体质指数与广州市女性乳腺癌发病

目的 研究体质指数与广州市女性乳腺癌发病的关系。方法 根据广州地区1996年－1999年开展的一项大规模的女性乳腺癌人群基础上的病例对照研究,采用问卷调查的方式,共收集了病例563例,人群对照570例。结果 随着体质指数的增加,已闭经的妇女患乳腺癌的危险性增高。结论 肥胖与乳腺癌的关系密切,控制体重的增加,对预防女性乳腺癌的发生有一定的作用。     

体质指数与乳腺癌的关系

[目的]探讨体质指数（BMI）与乳腺癌的关系。[方法]分析比较200例乳腺癌患者和200例健康对照者的BMI情况。[结果]乳腺癌患者平均BMI为24.39±4.61kg/m2,健康对照组平均BMI为23.81±3.17kg/m2,有显著性差异（t=12.501,P=0.001）。按60岁分层分析显示,≥60岁和〈60岁乳腺癌组BMI均显著性高于健康对照组（P〈0.05）。乳腺癌组Logistic回归分析显示BMI是乳腺癌发生的危险因素（OR=1.395,95%CI：1.062～1.931）。[结论]乳腺癌的发生与BMI有关。     

体质指数与肺癌关系的流行病学研究进展

流行病学研究发现肥胖与一些常见恶性肿瘤有关,提示肥胖在恶性肿瘤的发生发展中可能起到一定的作用。肥胖与肺癌关系的研究结果尚不一致。文章对近年来体质指数（BMI）与肺癌关系的流行病学研究进展进行系统综述。     

原发性胃癌患者术后体质指数与预后的关系研究

目的 探讨原发性胃癌（PGC）患者术后体质指数（BMI）与预后的关系。方法 选取巴中市中心医院2011年1月至2016年12 月收治的362例PGC患者作为研究对象,根据BMI中国标准分为低体重（BMI<18.5 kg/m2 ）、正常体重（BMI 18.5~23.9 kg/m2 ）、超重（BMI 24.0~27.9 kg/m2 ）、肥胖（BMI≥28.0 kg/m2）四组,采用Kaplan⁃Meier法计算生存期和无病生存期,4组间的差异比较采用Log⁃rank检验, 采用Cox比例风险模型进行预后影响因素分析。结果 低体重、正常体重、超重和肥胖的PGC的3年无病生存率分别为：90.0%、77.4%、 78.9%和79.8%,经Log⁃rank检验,组间差异无统计学意义（χ2=1.110, P=0.832）;低体重、正常体重、超重和肥胖的PGC的5年总生存率 分别为：32.3%、86.9%、71.5%和69.0%,经Log⁃rank检验,组间差异有统计学意义（χ2=7.616, P=0.027）,且进一步两两比较发现,低体 重和肥胖患者的总生存率水平最低。多因素分析显示,相对于正常体重患者,肥胖（BMI≥28.0 kg/m2）患者（RR=1.559,95%CI= 1.262~ 2.420, P=0.022）、体重过低（BMI≤18.5 kg/m2）患者（RR=3.385,95%CI=1.698~6.767, P=0.002）是影响PGC患者术后生存的独立危险 因素。结论 术后体重过低及肥胖可作为影响原发性胃癌生存率的独立影响因素。     

结肠癌危险因素的病例对照研究

目的：研究结肠癌的危险因素,为监测和控制嘉善县结肠癌提供依据。方法：实施基于全人群的病例对照研究;以统一的调查表调查151例结肠癌病人和1540名健康对照者;应用STATA5．0软件包进行单因素、多因素非条件Logistic回归分析。结果：与结肠癌发病有关的主要危险因素有下消化道疾病史（OR＝3．910）,一级亲属结肠直肠癌病史（OR＝3．298）,心理情绪不佳（OR＝2．224）,饮酒（OR＝1．721）及职员职业（OR＝3．068）;保护因素有10年前蔬菜月均消耗量高（OR＝0．774）,使用冰箱（OR＝0．442）及10年前人均月收入低（OR＝0．725）。结论：下消化道疾病、一级亲属结直肠癌病史及心理情绪不良是结肠癌危险因素,蔬菜是预防结肠癌的保护因素。     

广州市结肠癌危险因素的病例对照研究

目的：研究广州市结肠癌患者发病的危险因素。方法：采取病例对照研究的方法,采用全国4个城市和地区统一的调查表调查结肠癌患者及健康人各150例,资料按统一数据库收录后,采用SAS软件包进行单因素及多因素统计学分析。建立主效应模型。结果：与结肠癌发病有关的主要危险因素有：长期精神压抑（OR=75）,一级亲属患结肠癌（OR=7.886),高血脂及高胆固醇血症（OR=3.443);保护因素有：目前玉米月用量（OR=0.219),目前蛋类月用量（OR=0.278),常吃大蒜（OR=0.352),常吃早餐（OR=0.115)。结论：精神压抑、一级亲属患结肠癌、高血脂及高胆固醇血症是患结肠癌的危险因素;常吃早餐、常吃大蒜、膳食纤维的高摄入是预防结肠癌的保护因素。     

成年期体质指数与膀胱癌关系的全人群病例对照研究

[目的]研究成年期体质指数(BMI)与上海市区居民膀胱癌危险性的关系.[方法]采用全人群病例对照研究,共调查1996年1月1日～1998年12月31日期间诊断的上海市区膀胱癌新发病例608例,以及性别、年龄配对的人群对照607例.采用非条件Logistic回归模型,调整可能的混杂因素,估计20岁时、成年期最高体重时及参...     

结肠癌根治术后复发转移危险因素分析

[目的]探讨结肠癌患者根治术后复发转移的相关临床病理因素.[方法]选择1994年1月至2004年1月行结肠癌根治术患者446例,Cox模型分析临床病理因素与复发转移的关系.[结果]全组复发转移率为19.28%.单因素分析显示,发病至手术的时间、术前CEA水平、分化程度、Dukes＇分期、淋巴结转移与术后复发转移有关;多因素分析显示淋巴结转移、分化程度、术前血清CEA水平是术后复发转移预后因素.[结论]分化程度、淋巴结转移、术前血清CEA水平是影响结肠癌患者根治术后复发转移的重要预后因素.     

血清瘦素水平及体质指数与乳腺癌发生的相关性研究

  目的 探讨血清瘦素水平及体质指数与乳腺癌发生的相关性，为乳腺癌的防治寻找科学依据。方法 收集术前乳腺癌患者90例，乳腺良性疾病患者32例，健康对照103例血清，采用放射免疫分析法测定瘦素水平，并进行体质指数的测量与计算。采用SPSS软件包进行统计学处理。结果 乳腺癌组血清瘦素水平与体质指数明显高于乳腺良性疾病和健康对照组，差异均具有统计学意义（P＜0.01）；三组人群瘦素水平与体质指数均呈正相关，相关系数分别为0.327（P＜0.001），0.416（P＜0.001），0.525（P＜0.001）；Logistic回归分析，血清瘦素水平的升高是乳腺癌发生的危险因素，OR值为1.14（95 %CI：1.076 ~ 1.209）。结论 血清瘦素水平、体质指数升高可能与乳腺癌发生有关。     

低氧反应与结肠癌的关系

结肠癌具有缺氧微环境,缺氧的本质是细胞对低氧状态的一种反应和适应性改变.结肠癌低氧反应在其发生发展过程中起重要作用,包括低氧反应产生缺氧诱导因子-1(HIF-1)α及活性氧簇对结肠癌的作用及低氧反应直接对肿瘤细胞凋亡、能量代谢的影响.近年来改变结肠癌低氧反应的肿瘤辅助治疗正成为肿瘤学研究热点.     

Effect of comorbidity and body mass index on the survival of African‐American and Caucasian patients with colon cancer

BACKGROUND:

There is a survival disparity between African Americans and Caucasians who have colon cancer. The objectives of the current study were to quantify the impact of comorbidity and body mass index (BMI) on survival and to assess whether these 2 variables account for the decreased survival among African Americans.

METHODS:

Data from patients (n = 496) who underwent surgery for a first primary colon cancer at the University of Alabama at Birmingham Hospital from 1981 to 2002 were analyzed. Hazard ratios (HRs) with 95% confidence intervals (CI) were obtained using Cox proportional hazards models for the association of race, comorbidity, BMI, and covariates with all‐cause mortality. The confounding influence of comorbidity and BMI for the increased risk of death associated with African‐American race was evaluated, and effect modification by disease stage for the association of comorbidity and BMI with mortality also was assessed.

RESULTS:

African Americans experienced an increased risk of death compared with Caucasians (HR, 1.34; 95% CI, 1.06‐1.68). The highest comorbidity burden was associated with an increased risk of all‐cause mortality (HR, 1.63; 95% CI, 1.24‐2.15). For BMI, being underweight increased the risk of death (HR, 1.54; 95% CI, 0.96‐2.45); however, being overweight/obese was protective (HR, 0.77; 95% CI, 0.61‐0.97). The effect of comorbidity was observed among those with early stage tumors, whereas the effect of BMI was confined to patients who had advanced tumors.

CONCLUSIONS:

Although comorbidity and BMI had an impact on the survival of patients with colon cancer after surgery, these variables were not contributing factors to the decreased survival observed among African Americans. Cancer 2009. © 2009 American Cancer Society.     

体质量指数与结直肠癌预后的关系

目的:探讨体质量指数与结直肠癌患者预后的关系.方法:回顾性分析2010年1月至2011年12月新疆医科大学附属肿瘤医院收治的353例行根治手术的结直肠癌患者临床病理资料.将患者分为低体重组(BMI<18.5kg/m2)、正常体重组(18.5kg/m2≤BMI<23kg/m2)、超重组(23kg/m2≤BMI<27.5kg/m2)、肥胖组(BMI≥27.5kg/m2).比较四组临床因素,分析BMI与结直肠癌患者5年生存率的关系.结果:BMI与患者术前CA199有统计学差异(P=0.020),对5年生存率无显著影响(P=0.254).民族、pT分期、术前放化疗、肿瘤分化程度均是结直肠癌独立预后因素(P<0.05).结论:BMI对结直肠癌患者的预后无显著影响.     

Body mass index and body size in early adulthood and risk of pancreatic cancer in a central European multicenter case-control study

The relationship between two measures of excess body weight, body mass index (BMI) and body size score, and risk of pancreatic cancer was examined among 574 pancreatic cancer cases and 596 frequency-matched controls from the Czech Republic and Slovakia enrolled between 2004 and 2009. Analyses using multivariable logistic regression showed an increased risk of pancreatic cancer associated with elevated quartiles of BMI at ages 20 [fourth quartile: odds ratio (OR) = 1.79, 95% confidence interval (CI): 1.23, 2.61] and 40 (fourth quartile: OR = 1.57, 95% CI: 1.09, 2.27) compared to the lowest quartile. Consistent results were observed for body size score at ages 20 (high versus low: OR = 1.66, 95% CI: 1.08, 2.57) and 40 (medium versus low: OR = 1.36, 95% CI: 1.00, 1.86), but no association was found for BMI and body size score at 2 years before the interview. Stronger risk estimates for BMI were observed in males than females, particularly at age 20, but the analysis of body size yielded similar estimates by sex. When considering excess body weight at both ages 20 and 40 jointly, the highest risk estimates were observed among subjects with elevated levels at both time periods in the analysis of BMI (OR = 1.86, 95% CI: 1.32, 2.62) and body size (OR = 1.53, 95% CI: 1.09, 2.13). These findings, based on two different measures, provide strong support for an increased risk of pancreatic cancer associated with excess body weight, possibly strongest during early adulthood.     

体质量指数与甲状腺乳头状癌临床病理特征的相关性分析

目的:分析体质量指数（body mass index,BMI）与甲状腺乳头状癌（papillary thyroid carcinoma,PTC）临床病理特征的相关性。方法:回顾性分析2017年1月至2018年6月于西京医院甲乳血管外科行手术的829例PTC患者临床资料,并将入组患者根据BMI的不同分为四组:较轻组（BMI＜18.5 kg/m2）、正常组（18.5≤BMI＜25 kg/m2）、超重组（25≤BMI＜30 kg/m2）及肥胖组（BMI≥30 kg/m2）。通过单因素分析及多元逻辑回归分析BMI与PTC临床病理特征相关性。结果:不同BMI组PTC患者的年龄、性别以及高血压病史之间具有统计学差异（P<0.001）。超重组患者与其他组相比平均年龄较大,肥胖组患者男性居多。单因素分析显示,BMI与肿瘤多灶性、BRAF V600E基因突变以及TNM分期显著相关（P<0.05）,而与病灶大小、病灶分布、是否侵犯包膜以及淋巴结转移数目和位置无关（P>0.05）。BMI正常组患者的肿瘤发生灶多为单灶（60.3%）,而非正常组患者多灶的发生率显著增加（P=0.040）。随着BMI的增长,BRAF V600E基因突变率显著提高（P=0.001）。经多元逻辑回归分析的校正,PTC患者的TNM分期与BMI无统计学差异（P>0.05）,肿瘤多灶性以及BRAF V600E基因突变仍与BMI显著相关。结论:在PTC患者中,非正常BMI组患者肿瘤多灶的发生率较正常BMI组显著增加,且BRAF V600E基因突变率与BMI呈正比,而除多灶性以外的侵袭性病理特征与BMI之间未发现相关性。     

Body mass index at diagnosis and survival among colon cancer patients enrolled in clinical trials of adjuvant chemotherapy

BACKGROUND:

Although obesity is an established risk factor for developing colon cancer, its prognostic impact and relation to patient sex in colon cancer survivors remains unclear.

METHODS:

The authors examined the prognostic and predictive impact of the body mass index (BMI) in patients with stage II and III colon carcinoma (N = 25,291) within the Adjuvant Colon Cancer Endpoints (ACCENT) database. BMI was measured at enrollment in randomized trials of 5‐fluorouracil–based adjuvant chemotherapy. Association of BMI with the time to recurrence (TTR), disease‐free survival (DFS), and overall survival (OS) were determined using Cox regression models. Statistical tests were 2‐sided.

RESULTS:

During a median follow‐up of 7.8 years, obese and underweight patients had significantly poorer survival compared with overweight and normal‐weight patients. In a multivariable analysis, the adverse prognostic impact of BMI was observed among men but not among women (P_interaction = .0129). Men with class 2 and 3 obesity (BMI ≥35.0 kg/m²) had a statistically significant reduction in DFS (hazard ratio [HR], 1.16; 95% confidence interval [CI], 1.01‐1.33; P = .0297) compared with normal‐weight patients. Underweight patients had a significantly shorter TTR and reduced DFS (HR, 1.18; 95% CI, 1.09‐1.28; P < .0001) that was more significant among men (HR, 1.31; 95% CI, 1.15‐1.50; P < .0001) than among women (HR, 1.11; 95% CI, 1.01‐1.23; P = .0362; P_interaction = .0340). BMI was not predictive of a benefit from adjuvant treatment.

CONCLUSIONS:

Obesity and underweight status were associated independently with inferior outcomes in patients with colon cancer who received treatment in adjuvant chemotherapy trials. Cancer 2013. © 2013 American Cancer Society.     

Co-twin control and cohort analyses of body mass index and height in relation to breast, prostate, ovarian, corpus uteri, colon and rectal cancer among Swedish and Finnish twins

Associations between anthropometric measures and cancer have been studied previously, but relatively few studies have had the opportunity to control for genetic and early shared environmental factors. In this study, we analyzed 2 twin cohorts from Sweden born 1886-1925 (n = 21,870) and 1926-1958 (n = 30,279) and 1 from Finland born 1880-1958 (n = 25,882) including in total 78,031 twins, and studied the association between BMI and height and risk of prostate, breast, ovarian, corpus uteri, colon and rectal cancer. The cohorts were both analyzed through a co-twin control method and as traditional cohorts. In co-twin control analyses, older obese (BMI > or = 30 kg/m(2)) subjects (median age 56 years at baseline) were at higher risk of cancer of the corpus uteri (OR = 3.0; 95% CI 0.9-10.6), colon (OR = 1.9; 95% CI 0.8-4.5) and breast (OR = 2.5; 95% CI 1.3-4.2). For younger obese women (median age 30 years at baseline), an inverse tendency was observed for breast cancer (OR = 0.6; 95% CI 0.3-1.5, p for trend = 0.05). The tallest women had an increased risk of breast (OR = 1.8; 95% CI 1.3-2.7) and ovarian cancer (OR = 1.7; 95% CI 0.8-3.5). No consistent associations were found for prostate cancer either for BMI or height. There are some suggestions in our study that uncontrolled genetic or early shared environmental factors may affect risk estimates in studies of anthropometric measures and cancer risk, but do not explain observations of increased cancer risks related to BMI or height.     

Childhood body mass index and later cancer risk: a 50-year follow-up of the Boyd Orr study

Associations between childhood BMI and adult cancer risk were investigated in a historical cohort study based on the Carnegie ("Boyd Orr") Survey of Diet and Health in Pre-War Britain (1937-9). In 14 centres in England and Scotland, children had their height and weight measured. We included 2,347 individuals aged between 2 and 14 years 9 months at the time of measurement, who were traced through the National Health Service Central Register. Relative cancer risk (registration or death) was estimated in relation to age- and sex-specific BMI SD scores. We studied associations with (i) all cancers, (ii) cancer groups stratified according to their relationship to smoking and (iii) certain site-specific cancers. In the 50 years of follow-up, 188 men and 192 women developed cancer. There was a 9% increase (95% CI -3 to 22%) in risk of cancer in adulthood per SD increase in BMI measured in childhood. There was no evidence of confounding by childhood or adulthood socioeconomic position, other anthropometric variables, childhood energy intake or birth order. There was a 30% increase (95% CI 10-54%) in risk of smoking-related cancers per SD increase in childhood BMI. There was no relationship between BMI and cancers not related to smoking. Associations for all cancers and non-smoking-related cancers tended to be stronger in children who were measured at an older (>8 years) rather than a younger (< or =8 years) age. We conclude that childhood BMI is related to increased risk of cancer in later life, particularly smoking-related cancers.     

Body mass index and risk of ovarian cancer

BACKGROUND:

Convincing epidemiologic evidence links excess body mass to increased risks of endometrial and postmenopausal breast cancers, but the relation between body mass index (BMI) and ovarian cancer risk remains inconclusive. Potential similarities regarding a hormonal mechanism in the etiology of female cancers highlight the importance of investigating associations according to menopausal hormone therapy (MHT) use. However, to the authors' knowledge, data addressing whether the relation between BMI and ovarian cancer differs by MHT use are very sparse.

METHODS:

The authors prospectively investigated the association between BMI and ovarian cancer among 94,525 US women who were followed between 1996 through 1997 to December 31, 2003. During 7 years of follow‐up, 303 epithelial ovarian cancer cases were documented.

RESULTS:

Compared with normal weight women (BMI of 18.5‐24.9 kg/m²), the multivariate relative risk (MVRR) of ovarian cancer for obese women (BMI of ≥30 kg/m²) in the cohort as a whole was 1.26 (95% confidence interval [95% CI], 0.94‐1.68). Among women who never used MHT, the MVRR for obese versus normal weight women was 1.83 (95% CI, 1.18‐2.84). In contrast, no relation between BMI and ovarian cancer was apparent among women who ever used MHT (MVRR = 0.96; 95% CI, 0.65‐1.43; P interaction = 0.02). Exploratory analyses also suggested a positive association between BMI and ovarian cancer among women without a family history of ovarian cancer (MVRR comparing obese vs normal weight women = 1.36; 95% CI, 1.00‐1.86), but no relation with BMI was apparent among women with a positive family history of ovarian cancer (MVRR = 0.74; 95% CI, 0.34‐1.62 [P interaction = .02]).

CONCLUSIONS:

Based on the results of the current study, the authors suspect that obesity is associated with enhanced ovarian cancer risk through a hormonal mechanism. Cancer 2009. Published 2009 by the American Cancer Society.