江苏省恶性肿瘤低发区食管癌危险因素研究

[目的]探讨江苏省恶性肿瘤低发地区食管癌发病的有关危险因素及保护因素.[方法]在江苏省恶性肿瘤低发的赣榆地区进行了食管癌1:1配对病例对照研究,共调查病例与对照各95例,应用条件Logistic回归对相关因素进行单因素和多因素分析.[结果]热烫饮食(OR=2.066,95%CI=1.116～3.828)、饮酒(OR=3.206,95%CI=1.866～5.509)为该地区食管癌发病的主要危险因素,而生吃大蒜(OR=0.423,95%CI=0.209～0.856)、喜食蔬菜(OR=0.485,95%CI=0.267～0.881)、喜食干果(OR=0.333,95%CI=0..168～0.660)和性格开朗(OR=0.469,95%CI=0.254～0.866)则为该地区食管癌的主要保护因素.[结论]在江苏肿瘤低发区热烫饮食、饮酒仍是食管癌的危险因素,而生吃大蒜、蔬菜、干果和性格开朗是保护因素.     

中国妇女行为危险因素与子宫颈癌发病关系的Meta分析

目的:应用Meta分析法研究行为因素在中国妇女子宫颈癌发病中的危险性。方法:用Review Manger 5.0对国内8篇最近文献的病例-对照研究结果进行固定(FEM)或随机效应模型(REM)的定量综合分析。结果:各因素合并比值比OR(95%CI)分别为:首次性交年龄<20岁,OR=2.32(1.41~3.80);首次怀孕年龄≤21岁,OR=2.96(1.36~6.42);孕次>3,OR=1.93(1.13~3.31);性伴侣数>2,OR=2.18(1.24~3.84);绝经,OR=2.62(1.76~3.91);主动或被动吸烟,OR=2.33(1.46~3.70);教育程度≤9年,OR=3.34(1.53~7.28)。结论:多行为因素Meta分析证实,首次性交年龄<20岁、首次怀孕年龄≤21岁、孕次>3、性伴侣数>2、绝经、主动或被动吸烟及教育程度≤9年与子宫颈癌的发生有关,是子宫颈癌发病的危险因素。而首次性交年龄20~22岁或≥23岁、首次生育年龄≤21岁、产次>2、口服避孕药及居住地与子宫颈癌发病无相关。     

IGF-1和IGFBP-3基因多态性与前列腺癌易感性的相关性

目的探讨中国人群中IGF-1和IGFBP-3多态性与前列腺癌易感性的相关性。方法采用以医院为基础的病例对照研究模式,应用Taq Man探针法对IGF-1和IGFBP-3的9个SNPs进行基因分型,检测664例患者和702例对照者的基因型,分层分析与前列腺癌发生有关的可能因素。结果前列腺癌组和对照组进行比较时,rs6218,rs35767和rs5742612的基因型和等位基因频率分布存在显著差异(P=0.005、0.005和0.020)。在综合分析中,具有2~6个风险等位基因的个体患前列腺癌的风险显著高于具有0~1个风险等位基因的个体。研究还发现,组合风险等位基因与前列腺癌风险之间的关联主要表现在以下几组:年龄71岁(OR=1.41,95%CI=1.05~1.91,P=0.020),不吸烟(OR=1.68,95%CI=1.21~2.32,P=0.002),不喝酒(OR=1.32,95%CI=1.02~1.61,P=0.002),前列腺癌家族史(OR=1.28,95%CI=1.02~1.71,P=0.022)。结论在中国人群中,3个单核苷酸多态性(rs6218,rs35767和rs5742612)和具有2~6个风险等位基因的联合基因型可能与前列腺癌的易感性相关,而与前列腺癌的进展无关。     

乙醇脱氢酶2和乙醛脱氢酶2基因多态性及饮酒习惯与直肠癌易感性的研究

目的:研究乙醇脱氢酶2(ADH2)、乙醛脱氢酶2(ALDH2)基因多态性与直肠癌易感性的关系。方法:采用病例-对照研究方法,以PCR-DH-PLC检测研究对象的ADH2/ALDH2基因型,比较不同的基因型及生活习惯与直肠癌的关系。结果:1)与不饮酒者相比较,饮酒者患直肠癌的危险性显著增高(OR=2.20,95%CI:1.47～3.28,P=0.000);2)多因素分析结果未发现ADH2、ALDH2各基因型与直肠癌的危险性有关。3)对ADH2、ALDH2基因多态相互作用的分层分析发现,同时携带ADH2A/A和ALDH2G/G基因型者,发生直肠癌的危险性显著增高(性别、年龄和吸烟调整OR=1.82,95%CI:1.07～3.09)。4)在饮酒者中,ADH2A/A、A/G G/G基因型者患直肠癌的调整OR分别为2.56(95%CI:1.38～4.73)和2.10(95%CI:1.15～3.84);ALDH2G/G基因型者发生直肠癌的调整OR为1.82(95%CI:1.07～3.09)。结论:饮酒是直肠癌的危险因素;ADH2A/A与ALDH2G/G基因型在增加直肠癌易感性上有协同作用;ALDH2G/A A/A基因型可减弱饮酒患直肠癌的危险性。     

福建省贲门癌发病因素的病例对照研究

 目的　探讨贲门癌发生的危险因素。方法采用病例对照研究方法 ,研究对象 5 82例 ,其中贲门癌新病例 2 91例 ,对照 2 91例。应用统一制订的调查表进行流行病学调查。对资料进行单因素和多因素Logistic回归分析。 结果　贲门癌的危险因素有 :三餐不按时 (OR =1.4 4,95 %CI :1.15 1.81)、进食快 (OR=1.4 0 ,95 %CI :1.0 9 1.80 )、食用猪油 (OR =1.6 7,95 %CI :1.19 2 .35 )、饮用井水 (OR =1.90 ,95 %CI :1.2 7 2 .84 )、吸烟 (OR =1.2 8,95 %CI :1.0 5 1.5 8)和家庭肿瘤史 (OR =3.15 ,95 %CI :1.97 5 .0 4 )。常吃新鲜蔬菜(OR =0 .5 3,95 %CI :0 .2 8 0 .99)、水果 (OR =0 .75 ,95 %CI :0 .5 6 1.0 0 )、牛奶 (OR =0 .5 2 ,95 %CI :0 .2 9 0 .93)及文化程度高者 ,其胃癌发生风险低。结论　本研究首次发现不良的饮食方式是贲门癌的危险因素 ,对...     

非吸烟女性肺癌危险因素的研究

背景与目的肺癌是世界上一个重大的公共卫生问题,在我国肺癌是大中城市中恶性肿瘤的第一死因,且发病率和死亡率增长迅速。其中女性肺癌死亡率正逐年上升,而病例中以非吸烟者占多数,其危险因素尚不清楚。本研究通过流行病学调查来研究女性肺癌发生的危险因素。方法采用以医院患者为基础的病例-对照研究方法,包括女性肺癌患者618人,对照872人,进行流行病学调查。内容包括人口特征、被动吸烟史、烹饪油烟暴露史、燃料种类、煤烟暴露、亲属患癌史、职业史与饮食史等。结果女性肺癌患者与对照组比较,儿童时期被动吸烟(OR=1.81,95%CI=1.46~2.24)、烹饪油烟暴露(OR=3.18,95%CI=2.55~3.97)、煤烟暴露(OR=2.56,95%CI=1.83~4.55)、肺部疾病史(OR=1.80,95%CI=1.43~2.27)、肺结核史(OR=1.63,95%CI=1.31~2.03)、肿瘤家族史(OR=2.09,95%CI=1.46~3.00)和肺癌家族史(OR=2.46,95%CI=1.55~3.90)是危险因素。结论本研究显示儿童时期被动吸烟、烹饪油烟暴露、煤烟暴露、肺部疾病史、肺结核史及肿瘤或肺癌家族史是非吸烟女性肺癌的危险因素。     

预防直肠癌术后吻合口瘘发生的循证护理

目的:探讨国内直肠癌术后吻合口瘘的危险因素,为直肠癌患者术前护理决策的制定提供科学依据.方法:运用Meta分析方法对我国1999年1月份至2009年1月份公开发表的有关国内直肠癌术后吻合口瘘的危险因素的15篇文献资料进行综合分析.结果:年龄≥60岁直肠癌患者吻合口瘘的发生率高于<60岁者,合并OR值为0.50(95%CI:0.33-0.76)(P<0.01);男性直肠癌患者吻合口瘘的发生率高于女性,合并OR值为2.17(95%CI:1.38-3.42)(P<0.01);术前接受新辅助放疗直肠癌患者吻合口瘘的发生率高于未进行新辅助放疗者,合并OR值为3.66(95%CI:2.19-6.09)(P<0.01);术前患有糖尿病的直肠癌患者吻合13瘘发生率低于无糖尿病者,合并OR值为3.16(95%CI:2.27-4.39)(P<0.01);急诊手术直肠癌患者吻合口瘘发生率高于择期手术者,合并0R值为0.27(95%CI:0.13-0.56)(P<0.01).结论:根据患者年龄、性别、是否糖尿病患者、术前是否进行新辅助放疗及可能的手术方式,术前进行有针对性更全面的护理,是可能降低直肠癌吻合口瘘发生率的有效途径.     

老年肿瘤患者发生心律失常的危险因素分析

目的:分析老年肿瘤患者发生心律失常的危险因素。方法:回顾性分析2015年8月至2018年9月我院诊治的324例老年肿瘤患者临床资料，发生心律失常者纳入观察组，未发生心律失常者纳入对照组，对比两组临床相关资料，分析影响老年肿瘤患者发生心律失常的因素。结果:324例患者中98例于住院期间发生心律失常，心律失常发生率为30.25%（98/324）；单因素及多因素Logistic回归分析发现，年龄、心血管病史、心律失常史、其他疾病的并发症、酸碱平衡、慢阻肺、甲状腺功能减退、脑损伤、低钾血症、新辅助化疗为老年肿瘤患者发生心律失常的危险因素（OR=1.166，95%CI 1.005～1.354；OR=1.279，95%CI 1.027～1.593；OR=1.359，95%CI 1.100～1.680；OR=1.324，95%CI 1.080～1.624；OR=1.405，95%CI 1.033～1.911；OR=1.507，95%CI 1.229～1.848；OR=1.443，95%CI1.072～1.944；OR=1.361， 95%CI 1.076～1.722；OR=1.581，95%CI 1.041～2.400；OR=1.293，95%CI 1.110～1.507，P＜0.05），而术后镇痛为保护因素（OR=0.662，95%CI 0.548～0.799，P＜0.05）。结论:引起老年肿瘤患者心律失常的因素较多，应加强心律失常的监控，重视危险因素，及早预防及治疗，提高其晚期生活质量。     

沈阳市子宫颈癌发病危险因素的病例对照研究

目的通过沈阳市子宫颈癌患者与沈阳市地区居民的病例对照研究,探讨子宫颈癌发病的危险因素。方法 以在辽宁省肿瘤医院住院的沈阳市子宫颈癌患者100例为病例,以沈阳市大东区二台子街道随机抽取的1000名子宫颈癌及癌前病变筛查的城市居民中非癌对象为对照,进行流行病学调查,采集HPV标本及宫颈脱落上皮液基细胞学检测标本,对获得的数据采用SPSS 13.0统计软件进行单因素卡方分析、logistic回归分析以及多因素logistic回归分析。结果 HPV感染(OR=221.62,95%CI:28.53~1721.51)、初次性生活年龄小于21岁(OR=6.65,95%CI:1.88~23.51)是子宫颈癌发病的危险因素,使用避孕套(OR=0.05,95%CI:0.01~0.18)是避免患宫颈癌的保护性因素。结论 清除HPV感染、倡导使用避孕套、树立科学的性生活观念、避免过早性体验,对降低沈阳地区子宫颈癌的发病具有重要意义。     

鼠双微体同源基因2遗传多态与结直肠癌患病风险的相关性

目的 探讨p53 72 Arg→Pro和鼠双微体同源基因2(MDM2) 309 T→G多态与结直肠癌(CRC)发生发展的关系.方法 采用病例-对照关联研究方法,分析1000例CRC和1300例正常对照中p53 72 Arg→Pro和MDM2 309 T→G的基因型.以多因素Logistic回归模型计算各基因型的比值比(OR)及其95%可信区间(CI).结果 携带MDM2 309 GG或TG基因型者患CRC的风险比TT基因型者显著增高,OR分别为2.06(95%CI为1.62～2.62)和1.31(95%CI为1.06～1.62).p53 72 Arg→Pro多态与CRC风险不相关.两个基因多态联合分析表明,既携带MDM2 309 GG,又携带p53 72 Pro/Pro基因型者,患CRC的OR显著高于携带MDM2 309 TT和p53 72 Pro/Pro基因型者[2.75(95%CI为1.60～4.70)比1.09(95%CI为0.63～1.88);χ2=9.83,P=0.002].结论 MDM2基因的遗传多态可能是CRC的遗传易感性因素.     

Sexual behaviour, STDs and risks for prostate cancer

A population-based case-control study was carried out among 981 men (479 black, 502 white) with pathologically confirmed prostate cancer and 1315 controls (594 black, 721 white). In-person interviews elicited information on sexual behaviour and other potential risk factors for prostate cancer. Blood was drawn for serologic studies in a subset of the cases (n = 276) and controls (n = 295). Prostate cancer risk was increased among men who reported a history of gonorrhoea or syphilis (odds ratio (OR) = 1.6; 95% confidence internal (CI) 1.2-2.1) or showed serological evidence of syphilis (MHA-TP) (OR = 1.8; 95% CI 1.0-3.5). Patterns of risk for gonorrhoea and syphilis were similar for blacks (OR = 1.7; 95% CI 1.2-2.2) and whites (OR = 1.6; 95% CI 0.8-3.2). Risks increased with increasing occurrences of gonorrhoea, rising to OR = 3.3 (95% CI 1.4-7.8) among subjects with three or more events (Ptrend = 0.0005). Frequent sexual encounters with prostitutes and failure to use condoms were also associated with increased risk. Syphilis, gonorrhoea, sex with prostitutes and unprotected sexual intercourse may be indicators of contact with a sexually transmissible factor that increases the risk of prostate cancer.     

Association of prostate cancer family history with histopathological and clinical characteristics of prostate tumors

Genetic factors may be used not only to assess risk of prostate cancer development but also to evaluate prostate cancer outcomes including clinical prognosis, treatment methods, and treatment response. To assess the role of family history on prostate cancer outcomes, we evaluated tumor characteristics, diagnostic precursors and biochemical (prostate specific antigen) relapse-free survival in men with and without a family history of prostate cancer. A total of 684 prostate cancer cases unselected for family history were identified from an ongoing hospital based prostate cancer case-control study between 1995 and 2002. Self-reported family history was grouped within the following categories: none, any, moderate (one affected first or second degree relative) and high (2 or more affected first or second degree relatives). We further considered groups defined by early (before age 60) and late (after age 60) age at diagnosis. Overall, tumor stage was not significantly associated with any (odds ratio [OR] = 1.43 95% confidence interval [CI] = 1.00-2.05) or moderate (OR = 1.48, 95% CI = 1.0-2.19) family histories. Men diagnosed before age 60, however, had higher tumor stages if they had any (OR = 2.19, 95% CI = 1.28-3.75) or moderate (OR = 2.15, 95% CI = 1.2-3.9) family histories. Men diagnosed after age 60 with any family history were significantly more likely to experience biochemical (PSA) failure (Hazard ratio [HR] = 2.60, 95%CI = 1.08-6.25). Men with any and moderate family histories were at significantly increased risk of biochemical failure (HR = 2.49, 95%CI = 1.25-4.95 and HR = 2.46, 95% CI = 1.17-5.16, respectively). Moderate family history increased probability of seminal vesicle invasion (OR = 2.14, 95%CI = 1.06-4.34). Our results suggest that a family history of prostate cancer may be associated with predictors of clinical outcome in prostate cancer cases unselected for a family history of prostate cancer.     

Obesity, diabetes, and risk of prostate cancer: results from the prostate cancer prevention trial.

Studies on the relationship between obesity and prostate cancer incidence are inconsistent. In part, this inconsistency may be due to a differential effect of obesity on low-grade and high-grade cancer or confounding of the association of obesity with prostate cancer risk by diabetes. We investigated the associations of obesity and diabetes with low-grade and high-grade prostate cancer risk. Data were from 10,258 participants (1,936 prostate cancers) in the Prostate Cancer Prevention Trial who all had cancer presence or absence determined by prostate biopsy. Multiple logistic regression was used to model the risk of total prostate cancer, and polytomous logistic regression was used to model the risk of low-grade and high-grade prostate cancer. Compared with men with body mass index < 25, obese men (body mass index > or =30) had an 18% [odds ratio (OR), 0.82; 95% confidence interval (95% CI), 0.69-0.98] decreased risk of low-grade prostate cancer (Gleason <7) and a 29% (OR, 1.29; 95% CI, 1.01-1.67) increased risk of high-grade prostate cancer (Gleason > or =7) or, alternatively, a 78% (OR, 1.78; 95% CI, 1.10-2.87) increased risk defining high-grade cancer as Gleason sum 8 to 10. Diabetes was associated with a 47% (OR, 0.53; 95% CI, 0.34-0.83) reduced risk of low-grade prostate cancer and a 28% (OR, 0.72; 95% CI, 0.55-0.94) reduced risk of high-grade prostate cancer. Associations of obesity or diabetes with cancer risk were not substantially changed by mutually statistical controlling for each other. Obesity increases the risk of high-grade but decreases the risk of low-grade prostate cancer, and this relationship is independent of the lower risk for prostate cancer among men with diabetes.     

Vasectomy, cigarette smoking, and age at first sexual intercourse as risk factors for prostate cancer in middle-aged men

A population-based case-control study was conducted in men aged 60 or less to assess the risk of prostate cancer associated with vasectomy and other factors. Data were obtained from 216 case-control pairs by telephone interviews; this number represented 55% of all eligible cases. The matched pairs relative risk (RR) for vasectomy in ever married men was 1.4 with a 95% confidence interval (CI) of 0.9-2.3. There was a positive association between the number of years since vasectomy and prostate cancer risk (1-sided P = 0.01). Early age at first sexual intercourse was associated with increased prostate cancer risk (age less than 17 vs. 21+, RR = 2.3, 95% CI = 1.3, 4.0) but there were no consistent associations with number of sexual partners or frequency of sexual intercourse. Cigarette smoking was also associated with increased risk of prostate cancer (RR = 1.9, 95% CI = 1.2, 3.0) and there was a positive dose-response relationship with years of smoking (1-sided P = 0.001). We discuss the possible implication of the low response rate on each of these findings. To determine whether the association with vasectomy might have a hormonal basis, we compared levels of testosterone (T) and testosterone binding globulin-binding capacity (TeBG-bc) in 33 of the vasectomized control men with levels in 33 non-vasectomized controls of the same age, weight and height. T levels were higher in vasectomized than in non-vasectomized controls (1-sided P = 0.06). The ratio of T to TeBG-bc (an index of bioavailable T) was 13.5% higher in vasectomized men (1-sided P = 0.03).     

Screen-detected prostate cancer and the insulin-like growth factor axis: results of a population-based case-control study

Higher circulating levels of IGF-I have been associated with increased risk of prostate and some other cancers. Most research on prostate cancer has been based on men with symptoms or identified following treatment of benign disease. However, increasing numbers of cancer cases are now detected in asymptomatic men following prostate-specific antigen (PSA) tests. We therefore used a population-based case-finding exercise using the PSA test to examine whether associations between the IGF axis and cancer risk were apparent in this population. A matched case-control study was conducted among 7,383 men (50-70 years) receiving a PSA test as part of a case-finding exercise. Assays of IGF-I, IGF-II, IGFBP-2 and IGFBP-3 were performed on cases and 2 controls matched on age, recruitment center and calendar time. Analyses were based on 176 cases and 324 matched controls. The risk of prostate cancer increased across quartiles of IGF-I (highest vs. lowest quartile, OR = 2.34; 95% CI = 1.26-4.34; p(trend) = 0.02) and IGF-II (OR = 1.78; 95% CI = 0.94-3.15; p(trend) = 0.09). Controlling for smoking history and IGFBP-3 strengthened associations with cancer for both IGF-I (OR = 3.00; 95% CI = 1.50-6.01; p(trend) 0.005) and IGF-II (OR = 2.02; 95% CI = 1.07-3.84; p(trend) = 0.04) Associations between the IGFs and cancer risk were stronger for advanced cases. Our findings suggest that both IGF-I and IGF-II are associated with an increased risk of screen-detected prostate cancer.     

Family history of hormonal cancers and colorectal cancer risk: A case‐control study conducted in Ontario

Aggregation of cancers among families with highly penetrant genetic mutations such as hereditary nonpolyposis colorectal cancer is well‐described. However, there is a paucity of data regarding familial aggregation of hormonal cancers (cancers of the breast, endometrial, ovarian and prostate) and colorectal cancer (CRC) in the general population. We investigated the association between having a first‐degree family history of breast, endometrial, ovarian, or prostate cancer and CRC risk. Population‐based CRC cases and controls were recruited by the Ontario Familial Colorectal Cancer Registry (OFCCR). Logistic regression was conducted to obtain odds ratio (OR) estimates and 95% confidence intervals (95% CIs). First‐degree family history of breast cancer was associated with a modest, borderline statistically significant increased CRC risk (age‐, sex‐adjusted OR = 1.2, 95% CI = 1.0, 1.5). The magnitude of CRC risk was greatest if more than one first‐degree kin had breast cancer (age‐, sex‐adjusted OR = 1.7, 95% CI = 1.0, 2.0), as well as if the kin was diagnosed at >50 years of age (age‐, sex‐adjusted OR = 1.4, 95% CI = 1.1, 1.8). Family history of ovarian cancer was associated with reduced CRC risk (multivariate‐adjusted OR = 0.6, 95% CI = 0.3, 1.0). Although statistically significant increases in CRC risk were observed in the age‐, sex‐adjusted OR estimates for family history of endometrial and prostate cancers, the associations were no longer significant after multivariate‐adjustment. In conclusion, individuals with a first‐degree kin with breast cancer may have a modest increased risk for CRC compared to individuals without. © 2009 UICC     

Family history of cancer and the risk of prostate cancer and benign prostatic hyperplasia

We analysed the relation between family history of cancer in first-degree relatives and risk of prostate cancer (PC) and benign prostatic hyperplasia (BPH) using data from a multicentric case-control study conducted in Italy from 1991 to 2002 on 1,294 cases of incident, histologically confirmed PC, 1,369 cases of BPH and 1,451 men admitted to the same network of hospitals for acute, nonneoplastic conditions. Unconditional logistic regression was used to estimate odds ratios (OR) of PC and BPH, adjusted for age and other confounders. Men with a family history of PC had an OR of PC of 4.0 (95% confidence interval [CI] 2.5-6.5), and the risk was higher when the proband was younger, when 2 or more relatives were affected or when the affected relative was a brother. The risk of PC was also increased in men with a family history of cancer of the ovary (OR = 6.2, 95% CI 1.2-32), bladder (OR = 3.5, 95% CI 1.6-7.4) and kidney (OR = 3.1, 95% CI 1.1-8.5). An involvement of breast/ovarian cancer predisposition genes in a small proportion of PCs was suggested by the cluster of these cancers in female relatives of a few PC cases. The risk of BPH was increased in men with a family history of bladder cancer (OR = 2.2, 95% CI 1.0-5.0) but not PC (OR = 1.2, 95% CI 0.7-2.2). Our study adds further information on the association of family history of cancer and risk of PC and is, to our knowledge, the first comprehensive epidemiologic information on family history of cancer and risk of BPH.     

Prostate cancer risk from occupational exposure to polycyclic aromatic hydrocarbons interacting with the GSTP1 Ile105Val polymorphism

BACKGROUND: Variation in the glutathione S-transferase (GSTP1) gene and occupational polycyclic aromatic hydrocarbons (PAH) exposure are putative prostate cancer risk factors. An Ile/Val polymorphism in codon 105 of GSTP1 affects its enzymatic activity toward PAH detoxification, a possible mechanism in prostate carcinogenesis. METHODS: To determine whether the GSTP1 Ile105Val polymorphism modifies prostate cancer risk associated with occupational PAH exposure, we studied 637 prostate cancer cases and 244 controls of White and African-American race from the Henry Ford Health System in Detroit, Michigan. Occupational exposure to PAH from wood, petroleum, coal or other sources through respiratory and cutaneous routes was retrospectively assessed by expert review of job histories. The association of occupational PAH exposure and GSTP1 Ile105Val polymorphism with prostate cancer was tested in multiple logistic regression models adjusting for potential confounders. Cases were over sampled compared with controls to evaluate gene-environment interaction with the statistically efficient case-only analytic approach. RESULTS: Neither carriage of the GSTP1 Val(105) variant allele nor occupational PAH exposure was significantly associated with prostate cancer. However, case-only analyses revealed that carriage of the GSTP1 Val(105) variant allele was associated with increasing levels of occupational respiratory PAH exposures from any source and from petroleum (trend test p=0.01 for both). The GSTP1 Val(105) allele was observed most frequently in cases in the highest quartile of occupational respiratory PAH exposures from petroleum (OR=1.74; 95% CI=1.11-2.72) or from any source (OR=1.85; 95% CI=1.19-2.89). The gene-environment risk estimate in the highest PAH petroleum exposure quartile was greatest in men under age 60 (OR=4.52; 95% CI=1.96-10.41) or with a positive family history of prostate cancer (OR=3.02; 95% CI=1.15-7.92). CONCLUSIONS: Our results suggest men who carry the GSTP1 Val(105) variant and are exposed at high levels to occupational PAH have increased risk for prostate cancer. This increased risk is more pronounced in men under age 60 or with a family history of prostate cancer.     

Meat Consumption,Related Nutrients,Obesity and Risk of Prostate Cancer: a Case-Control Study in Uruguay

Background: In order to determine the role of meat consumption and related nutrients in the etiology of prostate cancer we conducted a case-control study among Uruguayan men in the time period 1998-2007. Results: The study included 464 cases and 472 controls, frequency matched for age and residence. Both series were drawn from the four major public hospitals in Montevideo. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95 % confidence intervals (95 % CI) of prostate cancer by quartiles of meat intake and related nutrients. The highest vs. the lowest quartile of intake of total meat (OR = 5.19, 95 % CI 3.46-7.81), red meat (OR = 4.64, 95 % CI 3.10-6.95), and processed meat (OR = 1.78, 95% CI 1.22-2.59) were associated with increased risk of prostate cancer. Meat nutrients were directly associated with the risk of prostate cancer (OR for cholesterol 5.61, 95 % CI 3.75-8.50). Moreover, both total meat and red meat displayed higher risks among obese patients. Conclusions: This study suggests that total and red meat and meat nutrients may play a role in the etiology of prostate cancer in Uruguay.     

Iron intake, oxidative stress-related genes (MnSOD and MPO) and prostate cancer risk in CARET cohort

Iron overload may increase prostate cancer risk through stimulation of oxidative stress, and endogenous pro- and antioxidant capabilities, i.e. manganese superoxide dismutase (MnSOD) and myeloperoxidase (MPO), may modify these associations. We investigated this hypothesis in the Carotene and Retinol Efficacy Trial cohort in a nested case-control study. Although there was no association between iron intake and risk overall, there was a suggestion of increased risk of clinically aggressive prostate cancer with higher iron intake [odds ratio (OR) = 1.4, 95% confidence interval (CI) = 0.9-2.0]. Associations were most notable for men with aggressive prostate cancer who were below the median consumption of total fruits and vegetables (OR = 1.8, 95% CI = 1.1-3.2). Associations between MPO -463 G to A genotype (rs2333227) and prostate cancer risk were only noted among men with aggressive cancer, with more than a 2-fold risk reduction among men with AA genotypes (OR = 0.4, 95% CI = 0.2-1.0); MnSOD was not associated with risk overall, but the MnSOD T to C (Val-9Ala, rs4880) polymorphism modified associations between risk of clinically aggressive prostate cancer and dietary iron intake (P for interaction = 0.02). Among aggressive cancer cases with the TT genotype, higher iron intake level was associated with >2-fold increase in risk (OR = 2.3, 95% CI = 1.0-4.9), whereas there was no association among men with CC genotypes (OR = 0.9, 95% CI = 0.4-2.3). Although interactions were not significant, there were similar patterns for MPO genotype, iron intake and risk. These findings suggest that higher iron intake may be associated with risk of clinically aggressive prostate cancer, and that endogenous antioxidant capabilities may modify these associations.