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Cheryl Ritenbaugh Janet L Stanford LieLing Wu James M Shikany Robert E Schoen Marcia L Stefanick Vicky Taylor Cedric Garland Gail Frank Dorothy Lane Ellen Mason S Gene McNeeley Joao Ascensao Rowan T Chlebowski 《Cancer epidemiology, biomarkers & prevention》2008,17(10):2609-2618
BACKGROUND: In separate Women's Health Initiative randomized trials, combined hormone therapy with estrogen plus progestin reduced colorectal cancer incidence but estrogen alone in women with hysterectomy did not. We now analyze features of the colorectal cancers that developed and examine the survival of women following colorectal cancer diagnosis in the latter trial. PARTICIPANTS AND METHODS: 10,739 postmenopausal women who were 50 to 79 years of age and had undergone hysterectomy were randomized to conjugated equine estrogens (0.625 mg/d) or matching placebo. Colorectal cancer incidence was a component of the monitoring global index of the study but was not a primary study endpoint. Colorectal cancers were verified by central medical record and pathology report review. Bowel exam frequency was not protocol defined, but information on their use was collected. RESULTS: After a median 7.1 years, there were 58 invasive colorectal cancers in the hormone group and 53 in the placebo group [hazard ratio, 1.12; 95% confidence interval (95% CI), 0.77-1.63]. Tumor size, stage, and grade were comparable in the two randomization groups. Bowel exam frequency was also comparable in the two groups. The cumulative mortality following colorectal cancer diagnosis among women in the conjugated equine estrogen group was 34% compared with 30% in the placebo group (hazard ratio, 1.34; 95% CI, 0.58-3.19). CONCLUSIONS: In contrast to the preponderance of observational studies, conjugated equine estrogens in a randomized clinical trial did not reduce colorectal cancer incidence nor improve survival after diagnosis. 相似文献
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《Annals of oncology》2015,26(1):221-230
BackgroundLung cancer is the leading cause of worldwide cancer deaths. While smoking is its leading risk factor, few prospective cohort studies have reported on the association of lung cancer with both active and passive smoking. This study aimed to determine the relationship between lung cancer incidence with both active and passive smoking (childhood, adult at home, and at work).Patients and methodsThe Women's Health Initiative Observational Study (WHI-OS) was a prospective cohort study conducted at 40 US centers that enrolled postmenopausal women from 1993 to 1999. Among 93 676 multiethnic participants aged 50–79, 76 304 women with complete smoking and covariate data comprised the analytic cohort. Lung cancer incidence was calculated by Cox proportional hazards models, stratified by smoking status.ResultsOver 10.5 mean follow-up years, 901 lung cancer cases were identified. Compared with never smokers (NS), lung cancer incidence was much higher in current [hazard ratio (HR) 13.44, 95% confidence interval (CI) 10.80–16.75] and former smokers (FS; HR 4.20, 95% CI 3.48–5.08) in a dose-dependent manner. Current and FS had significantly increased risk for all lung cancer subtypes, particularly small-cell and squamous cell carcinoma. Among NS, any passive smoking exposure did not significantly increase lung cancer risk (HR 0.88, 95% CI 0.52–1.49). However, risk tended to be increased in NS with adult home passive smoking exposure ≥30 years, compared with NS with no adult home exposure (HR 1.61, 95% CI 1.00–2.58).ConclusionsIn this prospective cohort of postmenopausal women, active smoking significantly increased risk of all lung cancer subtypes; current smokers had significantly increased risk compared with FS. Among NS, prolonged passive adult home exposure tended to increase lung cancer risk. These data support continued need for smoking prevention and cessation interventions, passive smoking research, and further study of lung cancer risk factors in addition to smoking.ClinicalTrials.govNCT00000611. 相似文献
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Michael S. Simon MD MPH Theresa A. Hastert PhD Ana Barac MD PhD Hailey R. Banack PhD Bette J. Caan DrPH Rowan T. Chlebowski MD PhD Randi Foraker PhD Gayane Hovsepyan BS Simin Liu MD MPH ScD Juhua Luo PhD JoAnn E. Manson MD DrPH Marian L. Neuhouser PhD RD Tochukwu M. Okwuosa DO Kathy Pan MD Lihong Qi PhD Julie J. Ruterbusch MS Aladdin H. Shadyab PhD Cynthia A. Thomson PhD RD Jean Wactawski-Wende PhD Nida Waheed MD MPH Jennifer L. Beebe-Dimmer PhD 《Cancer》2021,127(4):598-608
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Association of cigarette smoking with the risk of ovarian cancer 总被引:4,自引:0,他引:4
Pan SY Ugnat AM Mao Y Wen SW Johnson KC;Canadian Cancer Registries Epidemiology Research Group 《International journal of cancer. Journal international du cancer》2004,111(1):124-130
Cigarette smoking may be associated with ovarian cancer risk. This association may differ by histological type. The authors conducted a population-based case-control study in Canada of 442 incident cases of ovarian cancer and 2,135 controls 20-76 years of age during 1994-1997 to examine this association, overall and by histological type. Compared to women who never smoked, those who smoked had higher odds (odds ratio [OR] = 1.22; 95% confidence interval [CI] = 0.98-1.53) of having ovarian cancer, and the OR was larger for ex-smokers (1.30; 95% CI = 1.01-1.67) than for current smokers (1.10; 95% CI = 0.81-1.49). The association with cigarette smoking was stronger for mucinous tumors (OR = 1.77; 95% CI = 1.06-2.96) than for nonmucinous tumors (OR = 1.13; 95% CI = 0.89-1.44). In addition, the odds of smokers having mucinous tumors increased with years of smoking (OR = 1.36, 1.88, 1.19, 4.89 for <20, 21-30, 31-40 and >40 years, respectively; p for trend = 0.002), number of cigarettes smoked per day (OR = 1.55, 1.89, 2.28 for <10, 11-20 and >20 cigarettes/day, respectively; p for trend = 0.014) and smoking pack-years (OR = 1.13, 2.65, 1.77 and 2.39 for <10, 11-20, 21-30 and >30 pack-years, respectively; p for trend = 0.004). Our data suggest that cigarette smoking is associated with an increased risk of ovarian cancer, especially for mucinous types. 相似文献
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Luke J. Peppone Mary E. Reid Kirsten B. Moysich Gary R. Morrow Pascal Jean-Pierre Supriya G. Mohile Tom V. Darling Andrew Hyland 《Cancer causes & control : CCC》2010,21(8):1247-1255
Background
Studies published prior to 1980 failed to find an association between smoking and colorectal cancer, while subsequent studies reported an association after accounting for a three to four decade initiation period. The aims of this study were to determine the effect of accounting for secondhand smoke (SHS) exposure on the association between smoking and colorectal cancer and to determine the association between SHS and colorectal cancer. 相似文献7.
Cardiometabolic risk factors and survival after breast cancer in the Women's Health Initiative
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Michael S. Simon MD MPH Jennifer L. Beebe‐Dimmer PhD Theresa A. Hastert PhD JoAnn E. Manson MD DrPH Elizabeth M. Cespedes Feliciano ScD Marian L. Neuhouser PhD RD Gloria Y. F. Ho PhD Jo L. Freudenheim PhD Howard Strickler MD Julie Ruterbusch MPH Ana Barac MD PhD Rowan Chlebowski MD PhD Bette Caan DrPH 《Cancer》2018,124(8):1798-1807
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Terry PD Miller AB Rohan TE 《International journal of cancer. Journal international du cancer》2002,99(3):480-483
Epidemiological studies have consistently found a positive association between cigarette smoking and risk of colorectal adenomas, so the absence of a clear association between smoking and colorectal cancer risk may seem paradoxical. However, if colorectal cancer develops only after an induction period of about 35 years, as has been proposed recently, then studies in which all subjects have fewer than about 35 years between smoking commencement and assessment of outcome would be unlikely to detect this association. Few studies have examined smoking of several decades' duration among women. Therefore, in the cohort study reported here, we used proportional hazards models to estimate hazard ratios relating cigarette smoking to colorectal cancer risk among 89,835 women aged 40-59 years at recruitment into the Canadian National Breast Screening Study, a randomized controlled trial of mammography screening for breast cancer. During an average 10.6 years of follow-up (936,433 person-years), a total of 527 women were diagnosed with incident colorectal cancer (363 colon and 164 rectal). We found that smoking was associated with increased risk of rectal cancer 30 years or more after commencement, and especially with smoking of 40 years' duration or longer (hazard ratio=3.14, 95% CI=1.33-7.42). There was little evidence for altered risk of colon cancer. These results, along with those of other recent studies, support the hypothesis that tobacco smoking is an initiator, rather than a promoter, of rectal cancer. However, the results do not support an association with colon cancer risk, even with smoking of very long duration and high intensity. 相似文献
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Mona S?b? Camilla F Skjelbred Rebecca Breistein Inger Marie B Lothe Per Chr Hagen Gunter Bock Inger-Lise Hansteen Elin H Kure 《BMC cancer》2006,6(1):71
Background
The association between colorectal cancer (CRC) and smoking has not been consistent. Incomplete smoking history and association to a specific subset of CRC tumors have been proposed as explanations. The adenomatous polyposis coli (APC) gene has been reported to have a "gatekeeper" function in the colonic mucosa. 相似文献10.
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Theodore M. Brasky Roberta M. Ray Sandi L. Navarro Jeannette M. Schenk Alison M. Newton Marian L. Neuhouser 《International journal of cancer. Journal international du cancer》2020,147(5):1374-1384
We and others have reported associations between B vitamins principally involved in one-carbon metabolism and increased lung cancer risk; however, results for women have been inconsistent. Here we report on the association of supplemental vitamins B6, folic acid and B12 intake and lung cancer risk using data from the Women's Health Initiative (WHI) study of postmenopausal women. Between 1993 and 1998, 161,808 women were recruited to participate in the WHI at 40 clinical centers in the US. After exclusions, 159,232 women were available for analysis and followed prospectively for an average of 18.3 years. Among them, 3,836 incident lung cancer cases were diagnosed. At baseline, supplemental B vitamins from multivitamins, vitamin mixtures and individual supplements were assessed. Adjusted Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between supplemental B vitamin intake and lung cancer risk. Relative to no intake, women who took ≥50 mg/day of vitamin B6 had 16% (HR 0.84, 95% CI: 0.71–0.99) reduced lung cancer risk. Associations did not differ significantly by smoking status or lung cancer histology. Intakes of folic acid and vitamin B12 were not associated with risk. There is a need for replication of our findings from other large, prospective studies with similar high-quality measurement of supplement intakes before any recommendations can be made at present on B6 supplementation for lung cancer prevention in women. 相似文献
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Breast cancer and nonsteroidal anti-inflammatory drugs: prospective results from the Women's Health Initiative 总被引:18,自引:0,他引:18
Harris RE Chlebowski RT Jackson RD Frid DJ Ascenseo JL Anderson G Loar A Rodabough RJ White E McTiernan A;Women's Health Initiative 《Cancer research》2003,63(18):6096-6101
We analyzed data from the prospective Women's Health Initiative (WHI) Observational Study to examine the effects of regular use of aspirin, ibuprofen, and other nonsteroidal anti-inflammatory drugs (NSAIDs) on breast cancer risk. We studied a population of 80,741 postmenopausal women between 50 and 79 years of age who reported no history of breast cancer or other cancers (excluding nonmelanoma skin cancer), and we completed a personal baseline interview that elicited comprehensive health information including data on breast cancer risk factors and NSAID use. All of the cases were adjudicated by WHI physicians using pathology reports. Our analysis was based on 1392 confirmed cases of breast cancer. Relative risks (RRs) with 95% confidence intervals (CIs) were estimated with adjustment for age and other breast cancer risk factors. Regular NSAID use (two or more tablets/week) for 5-9 years produced a 21% reduction in the incidence of breast cancer (RR, 0.79; 95% CI, 0.60-1.04); regular NSAID use for 10 or more years produced a 28% reduction (RR, 0.72; CI, 0.56-0.91), and there was a statistically significant inverse linear trend of breast cancer incidence with the duration of NSAID use (P < 0.01). The estimated risk reduction for long-term use of ibuprofen (RR, 0.51; CI, 0.28-0.96) was greater than for aspirin (RR, 0.79; CI, 0.60-1.03). Subgroup analysis by breast cancer risk factors did not result in effect modification. Regular use of acetaminophen (an analgesic agent with little or no anti-inflammatory activity) or low-dose aspirin (<100 mg) was unrelated to the incidence of breast cancer. Our results indicate that the regular use of aspirin, ibuprofen, or other NSAIDs may have a significant chemopreventive effect against the development of breast cancer and underscore the need for clinical trials to confirm this effect. 相似文献
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Higginbotham S Zhang ZF Lee IM Cook NR Giovannucci E Buring JE Liu S;Women's Health Study 《Journal of the National Cancer Institute》2004,96(3):229-233
Although diet is believed to influence colorectal cancer risk, the long-term effects of a diet with a high glycemic load are unclear. The growing recognition that colorectal cancer may be promoted by hyperinsulinemia and insulin resistance suggests that a diet inducing high blood glucose levels and an elevated insulin response may contribute to a metabolic environment conducive to tumor growth. We prospectively followed a cohort of 38 451 women for an average of 7.9 years and identified 174 with incident colorectal cancer. We used baseline dietary intake measurements, assessed with a semiquantitative food-frequency questionnaire, to examine the associations of dietary glycemic load, overall dietary glycemic index, carbohydrate, fiber, nonfiber carbohydrate, sucrose, and fructose with the subsequent development of colorectal cancer. Cox proportional hazards models were used to estimate relative risks (RRs). Dietary glycemic load was statistically significantly associated with an increased risk of colorectal cancer (adjusted RR = 2.85, 95% confidence interval [CI] = 1.40 to 5.80, comparing extreme quintiles of dietary glycemic load; P(trend) =.004) and was associated, although not statistically significantly, with overall glycemic index (corresponding RR = 1.71, 95% CI = 0.98 to 2.98; P(trend) =.04). Total carbohydrate (adjusted RR = 2.41, 95% CI = 1.10 to 5.27, comparing extreme quintiles of carbohydrate; P(trend) =.02), nonfiber carbohydrate (corresponding RR = 2.60, 95% CI = 1.22 to 5.54; P(trend) =.02), and fructose (corresponding RR = 2.09, 95% CI = 1.13 to 3.87; P(trend) =.08) were also statistically significantly associated with increased risk. Thus, our data indicate that a diet with a high dietary glycemic load may increase the risk of colorectal cancer in women. 相似文献
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Red blood cell folate and plasma folate are not associated with risk of incident colorectal cancer in the Women's Health Initiative observational study
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Marian L. Neuhouser Ting‐Yuan David Cheng Shirley A.A. Beresford Elissa Brown Xiaoling Song Joshua W. Miller Yingye Zheng Cynthia A. Thomson James M. Shikany Mara Z. Vitolins Thomas Rohan Ralph Green Cornelia M. Ulrich 《International journal of cancer. Journal international du cancer》2015,137(4):930-939
The relationship between folate and colorectal cancer (CRC) risk is unclear. We investigated the association of two biomarkers of folate status, plasma folate and red blood cell (RBC) folate, with CRC risk using a nested case–control design in the Women's Health Initiative Observational Study. Postmenopausal women (n = 93,676) aged 50–79 years were enrolled in the Women's Health Initiative Observational Study (1993–1998). A fasting blood draw and extensive health, dietary and lifestyle data were collected upon enrollment. Through 2008, 988 incident CRC cases were reported and confirmed with medical records adjudication. Cases and controls were matched on age (±3 years), enrollment date (±1 year), race/ethnicity, blood draw date (±6 months) and hysterectomy status. Plasma and RBC folate were determined by radio assay. Folate biomarker values were divided into quartiles, and conditional logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CI) for the associations of folate with total CRC, by tumor site and by stage at diagnosis. Additional analyses examined whether risks varied across time periods corresponding to the United States folic acid fortification policy: prefortification (1994–1995), perifortification (1996–1997) and postfortification (1998). ORs for overall CRC risk comparing Q4 vs. Q1 were 0.91 (95% CI 0.67–1.24) and 0.91 (95% CI 0.67–1.23) for RBC and plasma folate, respectively. There were no changes in risk attributable to food supply fortification. These results do not support an overall association of folate with CRC risk and suggest that folic acid fortification of the US food supply did not alter the associations in these postmenopausal women. 相似文献
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Familial clustering of breast and prostate cancer and risk of postmenopausal breast cancer in the Women's Health Initiative Study
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Jennifer L. Beebe‐Dimmer MPH PhD Cecilia Yee MS Michele L. Cote MPH PhD Nancie Petrucelli MS Nynikka Palmer MPH DrPH Cathryn Bock MPH PhD Dorothy Lane MD MPH Ilir Agalliu MD ScD Marcia L. Stefanick PhD Michael S. Simon MD MPH 《Cancer》2015,121(8):1265-1272
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Jagtap D Rosenberg CA Martin LW Pettinger M Khandekar J Lane D Ockene I Simon MS 《Cancer》2012,118(20):5124-5131
BACKGROUND:
Melanoma is the most lethal form of skin cancer, with an estimated 68,130 new cases and 8700 deaths in the United States in 2010. The increasing incidence and high death rate associated with metastatic disease support the need to focus on prevention. The authors used data from the Women's Health Initiative (WHI) to assess whether 3‐hydroxy‐3 methylglutaryl coenzyme A inhibitors (statins) are associated with a decreased risk of melanoma.METHODS:
The study population consisted of 119,726 postmenopausal white women, in which 1099 cases of malignant melanoma were identified over an average (±standard deviation) of 11.6 ± 3.2 years. All diagnoses were confirmed by medical record review and pathology reports. Information on statin use was collected at baseline and during follow‐up. Self‐administered and interview‐administered questionnaires were used to collect information on other risk factors. Cox proportional hazards regression was used to calculate hazard ratios (HRs) with 95% confidence intervals (CIs). Analyses investigated the association of any statin use, type, potency, lipophilic status, and duration of use with melanoma.RESULTS:
Statins were used by 8824 women (7.4%) at baseline. The annualized rate of melanoma was 0.09% among statin users and 0.09% among nonusers The multivariable adjusted HR for statin users compared with nonusers was 1.14 (95% CI, 0.91‐1.43). There were no significant differences in risk based on statin type, potency, category, duration, or in time‐dependent models.CONCLUSIONS:
There was no significant association between statin use and melanoma risk among postmenopausal women in the WHI. Cancer 2012. © 2012 American Cancer Society. 相似文献19.
Mizobuchi S Furihata M Sonobe H Ohtsuki Y Ishikawa T Murakami H Kurabayashi A Ogoshi S Sasaguri S 《Japanese journal of clinical oncology》2000,30(10):423-428
BACKGROUND: It is generally accepted that cigarette smoking is closely associated with esophageal squamous cell carcinoma. This study investigated the molecular targets of cigarette smoke in carcinogenesis of the esophagus. METHODS: Seventy-four patients with esophageal squamous cell carcinoma (SCC) were grouped according to daily cigarette consumption: heavy smoking group (group H) (n = 26), moderate smoking group (group M) (n = 39) and non-smoking group (group N) (n = 9). We compared p53 and retinoblastoma (RB) expression among the three groups by immunohistochemistry. In addition, fresh tumor tissues from 30 smokers with esophageal SCC were tested for p53 mutations in exons 5-8 by direct sequencing. RESULTS: Staining for the p53 product was positive in 65.4% of group H, 38.5% of group M and 44.4% of group N. The frequency of positive staining in the group H was significantly higher than in group M (p = 0.033) and in group M + group N (p = 0.034). The difference with respect to the frequency of overexpression of RB was not significant. The patterns of p53 base-pair mutations in direct sequencing study were of five types, most commonly G:C to T:A transversion (35.3%). CONCLUSIONS: Our study suggests that one of the molecular targets of cigarette smoke is the p53 gene. The pattern of p53 point mutations involved a wide range of base-pair changes. 相似文献