Lee LT. Epidemiologic characteristics of pulmonary tuberculosis and association between pulmonary tuberculosis and lung cancer in Taiwan. Doctor thesis, Graduate Institute of Public Health, National Taiwan University, p225, 1993.
93.Rimington J. Smoking, chronic bronchitis, and lung cancer. Br J Med, 2: 373, 1971.
94.Christensen PH, Joergenson K, Munk J, et al. Hyper-frequency of pulmonary cancer in a population of 415 patients treated for laryngeal cancer. Laryngoscope, 97: 612-614, 1987.
95.Chan TK, Conrado P, Rom WN. Bronchogenic carcinoma in young patients at risk for acquired immunodeficiency syndrome. Chest, 103: 862-864, 1993.
96.Gao YT, Blot WJ, Wei Z, et al. Lung cancer among Chinese women. Int J Cancer, 40: 604-609, 1987.
97.Li S. Analysis of polycyclic aromatic hydrocarbons in cooking oil fumes. Arch Environ Health, 49 (2): 119-122, 1994.
98.Chaudhuri PK, Thomas PA, Walker MJ, et al. Steroid receptors in human lung cancer cytosols. Cancer Letters, 16: 327-332, 1982.
99.Doll R, Peto R. The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst, 66 (6): 1193-1261, 1981.
100.US Public Health Service. The health consequences of smoking: cancer. A report of the Surgeon General. Rockville, Maryland: US DHHS, Public Health Service, 1992.
101.Liaw KM, Chen CJ. Mortality attributable to cigarette smoking in Taiwan: a 12-year follow-up study. Tob Control, 7:141-148, 1998.
102.US Public Health Service. The health benefits of smoking cessation: A report of the Surgeon General. Rockville, Maryland: US DHHS, Public Health Service, 1990.
103.Samet JM. Health benefits of smoking cessation. Clin Chest Med, 12: 673, 1991.
104.Schwartz JL. Methods of smoking cessation. Med Clin North Am, 76(2): 451-476, 1992.
105.Mckenna JP, Cox JL. Transdermal nicotine replacement and smoking cessation. Am Fam Phys, 45 (6): 2595-2601, 1992.
106.Richmond RL, Anderson P. Research in general practices for smokers and excessive drinkers in Australia and the U.K. I. Interpretation of results. Addiction, 89: 35-40, 1994.
107.Richmond RL, Anderson P. Research in general practices for smokers and excessive drinkers in Australia and the U.K. II. Representativeness of the results. Addiction, 89: 41-47, 1994.
108.Richmond RL, Anderson P. Research in general practices for smokers and excessive drinkers in Australia and the UK. III. Dissemination of Interventions. Addiction, 89: 49-62, 1994.
109.Mulshine JL, Tockman MS, Smart CR. Considerations in the development of lung cancer screen tools. J Natl Cancer Inst, 81: 900-906, 1989.
110.Saccomanno G, Archer VE, Auerbach O, et al. Development of carcinoma of the lung as reflected in exfoliated cells. Cancer, 33: 256-270, 1974.
111.Frost JK, Ball WC, Levin ML, et al. Early lung cancer detection: Results of the initial radiologic and cytologic screen in the Johns Hopkins Study. Am Rev Respir Dis, 130: 549-554, 1984
112.Melamed MR, Flehinger BJ, Zaman MB, et al. Screen for early lung cancer: Results of the Memorial Sloan-Kettering Study in New York. Chest, 86: 44-53, 1984
113.Fontana RS, Sanderson DR, Taylor WF, et al. Early lung cancer detection: Results of the initial radiologic and cytologic screen in the Mayo Clinic Study. Am Rev Respir Dis, 130: 561-565, 1984.
114.Ebeling K, Nischan P. Screen for lung cancer: Results from a case-control study. Int J Cancer, 40: 141-144, 1987.
115.Kubik A, Parkin DM, Khlat M, et al. Lack of benefit from semi-annual screening for cancer of the lung: Follow-u p report of a randomized controlled trial on a population of high- risk males in Czechoslovakia. Int J Cancer, 45: 26-33, 1990.
116.Strauss GM, Cleason RE, Sugarbaker DJ. Chest X-ray screening improves outcome in lung cancer. Chest, 107 (suppl): 270s-279s, 1995.
117.Tockman MS, Gupta PK, Mayers JD, et al. Sensitive and specific monoclonal antibody recognition of human lung cancer antigen on preserved sputum cells: A new approach to early lung cancer detection. J Clin Oncol, 6: 1685-1693, 1988.
118.Slebos RJC, Rodenhuis S. The ras gene family in human non-small cell lung cancer. J Natl Cancer Inst, 13: 23-29, 1992.
119.Wong AJ, Ruppert JM, Eggleston J, et al. Gene amplification of c-myc and N-myc in small cell cancer of the lung. Science, 233: 461-464, 1986.
120.Kern JA, Schwartz DA, Nordberg JE, et al. p185neu expression in human lung adenocarcinoma predicted shortened survival. Cancer Res, 50: 5184-5191, 1990.
121.Harbour JW, Lai SL, Whang PJ, et al. Abnormalities in structure and expression of human retinoblastoma gene in the SCLC. Science, 241: 353-357, 1988.
122.Takahashi T, Nau MM, Chiba I, et al. p53: A frequent target for genetic abnormalities in lung cancer. Science, 246: 491-494, 1989.
123.Whang PJ, Kao-Shan CS, Lee EC, et al. Specific chromosome defect associated with human small cell lung cancer: Deletion 3p (14-23). Science, 215: 181-182, 1982.
124.Sozzi G, Miozzo M, Donghi R, et al. Deletion of 17p and p53 mutation in preneoplastic lesions of the lung. Cancer Res, 52: 6079-6082, 1992.
125.Guttita F, Carney DN, Mulshine J, et al. Bombesin-like peptides can function as autocrine growth factors in human small cell lung cancer. Nature, 316: 823-826, 1988.
126.Lam S, Palcic B, McLean D, et al. Detection of early lung cancer using low dose photofrin II. Chest, 97: 333-337, 1990.
127.Palcic B, Lam S, Hung J, et al. Detection and localization of early lung cancer by imaging techniques. Chest, 99: 742-743, 1991.
128.Sporn MB, Dunlop NM, Newton DL, et al. Prevention of chemical carcinogenesis by vitamin A and its synthetic analogs (retinoids). Fed Proc, 35: 1332-1338, 1976.
129.Slaughter DP, Southvick HW, Smejkal W. Field cancerization in oral stratified squamous epithelium- clinical implications of multicentric origin. Cancer, 6: 963-968, 1953.
130.Farber E. The multistep nature of cancer development. Cancer Res, 44: 4217-4223, 1984.
131.Itri LM. Cancer Chemoprevention. Cancer, 72: 3374-3380, 1993.
132.Morse MA, Stoner GD. Cancer chemoprevention: principles and prospects. Carcinogenesis, 14 (9): 1737-1746, 1993.
133.de Vries N, van Zandwijk N, Pastorino U. The Euroscan study. Br J Cancer, 64: 985-989, 1991.
134.Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta-carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med, 334:1150-5, 1996.
135.Alpha-tocopherol, beta-carotene cancer prevention study group. N Engl J Med, 330: 1029-35, 1994.
136.Hennekens CH, Buring JE, Manson JE, et al. Lack of effect of long-term supplementation with beta-carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med, 334: 1145-9, 1996.
137.Blot WJ, Li JY, Taylor PR, et al. Nutrition intervention trials in Linxian, China. J Natl Cancer Inst, 85: 1483-92, 1993.
138.US Public Health Service. Smoking and health: A report of the Surgeon General. Rockville, Maryland: US DHHS, Public Health Service, Office on Smoking and Health, 1979.
139.US Public Health Service. Reducing the health consequences of smoking: A report of the Surgeon General. Rockville, Maryland: US DHHS, Public Health Service, Office on Smoking and Health, 1989.
140.Kuller LH. Cigarette smoking and mortality. Prev Med, 20: 638-654, 1991.
141.DeMorais SMF, Wilkinson GR, Blaisdell J, Meyer UA, Goldstein JA. The major genetic defect responsible for the polymorphism of (S)-mephenytoin metabolism of humans. J Biol Chem, 269: 15419-15422, 1994.
142.Tsuneoka Y, Fukushima K, Matsuo Y, Ichikawa Y, Watanabe Y. Genotype analysis of the CYP2C19 gene in the Japanese population. Life Science, 59: 1711-1715, 1996.
143.Nakajima M, Yokoi T, Mizutani M, Kinoshima M, Funayama M, Kamataki T. Genetic polymorphism in the 5’ flanking region of the human CYP1A2 gene effect on the CYP1A2 inducibility in humans. J Biochem, 125: 803-808, 1999.
144.Hanna IH, Dawling S, Roodi N, Guengerich FP, Parl FF. Cytochrome P450 1B1 (CYP1B1) pharmacogenetics: association of polymorphisms with functional differences in estrogen hydroxylation activity. Cancer Res. 60(13): 3440-4, 2000.
145.Bailey LR, Roodi N, Dupont WD, Parl FF. Association of cytochrome P450 1B1 (CYP1B1) polymorphism with steroid receptor status in breast cancer. Cancer Res, 58: 5038-5041, 1998.
146.Felgelson HS, Shames LS, Pike MC, et al. Cytochrome p450c17α gene (CYP17) polymorphism is associated with serum estrogen and progesterone concentrations. Cancer Res, 58: 585-587, 1998.
147.Felgelson HS, Coetzee GA, Kolonel LN, et al. A polymorphism in the CYP17 gene increases the risk of breast cancer. Cancer Res, 57: 1063-1065, 1997.
148.Dunning AM, Pharoah PDP, Foster NA, et al. No association between a polymorphism in the steroid metabolism gene CYP 17 and risk of breast cancer. Br J Cancer, 77: 2045-2047, 1998.
149.Brodie A, Lu Q, Nakumura J. Aromatase in the normal breast and breast cancer. J Steroid Biochem Mol Biol, 61: 281-286, 1997.
150.Kristensen VN, Andersen TI, Lindblom A, et al. A rare CYP19 (aromatase) variant may increase the risk of breast cancer. Pharmacogenet, 8: 43-48, 1998.
151.Haiman CA, Hankinson SE, Speizer FE, Hunter DJ. A tetranucleotide repeat polymorphism in CYP19 and breast cancer risk. Proc Am Assoc Cancer Res, 40: 194, 1999.
152.Cascorbi I, Brockmöller J, Mrozikiewicz PM, Bauer S, Loddenkemper R, Roots I. Homozygous rapid arylamine N-acetyltransferase (NAT2) genotype as a susceptibility factor for lung cancer. Cancer Res., 58: 3961-3966, 1996.
153.Hou SM, Ryberg D, Falt S, Deverill A, Tefre T, Borresen AL, Haugen A, Lambert B. GSTM1 and NAT2 polymorphisms in operable and non-operable lung cancer patients. Carcinogenesis, 21(1): 49-54, 2000.
154.Seow A, Zhao B, Poh WT, The M, Eng P, Wang YT, Tan WC, Lee EJ, Lee HP. NAT2 slow acetylator genotype is associated with increased risk of lung cancer among non-smoking Chinese women in Singapore. Carcinogenesis, 20(9): 1877-81, 1999.
155.Bouchardy C, Mitrunen K, Wikman H, Husgafvel-Pursiainen K, Dayer P, Benhamou S, Hirvonen A. N-acetyltransferase NAT1 and NAT2 genotypes and lung cancer risk. Pharmacogenetics, 8 (4): 291-8, 1998.
156.Wu X, Gwyn K, Amos CI, Makan N, Hong WK, Spitz MR. The association of microsomal epoxide hydrolase polymorphisms and lung cancer risk in African-Americans and Mexican-Americans. Carcinogenesis, 22 (6): 923-8, 2001.
157.Benhamou S, Reinikainen M, Bouchardy C, Dayer P, Hirvonen A. Association between lung cancer and microsomal epoxide hydrolase genotypes. Cancer Res, 58: 5291-5293, 1998.
158.Lavigne JA, Helzlsouer KJ, Huang HY, et al. An association between the allele coding for a low activity variant of catechol-O-methyltransferase and the risk of breast cancer. Cancer Res, 57: 5493-5497, 1997.
159.Thompson PA, Shield PG, Freudenheim JL, et al. Genetic polymorphisms in the catechol-O-methyltransferase, menopausal status, and breast cancer risk. Cancer Res, 58: 2107-2110, 1998.
160.Fugua SA, Chamness GC, McGuire WL. Estrogen receptor mutations in breast cancer. J Cell Biochem, 51: 135-139, 1993.
161.Andersen TI, Heimdal KR, Skrede M. et al. Estrogen receptor (ESR) polymorphisms and breast cancer susceptibility. Hum Genet, 94: 665-670, 1994.
162.Watanabe M, Ushijima T, Shiraishi T, Yatani R, Shimazaki J, Kotake T, Sugimura T, Nagao M. Genetic Alterations of Androgen Receptor Gene in Japanese Human Prostate Cancer. Jpn J Clin Oncol, 389-393, 1997.
163.Ruth ML, Ronald GL, Hsien LL, et al. XRCC1 polymorphisms: effect on aflatoxin B1-DNA adducts and glycophorin A variant frequency. Cancer Res, 59: 2557-2561, 1999.
164.Pierce AJ, Johnson RD, Thompson LH, et al. XRCC3 promotes homology-directed repair of DNA damage in mammalian cells. Gene Development, 13:2633-2638, 1999.
165.Benachenhou N, Guiral S, Gorska-Flipot I, et al. High resolution deletion mapping reveals frequent allelic losses at the DNA mismatch repair loci hMLH1 and hMSH3 in non-small cell lung cancer. Int J Cancer, 77: 173-180, 1998.
166.Office of population census and surveys. “Occupational Mortality. The Registry General’s Decennial supplement for England and Wales, 1970-72”. Her Majesty’s Stationary. Office, London, 1978.
167.MacLennan R, Da Costa J, Day NE, et al. Risk factors for lung cancer in Singapore Chinese, a population with high female with high female incidence rate. Int J Cancer, 20: 854-860, 1977.
168.Ko YC, Lee CH, Chen MJ, et al. Risk factors for primary lung cancer among non-smoking women in Taiwan. Int J Epidemiol, 26: 24-31, 1997.
169.Ko YC, Cheng-Li SC, Lee CH, et al. Chinese food cooking and lung cancer in nonsmoking women. Am J Epidemiol, 15:140-147, 2000.
170.Chiang TA, Wu PF, Wang LF, et al. Mutagenicity and polycyclic aromatic hydrocarbon content of fumes from heated cooking oils produced in Taiwan. Mutat Res, 381: 157-161, 1997.
171.Wu PF, Chiang TA, Ko YC, Lee H. Genotoxicity of fumes from heated cooking oils produced in Taiwan. Environ Res Section A, 80: 122-126, 1999.
172.Wu PF, Chiang TA, Wang LF, Chang CS, Ko YC. Nitro-polycyclic aromatic hydrocarbon contents of fumes from heated cooking oils and prevention of mutagenicity by cetechin. Mutat Res, 403: 29-34, 1998.
173.Beattle CW, Hansen NW, Thomas PA. Steroid receptors in human lung cancer. Cancer Res: 45, 4206-4214, 1985.
174.Cagle PT, Mody DR, Schwartz MR. Estrogen and progesterone receptors in bronchogenic carcinoma. Cancer Res: 50, 6632-6635, 1990.
175.Ollayos CW, Riodan GP, Rubin JM. Estrogen receptor detection in paraffin sections of adenocarcinomas of colon, pancreas, and lung. Arch Pathol Lab Med: 118, 630-632, 1994.
176.Canver CC, Memoli VA, Vanderveer PL, et al. Sex hormone receptors in non-small cell lung cancer in human beings. J Thorac Cardiovas Surg: 108, 153-157, 1994.
177.Su JM, Hsu HK, Chang H, et al. Expression of estrogen and progesterone receptors in non-small cell lung cancer: immunohistochemical study. Anticancer Res: 16, 3803-3806, 1996.
178.Kaiser U, Hofmann J, Schilli B, et al. Steroid-hormone receptors in cell lines and tumor biopsies of human lung cancer. Int J Cancer: 67, 357-364, 1996.
179.Taioli E, Wynder EL. Endocrine factors and adenocarcinoma of the lung in women. J Natl Cancer Inst, 86: 869-870, 1994.
180.Adami HO, Persson I, Hoover R, et al. Risk of cancer in women receiving hormone replacement therapy. Int J Cancer: 44, 833-839, 1989.
181.Sellers TA, Potter JD, Folsom AR. Association of incident lung cancer with family history of female reproductive cancers: The Iowa women’s health study. Genet Epidemiol: 8, 199-208, 1991.
182.Noronha RFX, Goodal CM. Enhancement by testosterone of dimethylnitrosamine carcinogenesis in lung, liver, and kidney of inbed NZR/Gd female rats. Carcinogenesis: 4, 613-616, 1983.
183.Risch HA, Howe GR, Jain M. Are female smoker at higher risk for lung cancer than male smokers? A case-control analysis by histologic type. Am J Epidemiol, 138: 281-293, 1993.
184.Lippman SM, Lee JJ, Karp DD, et al. Randomized phase III intergroup trial of isotretinoin to prevent second primary tumors in stage I non-small-cell lung cancer. J Natl Cancer Inst, 93(8): 605-618, 2001.
185.Wang YC, Lee HS, Chen SK, Yang SC, Chen CY. Analysis of K-ras gene mutations in lung carcinomas: correlation with gender, histological subtypes, and clinical outcome. : J Cancer Res Clin Oncol, 124(9): 517-22, 1998.
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1. 13.林永泰,1994,塑膠袋、容器裝食品之殺菌,食品工業,26 (3):24-33。
2. 10.吳錦祥、吳清得,1998,馬口鐵生產技術與馬口鐵罐優點簡介,食品市場資訊,8710:17-26
3. 9.吳全耀、吳黃素月、趙熹、鄭昌家,1994,田口式品質工程在食品加工上的應用─文蛤軟糖的製造,中國水產,493:29-40。
4. 6.李榮輝,2001,可殺菌軟袋之殺菌技術,食品工業,33(1):56-64。
5. 14.林永泰,1995,塑膠罐頭之開發,食品工業,27 (3):41-48。
6. 16.胡棟宏,1989,高真空裝罐技術簡介,食品工業,21 (1):25-32。
7. 17.高馥君,1992,反應曲面在食品開發上的應用,食品工業,24(3): 32-41。
8. 21.許玉芳、林文雄,1998,品質工程之田口式實驗設計,建國學報,17:427-443
9. 22.陳和賢、黃卓治、謝政峰、王志源,2000,應用田口品質工程於蛋黃酥桿捲製程改進之研究,臺灣農業化學與食品科學,38 (3):214-222。
10. 23.陳和賢、王志源,2001,灰色田口法應用於蛋黃酥油酥皮生產最佳化之研究,技術學刊,16(4):549-556
11. 24.陳勵生,2001,類神經網路應用於機台參數設定,機械工業,214:131-143。
12. 27.詹彩鑾,1993,簡介金屬塑膠複合罐,中華食品工業,15:48-53。
13. 32.萬一怒、盛中德、楊智超、何榮祥,1998,胴裂米以類神經網路檢測之研究,農業工程學報,44(1):67-80。
14. 方煒。1994。水牆設計與使用。農業機械學刊 3: 57-70。
15. 王鼎盛。1990。開放式畜舍內輻射量之模擬。農業工程學報36: 78-86。
 
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