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Purpose: To examine the associations between red blood cell (RBC) composition of polyunsaturated fatty acids (PUFAs) and mortality among women with breast cancer. Methods: This nested case-control study included 1,104 women from the Women's Healthy Eating and Living Study, a randomized controlled trial of a plant-based dietary change on breast cancer survival. Cases were women who died from any cause (n = 290) from 1995 to 2006. Controls were women who were alive at the end of follow-up matched to cases on age at diagnosis, years since randomization, intervention group, and stage (n = 814). RBC fatty acid composition was measured in blood samples collected at baseline using gas chromatography and included the proportions of four n-3 and seven n-6 PUFAS. We examined each PUFA individually as well as factor analysis-derived factors in association with all-cause and breast cancer-specific mortality using conditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results: In fully-adjusted models, all-cause mortality ORs were elevated among women with PUFAs >median (versus = median) for alpha-linolenic acid (ALA, C18:3n3; OR = 1.56; 95% CI = 1.14-2.14) and for linolenic acid (LnA, C18:2n6, OR = 1.54; 95% CI = 1.15-2.07), and breast cancer-specific mortality ORs were elevated for LnA (OR = 1.72, 95% CI = 1.24-2.38) and gamma-linolenic acid (GLA, C18:3n6; OR = 1.40; 95% CI = 0.97-2.00). Factor 1 [arachidonic acid, C20:4n6; adrenic acid, C22:4n6; and docosapentaenoic acid, C22:5n6] scores >median (versus =median) were associated with lower odds of all-cause (OR = 0.72; 95% CI = 0.53-0.98) and breast cancer-specific (OR = 0.67; 95% CI = 0.47-0.94) mortality, and Factor 4 [ALA and GLA] scores >median (versus =median) were associated with increased odds of breast cancer-specific mortality (OR = 1.42; 95% CI = 1.01-2.01). Additionally, 1-SD increase in Factor 4 scores were associated with ORs of 1.22 (95% CI = 1.04-1.42) for all-cause mortality and 1.24 (95% CI = 1.05-1.47) for breast cancer-specific mortality. Conclusions: RBC PUFA composition profiles are associated with all-cause and breast cancer-specific mortality risk among women with breast cancer. [ABSTRACT FROM AUTHOR]

Unlabelled: Development of potential cancer chemopreventive drugs involves the systematic evaluation of these drugs in preliminary Phase I and II studies in human beings to identify the optimal drug dose, drug toxicity, and surrogate end point biomarker modulation., Objectives: We tested the hypothesis that aspirin, at a single, once-daily 81-mg dose, will reduce colonic mucosal concentration of prostaglandin estradiol (E2) in individuals at high risk for colorectal cancer development similar to our prior observations in a young normal-risk population., Methods: Aspirin was administered at a dose of 81 mg once daily for 28 days in a cohort of 92 matched high-risk and normal-risk colorectal cancer subjects. Prostaglandin E2 and cyclooxygenase expression were assayed from distal sigmoid biopsies from all of the subjects before and after treatment., Results: The mean prostaglandin E2 for normal-risk subjects before aspirin treatment was 11.3 +/- 1.7 pg/microg (mean +/- SE) tissue protein and after aspirin treatment was 4.9 +/- 0.91 pg/microg tissue protein (P < 0.0001). In high-risk subjects, mean pretreatment prostaglandin E2 was 14.4 +/- 1.7 pg/microg tissue protein and after aspirin treatment was 4.7 +/- 0.70 pg/microg tissue protein (P < 0.0001). Aspirin treatment did not alter cyclooxygenase-1 protein expression., Conclusions: Aspirin treatment at a dose of 81 mg reduces colorectal mucosal prostaglandin E2 concentration after 28 daily doses. Risk for colorectal carcinoma did not modify colorectal mucosal baseline or post-aspirin prostaglandin E2, or cyclooxygenase expression. Colorectal mucosal prostaglandin concentration may be used as a "drug-effect surrogate biomarker," that is, a surrogate to assess sufficient delivery and tissue effect of a chemopreventive agent.

This study examined the extent of low-energy reporting and its relationship with demographic and lifestyle factors in women previously treated for breast cancer. This study used data from a large multisite clinical trial testing the efficacy of a dietary intervention to reduce risk for breast cancer recurrence (Women's Healthy Eating and Living Study). Using the Schofield equation to estimate energy needs and four 24-h dietary recalls to estimate energy intakes, we identified women who reported lower than expected energy intakes using criteria developed by G. R. Goldberg et al. (Eur. J. Clin. Nutr., 45: 569-581, 1991). We examined data from 1137 women diagnosed with stage I, stage II, or stage IIIA primary, operable breast cancer. Women were 18-70 years of age at diagnosis and were enrolled in the Women's Healthy Eating and Living Study between August 19, 1995, and April 1, 1998, within 4 years after diagnosis. The Goldberg criteria classified about one-quarter (25.6%) as low-energy reporters (LERs) and 10.8% as very LERs. Women who had a body mass index >30 were almost twice (odds ratio, 1.95) as likely to be LERs. Women with a history of weight gain or weight fluctuations were one and a half times as likely (odds ratio, 1.55) to be LERs as those who were weight stable or weight losers. Age, ethnicity, alcohol intake, supplement use, and exercise level were also related to LER. Characteristics (such as body mass index, age, ethnicity, and weight history) that are associated with low-energy reporting in this group of cancer survivors are similar to those observed in other populations and might affect observed diet and breast cancer associations in epidemiological studies.

The objective of this study was to examine serum concentrations of alpha-carotene, beta-carotene, lutein, lycopene, and beta-cryptoxanthin due to consumption of vegetable juice versus raw or cooked vegetables. Subjects included female breast cancer patients who had undergone surgical resection and who were enrolled in a feasibility study for a trial examining the influence of diet on breast cancer recurrence. A high-vegetable, low-fat diet was the focus of the intervention, and some of the subjects were specifically encouraged to consume vegetable juice. At 12 months, blood samples were collected and analyzed for carotenoid concentrations via high-performance liquid chromatography methodology. Matched analysis and paired t test were conducted on two groups: those who consumed vegetable juice (the juice group) and those who consumed raw or cooked vegetables (no juice group). Serum concentrations of alpha-carotene and lutein were significantly higher in the vegetable juice group than in the raw or cooked vegetable group (P < 0.05 and P = 0.05, respectively). Paired t test analysis did not demonstrate a significant difference in serum values of beta-carotene, lycopene, and beta-cryptoxanthin between subjects consuming juice and those not consuming any juice. These results suggest that alpha-carotene and lutein appear to be more bioavailable in the juice form than in raw or cooked vegetables. Therefore, the food form consumed may contribute to the variability in serum carotenoid response to vegetable and fruit interventions in clinical studies.

Epidemiological studies suggest that a high vegetable diet may reduce risk for breast cancer and may also improve prognosis after the diagnosis of breast cancer. Circulating carotenoids may serve as a biomarker of vegetable and fruit intake, although several factors affect their bioavailability from food sources and may influence concentrations. One purpose of this study was to identify factors predictive of serum carotenoid, retinol, and alpha-tocopherol concentrations in 79 postsurgically resected breast cancer patients at enrollment and at 12 months in a feasibility study of a high vegetable, low fat diet intervention to reduce risk for cancer recurrence. Another purpose was to identify variables associated with change in these serum concentrations 12 months after randomization into control and intervention groups. The diet intervention (versus control) group had significantly greater increases in carotenoid intakes (P < 0.03) and significantly greater increases in serum concentrations of lutein, alpha- and beta-carotene, lycopene, and retinol (P < 0.04). Stepwise multiple regression revealed the level of dietary intake to be predictive of most serum carotenoid concentrations at baseline and 12 months, with additional associations between selected micronutrient concentrations and serum cholesterol, body mass index, age, percentage of energy intake from fat, and alcohol intake also observed at these time points. Intervention group change in serum carotenoid concentrations was inversely associated with baseline level, age, and change in serum cholesterol concentration and positively associated with change in carotenoid and alcohol intake. Circulating carotenoid concentrations are responsive to a high vegetable diet intervention, which also included reduced dietary fat and increased fiber intakes, to reduce risk for breast cancer recurrence.

An association between serum carotenoid concentrations and risk for certain cancers has been observed in epidemiological studies. Determinants of serum carotenoid concentrations are known to include dietary intake, plasma lipid concentrations, and body mass. Menstrual cycle phase, which has not been adequately addressed in previous studies, has been suggested to be a possible additional factor to consider in the interpretation of these values in women. We evaluated hormonal status, serum carotenoids, cholesterol, and triglycerides in 48 healthy women at early follicular, mid-luteal, and late luteal phases of one menstrual cycle. Eating patterns were assessed with diet records at two 3-day intervals during the cycle. Analysis was focused on the 30 subjects who were determined to have ovulated during the menstrual cycle under observation. Serum cholesterol was significantly decreased (P < 0.05) in the late luteal phase of an ovulatory cycle. Lutein concentration was increased in the early follicular phase (P < 0.05) and alpha-carotene was increased in the mid-luteal phase (P < 0.05) only if uncorrected for total cholesterol. Other carotenoids did not vary across the menstrual cycle, whether corrected or uncorrected for total cholesterol concentration. In normal healthy ovulating women, serum carotenoids do not appear to vary with menstrual cycle phase when corrected for serum cholesterol concentrations.