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Simple Summary: Cancer is the second leading cause of death globally, and the causes of cancer are numerous and multifactorial, including genetic and environmental factors. There is a developing interest in the role of sleep and light at night (LAN) exposure in cancer development. The aim of our study is to further understand the relationship between LAN exposure and the risk of cancer by systematically reviewing existing literature assessing LAN exposure and the risk of various cancer types. We found a positive association between LAN exposure and breast cancer risk, but there was insufficient data to convincingly draw a conclusion for other cancer types. This emphasizes the need for further research not only assessing LAN exposure and the incidence of other cancers but also the pathophysiology of sleep interruption on the formation of cancer. Background: Emerging interest surrounds the role of environmental factors, notably exposure to light at night (LAN), as a potential cause of cancer. The aim of this study was to conduct a systematic review and, if possible, meta-analysis of observational studies on LAN and cancer risk of multiple types. Methods: A systematic literature search in PubMed, Web of Science, and Embase, spanning from inception to May 2023, was conducted. Studies focusing on the association between LAN exposure and cancer risk in adult populations were included. We used random effects models to calculate pooled risk estimates (RR) and 95% confidence intervals (CI). We assessed study quality using the Risk of Bias in Non-randomized Studies of Interventions. Results: Among 8492 initially identified studies, 26 met the inclusion criteria (13 were case–control and 13 were cohort studies). These studies were published from 2001 to 2023 and assessed diverse cancer types in North America, Asia, Europe, and Australia. Except for breast cancer, there was a paucity of site-specific cancer studies. In the meta-analysis of 19 breast cancer studies, higher exposure to indoor (summary RR, 1.08; 95% CI 1.01–1.15) and outdoor (summary RR, 1.10; 95% CI, 1.04–1.15) LAN were associated with increased risk. After excluding one low-quality study, the results were unchanged. Conclusions: We found a positive association between LAN exposure and breast cancer risk in women. However, data are lacking for other cancer types, and further studies are required to better understand the role of LAN on cancer. [ABSTRACT FROM AUTHOR]

Simple Summary: Our study aimed to delineate the variables associated with the link between chronic periodontitis and hematologic cancers. The hazard ratio for hematologic cancers in patients with chronic periodontitis was also evaluated. Comprehensive statistical analyses revealed a 1.25-fold risk of hematologic cancers in the chronic periodontitis group. Factors such as being male and having hypertension were identified as increased risk factors for hematologic cancers. This nuanced exploration, including a subtype analysis for leukemia and lymphoma, contributes valuable insights into the complex relationship between chronic periodontitis and specific hematologic cancer subtypes. These findings could enhance our understanding of potential cancer risk factors in Taiwan. Background: Chronic periodontitis, an inflammation-related disorder affecting global populations, has been revealed to be linked to diverse cancers. Numerous epidemiological studies have not shown a link between chronic periodontitis and blood cancers in Taiwan. Methods: This study included 601,628 patients, diagnosed with newly chronic periodontitis by the ICD-9-CM classification, who were enrolled from 2001 to 2021 in the National Health Insurance Research Database (NHIRD) in Taiwan. In this study, we employed comprehensive statistical analyses to investigate the association between chronic periodontitis and hematologic cancers. Initially, we calculated incidence density and used a Poisson regression to analyze relative risk. Subsequently, we compared the cumulative incidence of hematological cancer in both chronic and non-chronic periodontitis groups using the Kaplan–Meier method. Results: The results revealed a significantly lower cumulative incidence of hematologic cancer in individuals with non-chronic periodontitis over a 12-year follow-up period. To further explore the risk factors, a Cox proportional hazard regression analysis was conducted. Being male (adjusted hazard ratio [aHR] = 1.21, 95% CI: 1.04 to 1.42; p = 0.014) and having hypertension (aHR = 1.34, 95% CI: 1.06 to 1.69; p = 0.015) were demonstrated to be associated with an increased risk of hematologic cancers, respectively. In addition, in a subtype multivariate analysis for categorizing hematologic cancers into lymphoma and leukemia, the aHR for leukemia was 1.48 (95% CI: 1.13 to 1.93; p = 0.004) and aHR for lymphoma was 1.15 (95% CI: 0.96 to 1.37; p = 0.140). Conclusions: This study found that being male and having hypertension were the significant risk factors for hematological malignancies. Moreover, the association between chronic periodontitis and specific subtypes of hematologic cancers was confirmed. [ABSTRACT FROM AUTHOR]

Simple Summary: The study aimed to develop and validate a prediction model that can be used to classify women for tailored breast cancer screening based on their individual risk. The model included data on age, mammographic density, family history of breast cancer, body mass index, age at menarche, alcohol consumption, exercise, pregnancy, hormone replacement therapy, and benign breast disease for 57,411 women screened in BreastScreen Norway 2007–2019. The 4-year predicted risk of breast cancer ranged between 0.2% and 7.3%, with 95% of the population having a risk of 0.6–2.3%. The differences in the predicted risk favor personalized screening for breast cancer. Background: We aimed to develop and validate a model predicting breast cancer risk for women targeted by breast cancer screening. Method: This retrospective cohort study included 57,411 women screened at least once in BreastScreen Norway during the period from 2007 to 2019. The prediction model included information about age, mammographic density, family history of breast cancer, body mass index, age at menarche, alcohol consumption, exercise, pregnancy, hormone replacement therapy, and benign breast disease. We calculated a 4-year absolute breast cancer risk estimates for women and in risk groups by quartiles. The Bootstrap resampling method was used for internal validation of the model (E/O ratio). The area under the curve (AUC) was estimated with a 95% confidence interval (CI). Results: The 4-year predicted risk of breast cancer ranged from 0.22–7.33%, while 95% of the population had a risk of 0.55–2.31%. The thresholds for the quartiles of the risk groups, with 25% of the population in each group, were 0.82%, 1.10%, and 1.47%. Overall, the model slightly overestimated the risk with an E/O ratio of 1.10 (95% CI: 1.09–1.11) and the AUC was 62.6% (95% CI: 60.5–65.0%). Conclusions: This 4-year risk prediction model showed differences in the risk of breast cancer, supporting personalized screening for breast cancer in women aged 50–69 years. [ABSTRACT FROM AUTHOR]

Simple Summary: Hormonal contraception is widely used among reproductive-aged women. In spite of the high effectiveness of hormonal contraception, some users become pregnant, probably due to irregular use. We previously reported an increased morbidity of childhood cancer in a nationwide cohort of offspring exposed in utero to maternal use of hormonal contraception. However, it remains unknown if mortality is increased in offspring with and without cancer after in utero exposure to hormonal contraception. The present study indicates that in utero exposure to hormonal contraception has an influence on long-term child mortality and survival after a diagnosis of leukemia. These novel findings have potential use in guidelines for hormonal contraception use in relation to pregnancy and expand our understanding of the etiology and prognosis of childhood leukemia. Approximately 400 million women of reproductive age use hormonal contraceptives worldwide. Eventually, pregnancy sometimes occurs due to irregular use. Use in early pregnancy is found to be associated with child morbidities including cancer, the main reason for disease-related death in children. Here, we add the missing piece about in utero exposure to hormonal contraception and mortality in offspring, including assessments of prognosis in children with cancer. In utero exposure to hormonal contraception may be associated with death since we found a hazard ratio (HR) of 1.22 (95% confidence interval (CI) 1.01–1.48) compared to children of mothers with previous use. The HRs were 1.22 (95% CI 0.99–1.13) for oral combined products and 2.92 (95% CI 1.21–7.04) for non-oral progestin-only products. A poorer prognosis was also found in exposed children with leukemia (3.62 (95% CI: 1.33–9.87)). If causal, hormonal contraception in pregnancy seems detrimental for offspring health and a marker of poorer prognosis in children with leukemia. [ABSTRACT FROM AUTHOR]

Simple Summary: (Multi-)Morbidity shares common biological mechanisms or risk factors with breast cancer. However, the risk of breast cancer among women with (multi-)morbidity remains unclear. In this study, using data of 239,436 female participants aged 40–69 of the UK Biobank cohort, we identified five chronic disease patterns: no-predominant morbidity, psychiatric morbidities, respiratory/immunological morbidities, cardiovascular/metabolic morbidities, and unspecific morbidities. After a median follow-up of 7 years, 5326 women developed breast cancer. We found no association between breast cancer risk and either the number of chronic diseases or chronic disease patterns, apart from an increased risk among women aged younger than 50 with a psychiatric pattern. Women with any multi-morbidity were more likely to die or to be diagnosed with other cancers. Our findings suggest that multi-morbidity may not be a key factor to help identify patients at an increased risk of breast cancer. (Multi-)Morbidity shares common biological mechanisms or risk factors with breast cancer. This study aimed to investigate the association between the number of morbidities and patterns of morbidity and the risk of female breast cancer. Among 239,436 women (40–69 years) enrolled in the UK Biobank cohort who had no cancer history at baseline, we identified 35 self-reported chronic diseases at baseline. We assigned individuals into morbidity patterns using agglomerative hierarchical clustering analysis. We fitted Cox models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer risk. In total, 58.4% of women had at least one morbidity, and the prevalence of multi-morbidity was 25.8%. During a median 7-year follow-up, there was no association between breast cancer risk (5326 cases) and either the number of morbidities or the identified clinically relevant morbidity patterns: no-predominant morbidity (reference), psychiatric morbidities (HR = 1.04, 95%CI 0.94–1.16), respiratory/immunological morbidities (HR = 0.98, 95%CI 0.90–1.07), cardiovascular/metabolic morbidities (HR = 0.93, 95%CI 0.81–1.06), and unspecific morbidities (HR = 0.98, 95%CI 0.89–1.07), overall. Among women younger than 50 years of age only, however, there was a significant association with psychiatric morbidity patterns compared to the no-predominant morbidity pattern (HR = 1.25, 95%CI 1.02–1.52). The other associations did not vary when stratifying by age at baseline and adherence to mammography recommendations. In conclusion, multi-morbidity was not a key factor to help identify patients at an increased risk of breast cancer. [ABSTRACT FROM AUTHOR]

Simple Summary: We reviewed 21 epidemiological studies on breast cancer risk and exposure to traffic-related air pollution. The exposure assessment methodologies were heterogeneous. There was variability across studies on temporal concordance between the exposure periods relevant to breast cancer and the time period of the exposure assessment. There was little evidence of an association between traffic-related air pollution estimated with proxies and breast cancer risk. The random-effects meta-analysis of 13 studies on NO2 and NOx exposure showed an increased risk of breast cancer with NO2 exposure. Current evidence of an association of breast cancer (BC) risk with air pollution exposure, in particular from traffic exhaust, remains inconclusive, and the exposure assessment methodologies are heterogeneous. This study aimed to conduct a systematic review and meta-analysis on the association between traffic-related air pollution (TRAP) and BC incidence (PROSPERO CRD42021286774). We systematically reviewed observational studies assessing exposure to TRAP and BC risk published until June 2022, available on Medline/PubMed and Web of Science databases. Studies using models for assessing exposure to traffic-related air pollutants or using exposure proxies (including traffic density, distance to road, etc.) were eligible for inclusion. A random-effects meta-analysis of studies investigating the association between NO2/NOx exposure and BC risk was conducted. Overall, 21 studies meeting the inclusion criteria were included (seven case–control, one nested case–control, 13 cohort studies); 13 studies (five case–control, eight cohort) provided data for inclusion in the meta-analyses. Individual studies provided little evidence of an association between TRAP and BC risk; exposure assessment methods and time periods of traffic emissions were different. The meta-estimate on NO2 exposure indicated a positive association (pooled relative risk per 10 µg/m3 of NO2: 1.015; 95% confidence interval, CI: 1.003; 1.028). No association between NOx exposure and BC was found (three studies). Although there was limited evidence of an association for TRAP estimated with proxies, the meta-analysis showed a significant association between NO2 exposure, a common TRAP pollutant marker, and BC risk, yet with a small effect size. Our findings provide additional support for air pollution carcinogenicity. [ABSTRACT FROM AUTHOR]

Simple Summary: Non-steroidal anti-inflammatory drugs (NSAIDs) are a group of commonly used drugs which target inflammation. Because inflammation is a critical component in cancer development, NSAID was proposed to reduce the risk of breast cancer by some studies. However, the results are inconsistent between studies. Moreover, there are insufficient data regarding risk of breast cancer with different characteristics, for example cancer subtype and stage, and few studies have investigated whether the risk will differ by breast density or previous breast disorders. Therefore, we investigated the association between use of NSAIDs and risk of breast cancer using data on NSAID use and breast cancer diagnosis from women in Sweden in general and women from a breast cancer screening program. Overall, we did not have strong evidence to support an association between the use of NSAIDs and the risk of breast cancer. More studies in diverse demographic and geographical settings are needed to confirm our findings. A link has been proposed between the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of breast cancer. There is, however, insufficient data regarding the subtype and stage of breast cancer, and few studies have assessed the interaction between the use of NSAIDs and breast density or previous breast disorders. There is also a lack of data from population-based studies. We first conducted a nested case-control study within the general female population of Sweden, including 56,480 women with newly diagnosed breast cancer during 2006–2015 and five breast cancer-free women per case as controls, to assess the association of NSAID use with the risk of incident breast cancer, focusing on subtype and stage of breast cancer as well as the interaction between NSAID use and previous breast disorders. We then used the Karolinska Mammography Project for Risk Prediction of Breast Cancer (Karma) cohort to assess the interaction between NSAID use and breast density in relation to the risk of breast cancer. Conditional logistic regression was used to estimate the hazard ratio (HR) and a 95% confidence interval (CI) was used for breast cancer in relation to the use of aspirin and non-aspirin NSAIDs. In the nested case-control study of the general population, exclusive use of aspirin was not associated with the risk of breast cancer, whereas exclusive use of non-aspirin NSAIDs was associated with a modestly higher risk of stage 0–2 breast cancer (HR: 1.05; 95% CI: 1.02–1.08) but a lower risk of stage 3–4 breast cancer (HR 0.80; 95% CI: 0.73–0.88). There was also a statistically significant interaction between the exclusive use of NSAIDs and previous breast disorders (p for interaction: <0.001). In the analysis of Karma participants, the exclusive use of non-aspirin NSAIDs was associated with a lower risk of breast cancer among women with a breast dense area of >40 cm2 (HR: 0.72; 95% CI: 0.59–0.89). However, the possibility of finding this by chance cannot be ruled out. Overall, we did not find strong evidence to support an association between the use of NSAIDs and the risk of breast cancer. [ABSTRACT FROM AUTHOR]

Simple Summary: Breast cancer (BC) is the most common cancer in females worldwide. Although fat has been hypothesized to be involved in BC etiology, the results of available studies are inconclusive. The aim of this study was to assess the associations of dietary fat intake, including an individual's percentage of energy from dietary fat (Pfat) with peri- and postmenopausal breast cancer (BC) occurrence in women. The associations between Pfat and dietary patterns (DPs) were also examined. The current findings strengthen reports that a higher dietary fat intake may contribute to an increased incidence of BC, which indicates a need to reduce dietary fat intake in cancer prevention. The aim of this study was to assess the associations of dietary fat intake with BC occurrence and dietary patterns. This case-control study involved 420 women aged 40–79 years from northeastern Poland, including 190 newly diagnosed BC cases. Dietary data were collected using a food frequency questionnaire (62-item FFQ-6®). The Quick Food Scan of the National Cancer Institute and the Percentage Energy from Fat Screener scoring procedures were used to estimate the percentage energy from dietary fat (Pfat). The odds of BC occurrence was three times higher in the Pfat > 32%. The Pfat > 32% was positively associated with the 'Non-Healthy' DP and inversely associated with the Polish-aMED® score, 'Prudent' DP, and 'Margarine and Sweetened Dairy' DP. This case-control study suggests that a higher dietary fat intake (>32%) may contribute to an increased occurrence of peri- and postmenopausal breast cancer in women. Given the obtained results, an unhealthy dietary pattern characterized by the consumption of highly processed, high in sugar foods and animal fat foods should be avoided to reduce fat intake. Instead, the frequent consumption of low-processed plant foods, fish, and moderate consumption of low-fat dairy should be recommended since this pro-healthy diet is inversely associated with dietary fat intake. [ABSTRACT FROM AUTHOR]

Simple Summary: Night shift work (NSW) may disturb circadian rhythms. This could influence the risk of breast cancer (BC), but research papers have reported conflicting results. We reviewed, summarized, and combined the results of those studies that measured the effect of long-term nightshift work (≥15 years of NSW) in BC with special attention to menopausal status and time since retirement age. Women with long-term NSW had 13% more risk of BC than women without NSW. Postmenopausal women showed no increased risk, while premenopausal women had a 27% higher risk. Women with a higher probability of recent long-term NSW (women under retirement age) had a 23% higher risk than women without NSW. We concluded that long-term NSW may increase BC risk, especially in women before menopause or shortly after NSW discontinuation. This systematic review discusses long-term NSW and female BC risk, with special attention to differences between pre- and postmenopausal BC, to test the association with recent NSW. The review follows PRISMA guidelines (Prospero registry: CRD42018102515). We searched PubMed, Embase, and WOS for case–control, nested case–control, and cohort studies addressing long-term NSW (≥15 years) as risk exposure and female BC as outcome until 31 December 2020. Risk of bias was evaluated with the Newcastle–Ottawa scale. Eighteen studies were finally included (eight cohorts; five nested case–control; five case–control). We performed meta-analyses on long-term NSW and BC risk; overall and by menopausal status; a subanalysis on recent long-term NSW, based on studies involving predominantly women below retirement age; and a dose–response meta-analysis on NSW duration. The pooled estimate for long-term NSW and BC was 1.13 (95%CI = 1.01–1.27; 18 studies, I2 = 56.8%, p = 0.002). BC risk increased 4.7% per 10 years of NSW (95%CI = 0.94–1.09; 16 studies, I2 = 33.4%, p = 0.008). The pooled estimate for premenopausal BC was 1.27 (95%CI = 0.96–1.68; six studies, I2 = 32.0%, p = 0.196) and for postmenopausal BC 1.05 (95%CI = 0.90–1.24,I2 = 52.4%; seven studies, p = 0.050). For recent long-term exposure, the pooled estimate was 1.23 (95%CI = 1.06–1.42; 15 studies; I2 = 48.4%, p = 0.018). Our results indicate that long-term NSW increases the risk for BC and that menopausal status and time since exposure might be relevant. [ABSTRACT FROM AUTHOR]

Simple Summary: This study assessed the association between short-term weight change and mammographic density in premenopausal women losing weight through diet and exercise to reduce their risk of postmenopausal breast cancer. We aimed to understand whether a reduction in body mass index affects various components of the breast, which could indicate a potential pathway for the reduction in postmenopausal breast cancer risk seen with premenopausal weight loss. Understanding this pathway is useful for monitoring the effectiveness of prevention strategies based on lifestyle advice. We found that a short-term reduction in premenopausal body mass index through diet and exercise is associated with a reduction in breast fat, but it is unlikely to have a significant effect on the quantity of breast glandular tissue. Breast cancer risk determined by changes in breast density might not capture potential weight loss-induced breast cancer risk reduction, instead falsely ascribing an increased risk due to increased percent density. We evaluated the association between short-term change in body mass index (BMI) and breast density during a 1 year weight-loss intervention (Manchester, UK). We included 65 premenopausal women (35–45 years, ≥7 kg adult weight gain, family history of breast cancer). BMI and breast density (semi-automated area-based, automated volume-based) were measured at baseline, 1 year, and 2 years after study entry (1 year post intervention). Cross-sectional (between-women) and short-term change (within-women) associations between BMI and breast density were measured using repeated-measures correlation coefficients and multivariable linear mixed models. BMI was positively correlated with dense volume between-women (r = 0.41, 95%CI: 0.17, 0.61), but less so within-women (r = 0.08, 95%CI: −0.16, 0.28). There was little association with dense area (between-women r = −0.12, 95%CI: −0.38, 0.16; within-women r = 0.01, 95%CI: −0.24, 0.25). BMI and breast fat were positively correlated (volume: between r = 0.77, 95%CI: 0.69, 0.84, within r = 0.58, 95%CI: 0.36, 0.75; area: between r = 0.74, 95%CI: 0.63, 0.82, within r = 0.45, 95%CI: 0.23, 0.63). Multivariable models reported similar associations. Exploratory analysis suggested associations between BMI gain from 20 years and density measures (standard deviation change per +5 kg/m2 BMI: dense area: +0.61 (95%CI: 0.12, 1.09); fat volume: −0.31 (95%CI: −0.62, 0.00)). Short-term BMI change is likely to be positively associated with breast fat, but we found little association with dense tissue, although power was limited by small sample size. [ABSTRACT FROM AUTHOR]

Simple Summary: Menopausal hormone therapy (MHT) increases risk of developing breast cancer (BC), and women are often advised to avoid its use for this reason. In this analysis we examined the size of this effect using data from a large cohort of women attending breast cancer screening in Manchester, UK. We additionally explored the extent to which risk from MHT might be modified by current BMI, early adulthood body mass index (BMI) (age 20 years), and age of first pregnancy. Identifying modifying effects would help enable better estimation of risk associated with MHT for an individual woman. Results indicated that women using combined oestrogen and progestagen MHT were at greater risk than those receiving oestrogen-only MHT. The Relative risk associated with MHT was less for obese women than non-obese women. After adjustment for current BMI, the effect of MHT did not appear to be substantially modified by early BMI or age of pregnancy. Menopausal hormone therapy (MHT) has an attenuated effect on breast cancer (BC) risk amongst heavier women, but there are few data on a potential interaction with early adulthood body mass index (at age 20 years) and age of first pregnancy. We studied 56,489 women recruited to the PROCAS (Predicting Risk of Cancer at Screening) study in Manchester UK, 2009-15. Cox regression models estimated the effect of reported MHT use at entry on breast cancer (BC) risk, and potential interactions with a. self-reported current body mass index (BMI), b. BMI aged 20 and c. First pregnancy >30 years or nulliparity compared with first pregnancy <30 years. Analysis was adjusted for age, height, family history, age of menarche and menopause, menopausal status, oophorectomy, ethnicity, self-reported exercise and alcohol. With median follow up of 8 years, 1663 breast cancers occurred. BC risk was elevated amongst current users of combined MHT compared to never users (Hazard ratioHR 1.64, 95% CI 1.32–2.03), risk was higher than for oestrogen only users (HR 1.03, 95% CI 0.79–1.34). Risk of current MHT was attenuated by current BMI (interaction HR 0.80, 95% CI 0.65–0.99) per 5 unit increase in BMI. There was little evidence of an interaction between MHT use, breast cancer risk and early and current BMI or with age of first pregnancy. [ABSTRACT FROM AUTHOR]