Biomedical subjects

Yutaka Yasui

Publications and source records attributed to Yutaka Yasui.

At least 19 recordsLinked to original sources

PubMed2026

Integrating genetic predictors into subsequent breast cancer risk prediction in survivors of childhood cancer.

PURPOSE: Female survivors of childhood cancer are at high risk for developing breast cancer. The contributions of most general population primary breast cancer genetic predictors to this risk have not been explored. METHODS: Analyses included females who survived ≥5 years after their childhood cancer diagnosis with available array (N = 2096, subsequent breast cancer [SBC]=218) or whole-genome sequencing (WGS; N = 3292, SBC=101) data from the Childhood Cancer Survivor Study and St. Jude Lifetime Cohort. We computed 99 externally-validated primary breast cancer polygenic risk scores (PRS). Using deep-coverage WGS, ClinVar-annotated pathogenic/likely pathogenic (P/LP) variants in breast cancer susceptibility genes were identified. Cox proportional hazards models assessed associations with SBC risk, adjusting for treatments and genetic ancestry. RESULTS: Among 5388 female survivors (genetic ancestry, European: N = 4,752; African: N = 444; East Asian: N = 192), 319 developed SBC. Most (90.9%) PRSs were nominally associated with SBC risk (P < 0.05), but effect sizes varied substantially. PRSs with superior discriminatory ability had greater genome-wide coverage (e.g., 6.4 million-variant PRS, HR per SD = 1.71, 95% CI = 1.43 to 2.05; P = 4.2x10-9) and 7.7-fold higher odds (P = 7.0x10-4) of including variants in multiple DNA damage repair pathways compared with PRSs with weaker risk associations. Among survivors with WGS, 1.6% carried P/LP variants in clinical testing panel genes, which was associated with a 7.4-fold greater risk (95% CI = 3.16 to 17.19). Including genetic factors improved SBC risk prediction by age 40 (P < 0.001) compared to treatment exposures alone. CONCLUSIONS: Externally-validated primary breast cancer genetic susceptibility predictors are relevant for SBC risk prediction and should be prioritized for risk stratification in survivors.

Journal Article↗

PubMed2005

Evaluation of serum protein profiling by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry for the detection of prostate cancer: I. Assessment of platform reproducibility.

BACKGROUND: Protein expression profiling for differences indicative of early cancer has promise for improving diagnostics. This report describes the first stage of a National Cancer Institute/Early Detection Research Network-sponsored multiinstitutional evaluation and validation of this approach for detection of prostate cancer. METHODS: Two sequential experimental phases were conducted to establish interlaboratory calibration and standardization of the surface-enhanced laser desorption (SELDI) instrumental and assay platform output. We first established whether the output from multiple calibrated Protein Biosystem II SELDI-ionization time-of-flight mass spectrometry (TOF-MS) instruments demonstrated acceptable interlaboratory reproducibility. This was determined by measuring mass accuracy, resolution, signal-to-noise ratio, and normalized intensity of three m/z "peaks" present in a standard pooled serum sample. We next evaluated the ability of the calibrated and standardized instrumentation to accurately differentiate between selected cases of prostate cancer and control by use of an algorithm developed from data derived from a single site 2 years earlier. RESULTS: When the described standard operating procedures were established at all laboratory sites, the across-laboratory measurements revealed a CV for mass accuracy of 0.1%, signal-to-noise ratio of approximately 40%, and normalized intensity of 15-36% for the three pooled serum peaks. This was comparable to the intralaboratory measurements of the same peaks. The instrument systems were then challenged with sera from a selected group of 14 cases and 14 controls. The classification agreement between each site and the established decision algorithm were examined by use of both raw peak intensity boosting and ranked peak intensity boosting. All six sites achieved perfect blinded classification for all samples when boosted alignment of raw intensities was used. Four of six sites achieved perfect blinded classification with ranked intensities, with one site passing the criteria of 26 of 28 correct and one site failing with 19 of 28 correct. CONCLUSIONS: These results demonstrate that "between-laboratory" reproducibility of SELDI-TOF-MS serum profiling approaches that of "within-laboratory" reproducibility as determined by measuring discrete m/z peaks over time and across laboratories.

Calibration↗

PubMed2004

Human plasma ghrelin levels increase during a one-year exercise program.

Weight loss resulting from decreased caloric intake raises levels of the orexigenic hormone, ghrelin. Because ingested nutrients suppress ghrelin, increased ghrelin levels in hypophagic weight loss may result from decreased inhibitory input by ingested food, rather than from lost weight. We assessed whether ghrelin levels increase in response to exercise-induced weight loss without decreased caloric intake. We randomized 173 sedentary, overweight, postmenopausal women to an aerobic exercise intervention or stretching control group. At baseline, 3 months, and 12 months, we measured body weight and composition, food intake, cardiopulmonary fitness (maximal oxygen consumption), leptin, insulin, and ghrelin. Complete data were available for 168 women (97%) at 12 months. Exercisers lost 1.4 +/- 0.4 kg (P < 0.05 compared with baseline; P = 0.01 compared with stretchers) and manifested a significant, progressive increase in ghrelin levels, whereas neither measure changed among stretchers. Ghrelin increased 18% in exercisers who lost more than 3 kg (P < 0.001). There was no change in caloric intake in either group and no effect on ghrelin of exercise per se independent of its impact on body weight. In summary, ghrelin levels increase with weight loss achieved without reduced food intake, consistent with a role for ghrelin in the adaptive response constraining weight loss and, thus, in long-term body weight regulation.

Body Mass Index↗

PubMed2004

Methylenetetrahydrofolate reductase genotype affects risk of relapse after hematopoietic cell transplantation for chronic myelogenous leukemia.

PURPOSE: Methylenetetrahydrofolate reductase (MTHFR) directs intracellular folate toward homocysteine metabolism and away from nucleotide synthesis. Two common MTHFR polymorphisms, C677T and A1298C, are associated with reduced enzyme activity. We evaluated the association of these polymorphisms with risk of relapse and bcr-abl mRNA transcript detection among 336 Caucasian patients who underwent allogeneic hematopoietic cell transplantation for chronic myelogenous leukemia. EXPERIMENTAL DESIGN: Data on the transplant course and folate-related exposures were abstracted from medical records. MTHFR C677T and A1298C genotypes were determined using polymerase chain reaction/restriction fragment length polymorphism and TaqMan assays. Qualitative bcr-abl mRNA testing was conducted using a two-step reverse transcription-polymerase chain reaction assay. Cox regression analysis was used to assess the association between MTHFR genotypes and time to relapse and bcr-abl mRNA detection. RESULTS: A statistically significant decreased risk of relapse was observed in patients with the variant A1298C genotype [1298AC, hazard ratio (HR)=0.48 and 95% confidence interval (CI)=0.26-0.88; 1298CC, HR=0.28 and 95% CI=0.09-0.84; P-trend <0.01). For the joint C677T/A1298C genotype, variant genotypes were associated with a decreased risk of relapse when compared with the wild-type 677CC/1298AA genotype. This risk was lowest for the 677CC/1298CC genotype (HR, 0.23; 95% CI, 0.08-0.72). MTHFR genotypes were not associated with bcr-abl transcript detection. CONCLUSIONS: These findings suggest that individuals with the 677CC/1298AA genotype are at higher risk of relapse after hematopoietic cell transplantation and that the balance of intracellular folate metabolites available for nucleotide synthesis (regulated by the relative activity of the MTHFR enzyme) may affect the progression from bcr-abl positivity to clinical relapse.

Adolescent↗

PubMed2004

Breast cancer after childhood cancer: a report from the Childhood Cancer Survivor Study.

BACKGROUND: Survivors of childhood cancer are at risk for secondary breast cancer. Other than previous chest radiation therapy, risk factors for secondary breast cancer have not been established. OBJECTIVE: To identify risk factors for breast cancer among female survivors of childhood cancer. DESIGN: Retrospective cohort study. SETTING: The Childhood Cancer Survivor Study (CCSS), a multicenter study of persons who survived more than 5 years after childhood cancer diagnosed from 1970 to 1986. PARTICIPANTS: Among 6068 women in the CCSS, 95 women had 111 confirmed cases of breast cancer. MEASUREMENTS: Standardized incidence ratios for breast cancer were calculated by using age-specific incidence rates in the general population. Breast cancer incidence was evaluated with respect to primary cancer diagnosis and therapy, age at and time since primary diagnosis, menstrual and reproductive history, and family history of cancer. RESULTS: Breast cancer risk was increased in survivors who were treated with chest radiation therapy (standardized incidence ratio, 24.7 [95% CI, 19.3 to 31.0]) and survivors of bone and soft-tissue sarcoma who were not treated with chest radiation therapy (standardized incidence ratios, 6.7 and 7.6, respectively). Family history of breast cancer (relative rate, 2.7 [CI, 1.3 to 5.0]) and history of thyroid disease (relative rate, 1.7 [CI, 1.1 to 2.6]) were independently associated with increased risk, and exposure to pelvic radiation was protective (relative rate, 0.6 [CI, 0.4 to 0.9]). Age at primary cancer diagnosis and menstrual and reproductive histories did not statistically significantly modify risk. LIMITATIONS: This cohort has not yet attained an age at which breast cancer risk is greatest. CONCLUSION: Survivors of childhood sarcomas and those who received chest radiation therapy are at risk for secondary breast cancer. When assessing a survivor's risk, clinicians should consider primary diagnosis, previous radiation therapy, family cancer history, and history of thyroid disease.

Adult↗

PubMed2004

XRCC1 and glutathione-S-transferase gene polymorphisms and susceptibility to radiotherapy-related malignancies in survivors of Hodgkin disease.

BACKGROUND: One of the most serious late effects of treatment for childhood cancer is the occurrence of subsequent malignancy. Survivors of Hodgkin disease (HD), in particular, have been shown to be at high risk of subsequent malignancy, the occurrence of which has been associated strongly with exposure to radiotherapy. METHODS: In the current study, the authors investigated the association between polymorphisms in 3 genes--glutathione-S-transferase M1 (GSTM1), glutathione-S-transferase T1 (GSTT1), and XRCC1, with roles in protection from a variety of DNA-damaging agents-and the risk of subsequent malignancy in 650 survivors of HD enrolled in the Childhood Cancer Survivor Study who had received radiotherapy. RESULTS: Individuals lacking GSTM1 but not GSTT1 were at increased risk of any subsequent malignancy (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.0-2.3), and for subsequent cancer within the radiation field (OR, 1.4; 95% CI, 0.9-2.1). A nonsignificant increased risk of thyroid carcinoma was observed in individuals lacking either GSTM1 (OR, 2.9; 95% CI, 0.8-10.9) or GSTT1 (OR, 3.7; 95% CI, 0.6-23.5). Individuals having the genotype of the arginine/glutamine polymorphism at codon 399 in the XRCC1 gene (R399) showed a nonsignificant increased risk of breast carcinoma compared with those without (OR, 1.4; 95% CI, 0.7-2.7), and a nonsignificant decreased risk against a subsequent thyroid carcinoma (OR, 0.6; 95% CI, 0.2-1.6). No differences in genotype frequencies were observed between survivors with basal cell carcinoma when compared with survivors without a subsequent cancer. CONCLUSIONS: These data illustrated the potential value of incorporating the collection of genomic DNA in longitudinal cohort studies of populations with well defined, potentially carcinogenic exposures. Evaluation of additional genetic polymorphisms in this cohort may help define genes that influence individual sensitivity to radiotherapy.

Adolescent↗

PubMed2004

Genetic variation in the leptin receptor gene and obesity in survivors of childhood acute lymphoblastic leukemia: a report from the Childhood Cancer Survivor Study.

PURPOSE: Overweight (body mass index [BMI] 25 to 29 kg/m2) and obesity (BMI > or = 30 kg/m2) frequently follow treatment for childhood acute lymphoblastic leukemia (ALL). Recent studies suggest that risk is most apparent in females treated with cranial radiation at a younger age. Because radiation at a young age may affect the hypothalamus causing leptin receptor insensitivity, we hypothesized that a polymorphism in the leptin receptor (LEPR) gene, Gln223Arg, might influence susceptibility to obesity in survivors of childhood ALL. PATIENTS AND METHODS: We genotyped 600 non-Hispanic white adult ALL survivors enrolled onto the Childhood Cancer Survivor Study. BMI was compared between those with two copies of the Arg allele to those who had at least one copy of the Gln allele. RESULTS: Female survivors with BMI > or = 25 kg/m2 were more likely Arg homozygous than those with BMI less than 25 kg/m2 (24% v 12%; P =.007). This difference was not observed in males. Moreover, among females treated with > or = 20 Gy cranial radiation, Arg/Arg individuals had six times higher odds of having BMI > or = 25 kg/m2 (95% CI, 2.1 to 22.0) than those with a Gln allele (P =.04 for interaction). CONCLUSION LEPR polymorphism may influence obesity in female survivors of childhood ALL, particularly those exposed to cranial radiation. Because obesity is associated with increased morbidity and mortality in later life, identification of children at high risk might allow for early targeted interventions.

Adolescent↗

PubMed2004

p19Arf suppresses growth, progression, and metastasis of Hras-driven carcinomas through p53-dependent and -independent pathways.

Ectopic expression of oncogenes such as Ras induces expression of p19(Arf), which, in turn, activates p53 and growth arrest. Here, we used a multistage model of squamous cell carcinoma development to investigate the functional interactions between Ras, p19(Arf), and p53 during tumor progression in the mouse. Skin tumors were induced in wild-type, p19(Arf)-deficient, and p53-deficient mice using the DMBA/TPA two-step protocol. Activating mutations in Hras were detected in all papillomas and carcinomas examined, regardless of genotype. Relative to wild-type mice, the growth rate of papillomas was greater in p19(Arf)-deficient mice, and reduced in p53-deficient mice. Malignant conversion of papillomas to squamous cell carcinomas, as well as metastasis to lymph nodes and lungs, was markedly accelerated in both p19 (Arf)- and p53-deficient mice. Thus, p19(Arf) inhibits the growth rate of tumors in a p53-independent manner. Through its regulation of p53, p19(Arf) also suppresses malignant conversion and metastasis. p53 expression was upregulated in papillomas from wild-type but not p19( Arf)-null mice, and p53 mutations were more frequently seen in wild-type than in p19( Arf)-null carcinomas. This indicates that selection for p53 mutations is a direct result of signaling from the initiating oncogenic lesion, Hras, acting through p19(Arf).

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2004

UDP-glucuronosyltransferase and sulfotransferase polymorphisms, sex hormone concentrations, and tumor receptor status in breast cancer patients.

INTRODUCTION: UDP-glucuronosyltransferase (UGT) and sulfotransferase (SULT) enzymes are involved in removing sex hormones from circulation. Polymorphic variation in five UGT and SULT genes - UGT1A1 ((TA)6/(TA)7), UGT2B4 (Asp458Glu), UGT2B7 (His268Tyr), UGT2B15 (Asp85Tyr), and SULT1A1 (Arg213His)--may be associated with circulating sex hormone concentrations, or the risk of an estrogen receptor-negative (ER-) or progesterone receptor-negative (PR-) tumor. METHODS: Logistic regression analysis was used to estimate the odds ratios of an ER- or PR- tumor associated with polymorphisms in the genes listed above for 163 breast cancer patients from a population-based cohort study of women in western Washington. Adjusted geometric mean estradiol, estrone, and testosterone concentrations were calculated within each UGT and SULT genotype for a subpopulation of postmenopausal breast cancer patients not on hormone therapy 2-3 years after diagnosis (n = 89). RESULTS: The variant allele of UGT1A1 was associated with reduced risk of an ER- tumor (P for trend = 0.03), and variants of UGT2B15 and SULT1A1 were associated with non-statistically significant risk reductions. There was some indication that plasma estradiol and testosterone concentrations varied by UGT2B15 and SULT1A1 genotypes; women with the UGT2B15 Asp/Tyr and Tyr/Tyr genotypes had higher concentrations of estradiol than women with the Asp/Asp genotype (P = 0.004). Compared with women with the SULT1A1 Arg/Arg and Arg/His genotypes, women with the His/His genotype had elevated concentrations of testosterone (P = 0.003). CONCLUSIONS: The risk of ER- breast cancer tumors may vary by UGT or SULT genotype. Further, plasma estradiol and testosterone concentrations in breast cancer patients may differ depending on some UGT and SULT genotypes.

Adult↗

PubMed2004

Effect of exercise on serum estrogens in postmenopausal women: a 12-month randomized clinical trial.

Elevated circulating estrogens and a sedentary lifestyle increase risk for breast cancer. The effect of exercise on circulating estrogens in sedentary postmenopausal women is unknown. The objective of this study was to examine the effects of a 12-month moderate-intensity exercise intervention on serum estrogens. We randomly assigned 173 sedentary, overweight (body mass index > 24.0 kg/m(2), body fat > 33%), postmenopausal women, ages 50-75 years, not using hormone therapy, living in the Seattle, Washington, area for the next year, and willing to be randomly assigned to an exercise intervention or stretching control group. The exercise intervention included facility and home-based exercise (45 min, 5 days/week moderate intensity sports/recreational exercise). A total of 170 (98.3%) women completed the study with exercisers averaging 171 min/week of exercise. After 3 months, exercisers experienced declines in estrone, estradiol, and free estradiol of 3.8, 7.7, and 8.2%, respectively, versus no change or increased concentrations in controls (P = 0.03, 0.07, and 0.02, respectively). At 12 months, the direction of effect remained the same, although the differences were no longer statistically significant. The effect was limited to women who lost body fat: women whose percentage of body fat [by dual energy x-ray absortiometry (DEXA)] decreased by >/==" BORDER="0">2% had statistically significant (comparing exercisers versus controls) decreases at 12 months of 11.9, 13.7, and 16.7% for serum estrone, estradiol, and free estradiol, respectively. We concluded that a 12-month moderate-intensity exercise intervention in postmenopausal women resulted in significant decreases in serum estrogens. The association between increased physical activity and reduced risk for postmenopausal breast cancer may be partly explained by effects on serum estrogens.

Aged↗

PubMed2004

TGFbeta1 polymorphism (L10P) and risk of colorectal adenomatous and hyperplastic polyps.

BACKGROUND: Transforming growth factor-beta1 (TGFbeta1) is a multifunctional signalling molecule with a wide array of roles. Animal experiments suggest that TGFbeta1 plays a biphasic role in carcinogenesis by protecting against the early formation of benign epithelial growths, but promoting malignant transformation of those growths that do develop. A polymorphism in the signal peptide sequence of the TGFbeta1 gene (L10P) has been associated with increased levels of plasma TGFbeta1 in individuals with the P allele. METHODS: We investigated whether this polymorphism was associated with the risk of colorectal adenomatous or hyperplastic polyps in a case-control study of individuals from Minnesota. Risk of colorectal polyps was evaluated separately for individuals with adenomatous polyps (n = 513) and hyperplastic polyps (n = 191) relative to polyp-free controls (n = 606) using logistic regression analysis. RESULTS: No overall association was seen between the L10P polymorphism and risk of colorectal adenomatous polyps. The age- and sex-adjusted odds ratios (OR) of developing colorectal hyperplastic polyps were 1.0 (95% CI: 0.7, 1.4) and 0.7 (95% CI: 0.4, 1.1) for individuals with the LP and PP genotypes, respectively, compared with individuals with the LL genotype. When stratified by smoking, evidence for a decreased risk of hyperplastic polyps associated with the P allele was seen only among ever smokers (P for trend = 0.05). CONCLUSIONS: Whereas adenoma risk did not vary by TGFbeta1 L10P genotype, these results suggest that the L10P variant allele may have a protective role in the development of colorectal hyperplastic polyps, possibly consistent with its role as an inhibitor of epithelial growths.

Adenomatous Polyps↗

PubMed2004

Pap testing among Vietnamese women: health care system and physician factors.

Cervical cancer occurs more frequently among Vietnamese Americans than women of any other race/ethnicity. In addition, previous studies in California have documented low Papanicolaou (Pap) testing rates in Vietnamese communities. This study focused on health care system factors and physician characteristics associated with recent cervical cancer screening among Vietnamese women. A population-based survey was conducted in Seattle during 2002. In-person interviews were conducted by bilingual, bicultural female survey workers. The survey response rate was 82% and 518 women were included in the analysis. Seventy-four percent of the respondents reported having been screened for cervical cancer on at least one occasion, and 64% reported a Pap smear within the previous 2 years. Women with a regular doctor were more likely to have been recently screened than those without a regular doctor (OR = 2.33, 95% CI = 1.45-3.74). Among those with a regular doctor, having a male physician, receiving care at a private doctor's office (rather than a community, hospital, or multi-specialty clinic), and concern about the cost of health care were independently associated with lower screening rates. Physician ethnicity was not associated with recent Pap smear receipt. The findings support targeted interventions for Vietnamese women without a regular physician and private doctors' offices that serve Vietnamese Americans. The availability of low cost screening services should be publicized in Vietnamese communities.

Adolescent↗

PubMed2004

Hepatitis B testing among Vietnamese American men.

Vietnamese American men are over 10 times more likely to be diagnosed with liver cancer than their white counterparts. This health disparity is attributable to high rates of hepatitis B virus (HBV) infection. Our study objective was to examine factors associated with HBV testing among Vietnamese men. A population-based survey was conducted in Seattle. The questionnaire content was guided by an earlier qualitative study and the Health Behavior Framework. The survey was completed by 345 men (response rate: 80%). About one-third (34%) of the respondents reported they had not been tested for HBV. The following factors were associated (P < 0.01) with previous testing in bivariate comparisons: having a regular source of care and regular provider; knowing that HBV can be spread during childbirth; believing HBV can cause liver cancer; and doctor(s) had recommended testing as well as had asked doctor(s) for testing. Three variables were independently associated with HBV testing in a logistic regression model: regular source of care (OR = 4.5; 95% CI = 2.6-7.9), physician recommendation (OR = 2.3, 95% CI = 1.3-4.0), and knowing HBV can be spread during childbirth (OR = 2.1; 95% CI = 1.2-3.9). Low levels of HBV testing remain a public health problem in some Vietnamese American sub-groups. Health education about HBV transmission may stimulate patients to seek testing. Intervention programs should specifically target Vietnamese men without a regular source of health care and physicians who serve Vietnamese communities.

Adult↗

PubMed2004

Frequent intentional weight loss is associated with lower natural killer cell cytotoxicity in postmenopausal women: possible long-term immune effects.

OBJECTIVE: Weight-loss attempts are likely to become more frequent as the prevalence of obesity rises. Repeated cycles of loss and gain are a common consequence of failed weight-loss attempts. The question of whether this pattern has negative health effects is unresolved. The objective of this research was to investigate associations between weight-loss history and current measures of immune function. DESIGN: The study design was a cross-sectional study. SUBJECTS: One hundred fourteen healthy, overweight, sedentary, postmenopausal women were recruited for an exercise intervention study and were currently weight stable. METHODS: History of intentional weight loss was assessed by questionnaire. Flow cytometry was used to measure natural killer cell (NK) cytotoxicity at four effector-to-target (E:T) ratios and for enumerating and phenotyping lymphocytes. Multiple linear regression analysis was used to investigate associations between weight loss within the past 20 years and current immune function. RESULTS: Women who reported ever intentionally losing >or=10 pounds had lower measured NK cytotoxicity than those who did not (24.7%+/-12.1% vs 31.1%+/-14.7%, respectively, at E:T 25:1; P=.01). Increasing frequency of previous intentional weight loss was associated with lower NK cytotoxicity (P=.003, trend). As an independent predictor, longer duration of recent weight stability was associated with higher NK cytotoxicity (21.6%+/-11.9%, 24.4%+/-11.0%, and 31.9%+/-14.4% for 2 to 5 years of weight stability, respectively; P=.0002, trend). The frequency of weight loss episodes was also associated with differences in the number and proportion of NK cells. CONCLUSIONS: This study provides evidence that frequent intentional weight loss may have long-term effects on immune function.

Aged↗

PubMed2004

Influence of demographic, physiologic, and psychosocial variables on adherence to a yearlong moderate-intensity exercise trial in postmenopausal women.

BACKGROUND: Few studies have examined the long-term adherence to a yearlong exercise intervention among postmenopausal women. We examined the patterns of adherence to a yearlong exercise intervention and the influence of demographic, physiologic, and psychosocial variables on patterns of adherence among 173 sedentary, overweight, postmenopausal women. METHODS: We collected demographic, physical activity (PA), physiologic, psychosocial, and medical history information at baseline and 12 months. The exercise prescription consisted of at least 45 min of moderate-intensity exercise 5 days/week for 12 months. We calculated several adherence variables. Associations between baseline variables and adherence levels were assessed in bivariate analyses and in multiple regression models. RESULTS: Women randomized to the exercise group (N = 87) participated in moderate-intensity sports or recreational PA on 3.7 +/- 1.4 days/week (79% of the prescribed 5 days/week) for 171 +/- 88 min/week (87% of the prescribed 225 min/week) over the yearlong trial period. Sixty-eight percent of the exercisers had a yearlong average PA level exceeding the national recommendation of 150 min/week. Being in the preparation stage vs. the contemplation stage of the transtheoretical model and a history of participating in any sports or recreational PA were significant predictors of adherence. CONCLUSIONS: Our findings provide important information for the design of future PA interventions and health promotion programs.

Aged↗

PubMed2004

Breast cancer risk counseling improves women's functioning.

Helping people cope with health risks is an important area for research and practice. Counseling offers people the opportunity to relieve their distress and improve the ways in which they manage their health issues. This study was a randomized test of two different counseling methods, genetic and psychosocial counseling, compared to a control group. Eligibility requirements included being between 18 and 74 years old, having at least one relative with breast cancer, not having a family history consistent with carrying a BRCA1/2 mutation for breast cancer risk, having no personal history of breast or ovarian cancer, living within 60 miles of the research institute, and willingness to complete the research requirements of the project. Perceived risk decreased by 50% for participants in the two counseling groups relative to comparison participants. Cancer worry decreased in both counseling groups by one scale point (P < 0.05). These results indicate that counseling can relieve women's negative reactions to breast cancer risk.

Adult↗

PubMed2004

Optimism, perceived risk of breast cancer, and cancer worry among a community-based sample of women.

Optimism is frequently inversely associated with distress; however, less is known about the mechanisms underlying this relationship. Optimism can be defined as having a generalized positive expectancy about the future. The authors hypothesized that a specific expectancy might mediate the relationship between optimism and distress. That model was tested using perceived risk of breast cancer as a specific measure of expectancy and cancer worry as a measure of distress in a community-based sample of 1,366 women. It was hypothesized that optimism would be inversely associated with cancer worry and that perceived risk of breast cancer would mediate the relationship between optimism and cancer worry. Multiple regression analyses revealed that perceived risk partially mediated the relationship between optimism and cancer worry.

Adult↗

PubMed2004

The effect of CYP19 and COMT polymorphisms on exercise-induced fat loss in postmenopausal women.

OBJECTIVE: To examine whether genetic polymorphisms in CYP19 [intron 4 (TTTA)n; n = 7 to 13 and a 3-base pair deletion, which is in strong linkage disequilibrium with the seven repeat] and COMT (Val108/158Met) modified the change in BMI, total and percentage body fat, or subcutaneous and intra-abdominal fat during a year-long exercise intervention trial. These genes metabolize estrogens and androgens, which are important in body fat regulation. RESEARCH METHODS AND PROCEDURES: A randomized intervention trial was used, with an intervention goal of 225 min/wk of moderate-intensity exercise for one year. Participants (n = 173) were postmenopausal, 50 to 75 years old, sedentary, overweight or obese, and not taking hormone therapy at baseline. RESULTS: Exercisers with two vs. no CYP19 11-repeat alleles had a larger decrease in total fat (-3.1 kg vs. -0.5 kg, respectively, p = 0.01) and percentage body fat (-2.4% vs. -0.6%, respectively, p = 0.001). Exercisers with the COMT Met/Met vs. Val/Val genotype had a smaller decrease in percentage fat (-0.7% vs. -1.9%, respectively, p = 0.05). Among exercisers, women with the COMT Val/Val genotype and at least one copy of the CYP19 11-repeat allele vs. those with neither genotype/allele had a significantly larger decrease in BMI (-1.0 vs. +0.1 kg/m2, respectively, p = 0.009), total fat (-2.9 vs. -0.5 kg, respectively, p = 0.004), and percentage body fat (-2.6% vs. -0.4%, respectively, p < 0.001). DISCUSSION: Genetic polymorphisms in CYP19 and COMT may be important for body fat regulation and possibly modify the effect of exercise on fat loss in postmenopausal women.

Adipose Tissue↗