Understanding which factors influence participation in physical activity is important to improve the public health. The aim of the present review of reviews was to summarize and present updated evidence on personal and environmental factors associated with physical activity. MEDLINE and EMBASE were searched for reviews published up to 31 Jan. 2017 reporting on potential factors of physical activity in adults aged over 18 years. The quality of each review was appraised with the Assessing the Methodological Quality of Systematic Reviews (AMSTAR) checklist. The corrected covered area (CCA) was calculated as a measure of overlap for the primary publications in each review. Twenty-five articles met the inclusion criteria which reviewed 90 personal and 27 environmental factors. The average quality of the studies was moderate, and the CCA ranged from 0 to 4.3%. For personal factors, self-efficacy was shown as the strongest factor for participation in physical activity (7 out of 9). Intention to exercise, outcome expectation, perceived behavioral control and perceived fitness were positively associated with physical activity in more than 3 reviews, while age and bad status of health or fitness were negatively associated with participation in physical activity in more than 3 reviews. For environmental factors, accessibility to facilities, presence of sidewalks, and aesthetics were positively associated with participation in physical activity. The findings of this review of reviews suggest that some personal and environmental factors were related with participation in physical activity. However, an association of various factors with physical activity could not be established because of the lack of primary studies to build up the organized evidence. More studies with a prospective design should be conducted to understand the potential causes for physical activity.

Introduction: Although approximately 25 common genetic susceptibility loci have been identified to be independently associated with breast cancer risk through genome-wide association studies (GWAS), the genetic risk variants reported to date only explain a small fraction of the heritability of breast cancer. Furthermore, GWAS-identified loci were primarily identified in women of European descent. Methods: To evaluate previously identified loci in Korean women and to identify additional novel breast cancer susceptibility variants, we conducted a three-stage GWAS that included 6,322 cases and 5,897 controls. Results: In the validation study using Stage I of the 2,273 cases and 2,052 controls, seven GWAS-identified loci [5q11.2/MAP3K1 (rs889312 and rs16886165), 5p15.2/ROPN1L (rs1092913), 5q12/MRPS30 (rs7716600), 6q25.1/ESR1 (rs2046210 and rs3734802), 8q24.21 (rs1562430), 10q26.13/FGFR2 (rs10736303), and 16q12.1/TOX3 (rs4784227 and rs3803662)] were significantly associated with breast cancer risk in Korean women (P_trend < 0.05). To identify additional genetic risk variants, we selected the most promising 17 SNPs in Stage I and replicated these SNPs in 2,052 cases and 2,169 controls (Stage II). Four SNPs were further evaluated in 1,997 cases and 1,676 controls (Stage III). SNP rs13393577 at chromosome 2q34, located in the Epidermal Growth Factor Receptor 4 (ERBB4) gene, showed a consistent association with breast cancer risk with combined odds ratios (95% CI) of 1.53 (1.37-1.70) (combined P for trend = 8.8 × 10^-14). Conclusions: This study shows that seven breast cancer susceptibility loci, which were previously identified in European and/or Chinese populations, could be directly replicated in Korean women. Furthermore, this study provides strong evidence implicating rs13393577 at 2q34 as a new risk variant for breast cancer.

A systematic review and meta-analysis of randomized controlled trials (RCTs) and observational studies was conducted to assess the association between menopausal hormone therapy and cardiovascular disease. The PubMed and EMBASE databases were searched for articles published from 2000 to 2019, using review methods based on a previous Cochrane review. Quality assessment of RCTs and observational studies was conducted using the Jadad scale and the Newcastle–Ottawa Scale, respectively. A total of 26 RCTs and 47 observational studies were identified. The study populations in the RCTs were older and had more underlying diseases than those in the observational studies. Increased risks of venous thromboembolism [summary estimate (SE), 95% confidence interval (CI): RCTs, 1.70, 1.33–2.16; observational studies, 1.32, 1.13–1.54] were consistently identified in both study types, whereas an increased risk of stroke in RCTs (SE: 1.14, 95% CI: 1.04–1.25) and a decreased risk of myocardial infarction in observational studies (SE: 0.79, 95% CI: 0.75–0.84) were observed. Differential clinical effects depending on timing of initiation, underlying disease, regimen type, and route of administration were identified through subgroup analyses. These findings suggest that underlying disease and timing of initiation should be carefully considered before starting therapy in postmenopausal women.

Background: Older paternal age may increase the germ cell mutation rate in the offspring. Maternal age may also mediate in utero exposure to pregnancy hormones in the offspring. To evaluate the association between paternal and maternal age at birth with the risk of breast cancer in female offspring, a case-control study was conducted in Korea. Methods: Histologically confirmed breast cancer cases (n = 1,011) and controls (n = 1,011) with no present or previous history of cancer, matched on year of birth and menopausal status, were selected from several teaching hospitals and community in Seoul during 1995–2003. Information on paternal and maternal ages and other factors was collected by interviewed questionnaire. Odds ratio (OR) and 95% confidence interval (95% CI) were estimated by unconditional logistic regression model adjusting for family history of breast cancer in 1^st or 2^nd degree relatives, and lifetime estrogen exposure duration. Results: The risk of breast cancer significantly increased as the paternal age increased (p for trend = 0.025). The association was stronger after controlling for maternal age; women whose fathers were aged ≥40 years at their birth had 1.6-fold increased risk of breast cancer compared with fathers aged <30 years. This association was profound in breast cancer cases in premenopausal women (OR = 1.9, 95% CI = 1.12–3.26, for paternal aged ≥40 vs. <30) (p for trend = 0.031). Although the risk of breast cancer increased as maternal age increased up to the intermediate, and then reduced; the risks in women whose mother were aged 25–29, 30–34, and ≥35 yrs at birth compared to women whose mothers were aged <25 years, were 1.2, 1.4, and 0.8, respectively, the trend was not significant (p for trend = 0.998). Conclusion: These findings suggest that older paternal age increases the risk of breast cancer in their female offspring.

Background: Although the role of microRNA’s (miRNA’s) biogenesis pathway genes in cancer development and progression has been well established, the association between genetic variants of this pathway genes and breast cancer survival is still unknown. Methods: We used genotype data available from a previously conducted case–control study to investigate association between common genetic variations in miRNA biogenesis pathway genes and breast cancer survival. We investigated the possible associations between 41 germ-line single-nucleotide polymorphisms (SNPs) and both disease free survival (DFS) and overall survival (OS) among 488 breast cancer patients. During the median follow-up of 6.24 years, 90 cases developed disease progression and 48 cases died. Results: Seven SNPs were significantly associated with breast cancer survival. Two SNPs in AGO2 (rs11786030 and rs2292779) and DICER1 rs1057035 were associated with both DFS and OS. Two SNPs in HIWI (rs4759659 and rs11060845) and DGCR8 rs9606250 were associated with DFS, while DROSHA rs874332 and GEMIN4 rs4968104 were associated with only OS. The most significant association was observed in variant allele of AGO2 rs11786030 with 2.62-fold increased risk of disease progression (95% confidence interval (CI), 1.41-4.88) and in minor allele homozygote of AGO2 rs2292779 with 2.94-fold increased risk of death (95% CI, 1.52-5.69). We also found cumulative effects of SNPs on DFS and OS. Compared to the subjects carrying 0 to 2 high-risk genotypes, those carrying 3 or 4–6 high-risk genotypes had an increased risk of disease progression with a hazard ratio of 2.16 (95% CI, 1.18- 3.93) and 4.47 (95% CI, 2.45- 8.14), respectively (P for trend, 6.11E-07). Conclusions: Our results suggest that genetic variants in miRNA biogenesis pathway genes may be associated with breast cancer survival. Further studies in larger sample size and functional characterizations are warranted to validate these results.

Approximately 100 common breast cancer susceptibility alleles have been identified in genome-wide association studies (GWAS). The utility of these variants in breast cancer risk prediction models has not been evaluated adequately in women of Asian ancestry. We evaluated 88 breast cancer risk variants that were identified previously by GWAS in 11,760 cases and 11,612 controls of Asian ancestry. SNPs confirmed to be associated with breast cancer risk in Asian women were used to construct a polygenic risk score (PRS). The relative and absolute risks of breast cancer by the PRS percentiles were estimated based on the PRS distribution, and were used to stratify women into different levels of breast cancer risk. We confirmed significant associations with breast cancer risk for SNPs in 44 of the 78 previously reported loci at P < 0.05. Compared with women in the middle quintile of the PRS, women in the top 1% group had a 2.70-fold elevated risk of breast cancer (95% CI: 2.15–3.40). The risk prediction model with the PRS had an area under the receiver operating characteristic curve of 0.606. The lifetime risk of breast cancer for Shanghai Chinese women in the lowest and highest 1% of the PRS was 1.35% and 10.06%, respectively. Approximately one-half of GWAS-identified breast cancer risk variants can be directly replicated in East Asian women. Collectively, common genetic variants are important predictors for breast cancer risk. Using common genetic variants for breast cancer could help identify women at high risk of breast cancer.