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Articles by A McTiernan
Total Records ( 5 ) for A McTiernan
  A McTiernan , J Wactawski Wende , L Wu , R. J Rodabough , R Freeman , S Hendrix and R. Jackson
 

Background: The effects of dietary changes on osteoporosis, low bone density, and frequent falls are unestablished.

Objective: We assessed the effect of the Women's Health Initiative Dietary Modification low-fat and increased fruit, vegetable, and grain intervention on incident hip, total, and site-specific fractures and self-reported falls, and, in a subset, on bone mineral density (BMD).

Design: Postmenopausal women (n = 48,835) aged 50–79 y (18.6% of minority race-ethnicity) were randomly assigned to receive the Dietary Modification intervention (40%, n = 19,541) (daily goal: ≤20% of energy as fat, ≥5 servings of vegetables and fruit, and ≥6 servings of grains) or to a comparison group that received no dietary changes (60%; n = 29,294).

Results: After a mean 8.1 y of follow-up, 215 women in the intervention group and 285 women in the comparison group (annualized rate: 0.14% and 0.12%, respectively) experienced a hip fracture (hazard ratio: 1.12; 95% CI: 0.94, 1.34; P = 0.21). The intervention group (n = 5423; annualized rate: 3.44%) had a lower rate of reporting ≥2 falls than did the comparison group (n = 8695; annualized rate: 3.67%) (HR: 0.92; 95% CI: 0.89, 0.96; P < 0.01). There was a significant interaction according to hormone therapy use; those in the comparison group receiving hormone therapy had the lowest incidence of hip fracture. In a subset of 3951 women, hip BMD at years 3, 6, and 9 was 0.4–0.5% lower in the intervention group than in the comparison group (P = 0.003).

Conclusions: A low-fat and increased fruit, vegetable, and grain diet intervention modestly reduced the risk of multiple falls and slightly lowered hip BMD but did not change the risk of osteoporotic fractures. This trial was registered at clinicaltrials.gov as NCT00000611.

  C. J Crandall , A. K Aragaki , R. T Chlebowski , A McTiernan , G Anderson , S. L Hendrix , B. B Cochrane , L. H Kuller and J. A. Cauley
 

Background  Estrogen plus progestin therapy increases breast cancer incidence and breast tenderness. Whether breast tenderness during estrogen plus progestin therapy is associated with breast cancer risk is uncertain.

Methods  We analyzed data from the Women's Health Initiative Estrogen + Progestin Trial, which randomized postmenopausal women with an intact uterus to receive daily conjugated equine estrogens, 0.625 mg, plus medroxyprogesterone acetate, 2.5 mg (n = 8506), or placebo (n = 8102). At baseline and annually, participants underwent mammography and clinical breast examination. Self-reported breast tenderness was assessed at baseline and at 12 months. The incidence of invasive breast cancer was confirmed by medical record review (mean follow-up of 5.6 years).

Results  Of women without baseline breast tenderness (n = 14 538), significantly more assigned to receive conjugated equine estrogens plus medroxyprogesterone vs placebo experienced new-onset breast tenderness after 12 months (36.1% vs 11.8%, P < .001). Of women in the conjugated equine estrogens plus medroxyprogesterone group, breast cancer risk was significantly higher in those with new-onset breast tenderness compared with those without (hazard ratio, 1.48; 95% confidence interval, 1.08-2.03; P = .02). In the placebo group, breast cancer risk was not significantly associated with new-onset breast tenderness (P = .97).

Conclusions  New-onset breast tenderness during conjugated equine estrogens plus medroxyprogesterone therapy was associated with increased breast cancer risk. The sensitivity and specificity of the association between breast tenderness and breast cancer were similar in magnitude to those of the Gail model.

Trial Registration  clinicaltrials.gov Identifier: NCT00000611

  A. A Arslan , K. J Helzlsouer , C Kooperberg , X. O Shu , E Steplowski , H. B Bueno de Mesquita , C. S Fuchs , M. D Gross , E. J Jacobs , A. Z LaCroix , G. M Petersen , R. Z Stolzenberg Solomon , W Zheng , D Albanes , L Amundadottir , W. R Bamlet , A Barricarte , S. A Bingham , H Boeing , M. C Boutron Ruault , J. E Buring , S. J Chanock , S Clipp , J. M Gaziano , E. L Giovannucci , S. E Hankinson , P Hartge , R. N Hoover , D. J Hunter , A Hutchinson , K. B Jacobs , P Kraft , S. M Lynch , J Manjer , J. E Manson , A McTiernan , R. R McWilliams , J. B Mendelsohn , D. S Michaud , D Palli , T. E Rohan , N Slimani , G Thomas , A Tjonneland , G. S Tobias , D Trichopoulos , J Virtamo , B. M Wolpin , K Yu , A Zeleniuch Jacquotte and A. V. Patel
 

Background  Obesity has been proposed as a risk factor for pancreatic cancer.

Methods  Pooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, <18.5; normal weight, 18.5-24.9; overweight, 25.0-29.9; obese, 30.0-34.9; and severely obese, ≥35.0). Models were adjusted for potential confounders.

Results  In all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; Ptrend < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; Ptrend < .03), and in women it was 1.34 (95% CI, 1.05-1.70; Ptrend = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; Ptrend = .003) but less so in men.

Conclusions  These findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.

  H. J Thompson , P Wolfe , A McTiernan , W Jiang and Z. Zhu
 

The purpose of this investigation was to identify pathways by which physical activity, implemented as running in an activity wheel, inhibits carcinogenesis. The focus of this analysis was on 20 plasma biomarkers for glucose homeostasis, inflammation, cytokine function, and endocrine activity, known to be affected by a physically active lifestyle. Plasma for analysis was obtained from previously reported carcinogenesis experiments in which the effects on mammary carcinogenesis, induced by i.p. injection of 1-methyl-1-nitrosurea, of running on a motorized activity wheel or a nonmotorized free wheel were compared with sedentary controls. Wheel running reduced cancer incidence (P = 0.0004) and the number of cancers per animal (P = 0.005). Principal components analysis was used to reduce the 20 plasma biomarkers to a concise index that was significantly different by treatment group assignment (P < 0.0001). Statistical analyses provided evidence that supported the hypothesis of a mediational role of these molecules in accounting for the protective effect of wheel running on the carcinogenic process. In addition, the plasma biomarker index derived from principal components analysis was a good discriminator of treatment group assignment (only 4.5% of animals were misclassified). These findings suggest that the plasma biomarkers evaluated have utility in assessing the breast cancer response to a physical activity intervention. Identification of such biomarkers is critical in clinical studies for which evaluating the effects of physical activity on cancer outcomes (diagnosis, recurrence, or mortality) is not possible. Cancer Prev Res; 3(11); 1484–92. ©2010 AACR.

  P. B Mann , W Jiang , Z Zhu , P Wolfe , A McTiernan and H. J. Thompson
 

Emerging evidence indicates that intrinsic differences and induced changes in aerobic capacity are probably to play a critical role in the development of chronic diseases like cancer. This study was initiated: (i) to determine how citrate synthase activity, which is routinely used as a marker of aerobic capacity and mitochondrial density in skeletal muscle, was affected by voluntary running on either a motorized activity wheel or a non-motorized free wheel and (ii) to investigate the association between aerobic capacity and the carcinogenic response induced in the mammary gland by intraperitoneal injection of 1-methyl-1-nitrosurea. Overall, wheel running reduced cancer incidence (96 versus72%, P = 0.0006) and the number of cancers per animal (2.84 versus 1.78, P < 0.0001) and induced citrate synthase activity (276 versus 353 U/mg, P < 0.0001, sedentary control versus wheel running,respectively). Both motorized and free wheel running increased citrate synthase activity (373 ± 24, 329 ± 11 and 276 ± 9 U/mg protein, P < 0.0001) and reduced the average number of cancers per rat (2.84, 1.96 and 1.63, P < 0.01), sedentary control, free wheel and motorized wheel, respectively. However, regression analyses failed to provide evidence of a significant association between citrate synthase activity and either cancer incidence or cancer multiplicity. Citrate synthase activity is a single measure in a complex pathway that determines aerobic capacity. The multifaceted nature of intrinsic and inducible aerobic capacity limits the usefulness of citrate synthase activity alone in elucidating the relationship between aerobic capacity and the carcinogenic response.

 
 
 
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