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BACKGROUND: Environmental exposure to polychlorinated biphenyls (PCBs) and p,p'-dichlorodiphenyldichloroethylene (p, p'-DDE) has been associated with the risk of non-Hodgkin lymphoma. METHODS: We conducted a case-control study nested within the Physicians' [...]

Earth's rotation around its axis has pressured its inhabitants to adapt to 24 h cycles of day and night. Humans adapted their own circadian rhythms to the Earth's rhythms with a light-aligned awake–sleep cycle. As a consequence, metabolism undergoes drastic changes throughout the circadian cycle and needs plasticity to cope with opposing conditions in the day (when there is an increase in energy demands and food availability), and during the night (when prolonged fasting couples with cyclic changes in the energy demands across the sleep stages). In the last century, human behavior changed dramatically with a disregard for the natural circadian cycles. This misalignment in sleep and eating schedules strongly modulates the metabolism and energy homeostasis, favoring the development of obesity, metabolic syndrome, and metabolic dysfunction-associated steatotic liver disease (MASLD). This review summarizes the effects of circadian disruption, with a particular focus on the feeding and sleep cycles in the development of MASLD and hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

Artificial sweeteners, as low-calorie sugar substitutes, have attracted much attention in recent years, especially in terms of their potential health effects. Although they add almost no calories, studies have shown that artificial sweeteners may affect metabolism by stimulating insulin secretion and changing the intestinal microbiota, increasing the risk of metabolic syndrome and type 2 diabetes. Breast cancer, as the most common cancer in the world, is related to multiple factors such as genetics and hormone levels. The results of studies on artificial sweeteners and breast cancer risk are conflicting, with some showing a positive correlation between the two and others failing to confirm it. Differences in study design, participant characteristics, and the types of sweeteners have led to this ambiguity. Although some studies have focused on mechanisms such as hormone disorders, insulin response, and changes in the intestinal microbiota, further exploration is needed to establish a causal relationship. Our review aims to comprehensively analyze the potential association between artificial sweeteners and breast cancer and its mechanisms, as well as encourage future studies to reveal its long-term health effects. [ABSTRACT FROM AUTHOR]

Background/Objectives: Radiotherapy represents the only treatment option for patients with inoperable endometrial cancer (EC). The aim of our study was to evaluate the efficacy and safety of brachytherapy (BT) in this selected patient population. Methods: Between 1990 and 2019, 18 patients with inoperable EC in stage FIGO I–IV were treated with intracavitary brachytherapy using the "Heyman Packing technique". BT was performed either as sole PDR- or HDR-brachytherapy with a median cumulative dose up to 60.0 Gy (67.9 Gy EQD2 α/β = 3Gy) and 34.0 Gy (75.6 Gy EQD2 α/β = 3Gy), respectively. Results: The median follow-up was 46 months (6–219). The mean age was 71 years. The 5-year cumulative local recurrence rate (CLRR) for the whole cohort was 27.3%. The 5-year overall survival (OS), distant metastasis-free survival (DMFS), and disease-free survival (DFS) were 51%, 79%, and 69%. The 5-year DFS for low-, intermediate-, and high-risk EC was 89%, 50%, and 44% (p = 0.51). No significant difference in DFS was observed in patients over 70 (p = 0.526). No late side effects of grade > 1 were documented. Conclusions: Brachytherapy for inoperable EC is a safe and effective treatment option, offering good local control and OS with minimal toxicity. Moreover, brachytherapy effectively controls hemoglobin-relevant bleeding. Therefore, BT should be considered a viable alternative to non-curative treatment strategies in gynecological multidisciplinary conferences. [ABSTRACT FROM AUTHOR]

Objective: This scoping review aims to investigate the complex interplay between the built environment, health, and well-being and to provide a comprehensive overview of the knowledge needed for crucial health and well-being enhancement in cities. Method: A scoping review method has been chosen using four databases. The first sample was reduced from 2819 papers to 71 papers by implementing exclusion criteria, snowballing, and direct searches to find a relevant final sample. Results: Built environmental elements such as the neighborhood, urban architecture, activities, public spaces, greenery, lights, safety, aesthetics, and amenities were identified to be impactful on health and well-being outcomes. The two-way association of each environmental factor and its criteria with specific types of health and well-being issues such as cancer, cardiovascular diseases, stress, etc. was determined to identify solutions and ways for improvement. Conclusions: This scoping review provides a comprehensive overview of the intricate interplay between the built environment, health, and well-being. By synthesizing existing knowledge of the built environmental factors, it explores the basis for evidence-based strategies to enhance health and well-being. By illuminating theoretical knowledge of the built environment on health and well-being, our findings will provide a deeper foundation of sources and practical insights for related fields. [ABSTRACT FROM AUTHOR]

Breast cancer remains one of the primary causes of cancer-related deaths among women globally. Early detection via mammography is essential for improving prognosis and survival rates. However, mammogram diagnostic accuracy is severely hindered by dense breast tissue, which can obstruct potential malignancies, complicating early detection. To tackle this pressing issue, this study introduces an innovative approach that leverages Generative Adversarial Networks (GANs), specifically CycleGAN and GANHopper, to transform breast density in mammograms. The aim is to diminish the masking effect of dense tissue, thus enhancing the visibility of underlying malignancies. The method uses unsupervised image-to-image translation to gradually alter breast density (from high (ACR-D) to low (ACR-A)) in mammographic images, detecting obscured lesions while preserving original diagnostic features. We applied this approach to multiple mammographic datasets, demonstrating its effectiveness in diverse contexts. Experimental results exhibit substantial improvements in detecting potential malignancies concealed by dense breast tissue. The method significantly improved precision, recall, and F1-score metrics across all datasets, revealing previously obscured malignancies and image quality assessments confirmed the diagnostic relevance of transformed images. The study introduces a novel mammogram analysis method using advanced machine-learning techniques, enhancing diagnostic accuracy in dense breasts and potentially improving early breast cancer detection and patient outcomes. [ABSTRACT FROM AUTHOR]

Endometrial atypical hyperplasia (EAH) is a premalignant condition with a substantial risk of progression to endometrial cancer (EC), with the endometrioid subtype being the most common. EAH is characterized by abnormal endometrial gland proliferation and cellular atypia, often resulting from prolonged unopposed estrogen exposure. This review aims to explore the clinical significance of EAH, its risk of progression to EC, and the current approaches to management. The risk of EAH progressing to EC ranges from 20 to 50%, influenced by factors such as histopathology and genetic mutations including PTEN and KRAS. Key risk factors include obesity, polycystic ovary syndrome, and postmenopausal status. Abnormal uterine bleeding is a hallmark symptom of EAH and early-stage EC, necessitating diagnostic evaluation through endometrial biopsy and transvaginal ultrasonography. Therapeutic management strategies depend on patient risk and fertility considerations. Hormonal therapy, particularly progestins, is the mainstay for fertility preservation, while hysterectomy is preferred for higher-risk patients. Regular monitoring with biopsies is essential for those undergoing conservative treatment. Recent advancements in the management of EAH and EC have shifted towards incorporation of molecular diagnostics and targeted therapies, enabling better risk stratification and individualized care. Biomarkers and minimally invasive surgical techniques are emerging as promising approaches in improving outcomes for women with EAH. This review underscores the importance of early diagnosis and personalized management in preventing the progression of EAH to EC, highlighting current clinical practices and potential future developments in this field. [ABSTRACT FROM AUTHOR]

Ultra violet (UV) solar energy can cause several negative effects to the skin and eyes in case of overexposure. To protect people from erythemal damage, personal erythemal exposure must be carefully assessed when outdoor activities are carried out. The direct measure with scientific instruments is impracticable to common people, and indirect methods assess the exposure only on the horizontal plane: this work developed a mathematical model to assess erythemal exposure to all the body districts. UVA irradiance and erythemal irradiance were measured on several inclined planes, oriented to the four cardinal directions, in seven environments with multiple sky conditions. The UV erythemal (UVE) ratio between erythemal irradiance on an inclined plane (Iery°) and UVA irradiance on a horizontal plane (IUVAh) was calculated. The results indicate that the UVE = Iery°/IUVAh is variable across the day and depends on the plane orientation, its degree of inclination, and sky conditions. Mathematical models to calculate erythemal exposure in clear, intermediate and overcast sky conditions on planes with different inclinations and orientations were derived from the daily trends of the UVE = Iery°/IUVAh. The application procedure of the mathematical model to the vertical plane oriented to the south is provided as an example. [ABSTRACT FROM AUTHOR]

Understanding the genetic basis of sweet taste preference is crucial for potential implications in diet-related health outcomes, such as obesity. This study identified genes and single nucleotide polymorphisms (SNPs) associated with sweet taste preferences over time. Data from the American Nurses' Health Study (NHS1) and Health Professionals Follow-up Study (HPFS) cohorts were analyzed. Using tools like PLINK and METAL for genetic associations and FUMA for functional annotation, the study identified eight SNPs associated with sweet taste preferences. Notably, rs80115239 and rs12878143 were identified as key determinants of the highest and lowest associations with sweet taste preferences, respectively. Individuals with the rs80115239 (AA) genotype displayed a higher preference for sweet tastes, including chocolate and cake, but a lower preference for physical activity, fruits, and vegetables, particularly in females from the NHS1 cohort, linking this genotype to a higher obesity risk. Conversely, those with the rs12878143 (CC) genotype preferred fruits, vegetables, coffee, and tea, with a lower preference for sweetened beverages, but the correlation with obesity risk was less clear due to inconsistent data. In conclusion, these findings highlight the genetic influences on sweet taste preference and their potential role in personalized dietary recommendations and obesity management strategies. [ABSTRACT FROM AUTHOR]

Environmental exposure to a mixture of chemical xenobiotics acts as a double-edged sword, promoting or suppressing tumorigenesis and the development of breast cancer (BC). Before anything else, we are what we eat. In this review, we highlight both "the good" and "the bad" sides of the daily human diet and dietary patterns that could influence BC risk (BCR) and incidence. Thus, regularly eating new, diversified, colorful, clean, nutrient-rich, energy-boosting, and raw food, increases apoptosis and autophagy, antioxidation, cell cycle arrest, anti-inflammation, and the immune response against BC cells. Moreover, a healthy diet could lead to a reduction in or the inhibition of genomic instability, BC cell stemness, growth, proliferation, invasion, migration, and distant metastasis. We also emphasize that, in addition to beneficial compounds, our food is more and more contaminated by chemicals with harmful effects, which interact with each other and with endogenous proteins and lipids, resulting in synergistic or antagonistic effects. Thus, a healthy and diverse diet, combined with appropriate nutritional behaviors, can exert anti-carcinogenic effects and improve treatment efficacy, BC patient outcomes, and the overall quality of life of BC patients. [ABSTRACT FROM AUTHOR]

Background/Objectives: High breast density is a risk factor for breast cancer and can reduce the sensitivity of mammography. Given the influence of breast density on patient risk stratification and screening accuracy, it is crucial to monitor the prevalence of extremely dense breasts within local populations. Moreover, there is a lack of comprehensive understanding regarding breast density prevalence in Switzerland. Therefore, this study aimed to determine the prevalence of breast density in a selected Swiss population. Methods: To overcome the potential variability in breast density classifications by human readers, this study utilized commercially available deep convolutional neural network breast classification software. A retrospective analysis of mammographic images of women aged 40 years and older was performed. Results: A total of 4698 mammograms from women (58 ± 11 years) were included in this study. The highest prevalence of breast density was in category C (heterogeneously dense), which was observed in 41.5% of the cases. This was followed by category B (scattered areas of fibroglandular tissue), which accounted for 22.5%. Conclusions: Notably, extremely dense breasts (category D) were significantly more common in younger women, with a prevalence of 34%. However, this rate dropped sharply to less than 10% in women over 55 years of age. [ABSTRACT FROM AUTHOR]

To fill a research gap on firefighter exposures and breast cancer risk, and guide exposure reduction, we aimed to identify firefighter occupational exposures linked to breast cancer. We conducted a systematic search and review to identify firefighter chemical exposures and then identified the subset that was associated with breast cancer. To do this, we compared the firefighter exposures with chemicals that have been shown to increase breast cancer risk in epidemiological studies or increase mammary gland tumors in experimental toxicology studies. For each exposure, we assigned a strength of evidence for the association with firefighter occupation and for the association with breast cancer risk. We identified twelve chemicals or chemical groups that were both linked to breast cancer and were firefighter occupational exposures, including polycyclic aromatic hydrocarbons, volatile aromatics, per- and polyfluoroalkyl substances, persistent organohalogens, and halogenated organophosphate flame retardants. Many of these were found at elevated levels in firefighting environments and were statistically significantly higher in firefighters after firefighting or when compared to the general population. Common exposure sources included combustion byproducts, diesel fuel and exhaust, firefighting foams, and flame retardants. Our findings highlight breast-cancer-related chemical exposures in the firefighting profession to guide equitable worker's compensation policies and exposure reduction. [ABSTRACT FROM AUTHOR]

Intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin are cell adhesion molecules that play a significant role in inflammation and are implicated in the pathophysiology of preeclampsia development and HIV infection. More specifically, the immune expression of ICAM-1, VCAM-1, and E-selectin within cyto- and syncytiotrophoblast cells are dysregulated in preeclampsia, indicating their role in defective placentation. This study investigates the associations of ICAM-1, VCAM-1, and E-selectin gene variants (rs3093030, rs3783605, and rs1805193, respectively) with preeclampsia comorbid with HIV infection in women of African ancestry. It also examines the susceptibility to preeclampsia development and the effect of highly active antiretroviral therapy (HAART). A total of 405 women were enrolled in this study. Out of these women, 204 were preeclamptic and 201 were normotensive. Clinical characteristics were maternal age, weight, blood pressure (systolic and diastolic), and gestational age. Whole blood was collected, DNA was extracted, and genotyping of the ICAM-1 (rs3093030 C>T), VCAM-1(rs3783605 A>G), and E-selectin (rs1805193 A>C) gene polymorphisms was performed. Comparisons were made using the Chi-squared test. Our results demonstrated that preeclamptic women exhibited a higher frequency of analyzed variants, in contrast to those with the duality of preeclampsia and HIV infection. Additionally, the C allele of the ICAM-1 (rs3093030 C>T) and G allele of the VCAM-1 (rs3783605 A>G) genes were found to have a greater role in the co-morbidity and may be considered as a risk factor for preeclampsia development in women of African ancestry. In contrast, the SNP of rs1805193 of the E-selectin gene indicated that A>C was only significantly associated with HIV infection and not with preeclampsia. These findings highlight a strong association of the rs3093030 SNP of the ICAM-1 gene and of the VCAM-1 rs3783605 gene with the development of preeclampsia, indicating their role in the defective trophoblast invasion of preeclampsia. Sub-group analysis further reveals an association of the AA genotype with late-onset preeclampsia, a less severe form of disease indicating differing genetic predispositions between early and late-onset forms. [ABSTRACT FROM AUTHOR]

Over the past few decades, the scientific community has been highly concerned about the obesity epidemic. Artificial sweeteners are compounds that mimic the sweet taste of sugar but have no calories or carbohydrates; hence, they are very popular among patients suffering from diabetes or obesity, aiming to achieve glycemic and/or weight control. There are four different types of sweeteners: artificial, natural, rare sugars, and polyols. Artificial and natural sweeteners are characterized as non-nutritional sweeteners (NNSs) since they do not contain calories. The extended use of sweeteners has been reported to have a favorable impact on body weight and glycemic control in patients with type 2 diabetes (T2DM) and on tooth decay prevention. However, there is concern regarding their side effects. Several studies have associated artificial sweeteners' consumption with the development of insulin resistance, nonalcoholic fatty liver disease (NAFLD), gastrointestinal symptoms, and certain types of cancer. The present review focuses on the description of different types of sweeteners and the benefits and possible deleterious effects of the chronic consumption of NNSs on children's health. Additionally, possible underlying mechanisms of the unfavorable effects of NNSs on human health are described. [ABSTRACT FROM AUTHOR]

Endometrial cancer is reported to be one of the most prevalent cancers of the female reproductive organs worldwide, with increasing incidence and mortality rates over the past decade. Early diagnosis is critical for effective treatment. Recently, there has been a growing focus on the role of nutrition and micronutrient and macronutrient status in patients with gynecologic cancers, including endometrial cancer. In the following paper, we have conducted an in-depth narrative literature review with the aim of evaluating the results of metallomic studies specifically concerning the micro- and macronutrient status of patients with endometrial cancer. The main objective of the paper was to analyze the results regarding the nutritional status of endometrial cancer patients and describe the role of chosen elements in the onset and progression of endometrial carcinogenesis. Further, we have focused on the evaluation of the usage of the described elements in the potential treatment of the abovementioned cancer, as well as the possible prevention of cancer considering proper supplementation of chosen elements in healthy individuals. Calcium supplementation has been proposed to reduce the risk of endometrial cancer, although some studies offer conflicting evidence. Deficiencies in phosphorus, selenium, and zinc have been inversely associated with endometrial cancer risk, suggesting they may play a protective role, whereas excessive levels of iron, copper, and cadmium have been positively correlated with increased risk. However, the molecular mechanisms by which these elements affect endometrial carcinogenesis are not fully understood, and current findings are often contradictory. Further research is needed to clarify these relationships and to evaluate the potential of nutritional interventions for the prevention and treatment of endometrial cancer. [ABSTRACT FROM AUTHOR]

Both periodontal disease and cancer are prevalent conditions with significant impacts on individuals and society. Extensive research has suggested a potential link between these two diseases. This study conducted a bibliometric analysis using the Thomson Reuters Web of Science Core Collection database, focusing on publications from 2014 to 2023. The analysis included data extraction and examination of authors, affiliations, publication dates, journals, countries, citation counts, keywords, and the H-index. A total of 253 relevant articles were identified, showing an increasing trend in both publications and citations over the years. The analysis highlighted the most productive authors, institutions, and countries/regions, with Michaud DS and Abnet CC leading in the number of publications. Highly cited articles emphasized the role of specific oral microbiota, particularly F. nucleatum and P. gingivalis, in various cancers, suggesting their potential as diagnostic markers and therapeutic targets. Four key thematic clusters emerged from the keyword analysis: the broader health implications of periodontal disease, the microbiome's role in carcinogenesis, inflammation, and specific bacteria in cancer, and epidemiological methods in studying the disease–cancer association. This bibliometric analysis underscores the growing interest in the connection between periodontal disease and cancer. Future research should adopt interdisciplinary approaches, focus on large-scale microbiome studies and longitudinal research to understand the systemic effects of periodontal disease, identify cancer-associated bacterial profiles, and investigate the molecular mechanisms of bacterial carcinogenesis. Additionally, public health interventions aimed at improving oral hygiene and reducing cancer risk factors are recommended. [ABSTRACT FROM AUTHOR]

Our study aimed to identify sweetness preference-associated single-nucleotide polymorphisms (SNPs), characterize the related genetic loci, and develop SNP-based polygenic risk scores (PRS) to analyze their associations with obesity. For genotyping, we utilized a pooled genome-wide association study (GWAS) dataset of 18,499 females and 10,878 males. We conducted genome-wide association analyses, functional annotation, and employed the weighted method to calculate the levels of PRS from 677 sweetness preference-related SNPs. We used Cox proportional hazards modeling with time-varying covariates to estimate age-adjusted and multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for obesity incidence. We also tested the correlation between PRS and environmental factors, including smoking and dietary components, on obesity. Our results showed that in males, the TT genotype of rs4861982 significantly increased obesity risk compared to the GG genotype in the Health Professionals Follow-up Study (HPFS) cohort (HR = 1.565; 95% CI, 1.122–2.184; p = 0.008) and in the pooled analysis (HR = 1.259; 95% CI, 1.030–1.540; p = 0.025). Protein tyrosine phosphatase receptor type O (PTPRO) was identified as strongly associated with sweetness preference, indicating a positive correlation between sweetness preference and obesity risk. Moreover, each 10 pack-year increment in smoking was significantly associated with an increased risk of obesity in the HPFS cohort (HR = 1.024; 95% CI, 1.000–1.048) in males but not in females. In conclusion, significant associations between rs4861982, sweetness preference, and obesity were identified, particularly among males, where environmental factors like smoking are also correlated with obesity risk. [ABSTRACT FROM AUTHOR]

Simple Summary: The circadian clock controls the rhythmic timing of nearly every aspect of physiology, including sleep, body temperature, hormone fluctuation, and overall metabolism on a daily basis. Research shows that disruption to this control contributes to the development of diseases, including cancer. Evidence also suggests that cancers may be amenable to treatments that target the circadian clock, which maximizes benefits while minimizing side effects. Here, the rhythmic influence over cancers of the liver and gut will be reviewed, and treatments that take into account the circadian clock will be discussed. Circadian rhythms dictate the timing of cellular and organismal physiology to maintain homeostasis. Within the liver and gut, circadian rhythms influence lipid and glucose homeostasis, xenobiotic metabolism, and nutrient absorption. Disruption of this orchestrated timing is known to negatively impact human health and contribute to disease progression, including carcinogenesis. Dysfunctional core clock timing has been identified in malignant growths and may be used as a molecular signature of disease progression. Likewise, the circadian clock and its downstream effectors also represent potential for novel therapeutic targets. Here, the role of circadian rhythms in the pathogenesis of cancers of the liver and gut will be reviewed, and chronotherapy and chronopharmacology will be explored as potential treatment options. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is the most prominent tumor type among women, accounting for 32% of newly diagnosed cancer cases. BC risk factors include inherited germline pathogenic gene variants and family history of disease. However, the etiology of the disease remains occult in most cases. Therefore, in the absence of high-risk factors, a polygenic basis has been suggested to contribute to susceptibility. This information is utilized to calculate the Polygenic Risk Score (PRS) which is indicative of BC risk. This study aimed to evaluate retrospectively the clinical usefulness of PRS integration in BC risk calculation, utilizing a group of patients who have already been diagnosed with BC. The study comprised 105 breast cancer patients with hereditary genetic analysis results obtained by NGS. The selection included all testing results: high-risk gene-positive, intermediate/low-risk gene-positive, and negative. PRS results were obtained from an external laboratory (Allelica). PRS-based BC risk was computed both with and without considering additional risk factors, including gene status and family history. A significantly different PRS percentile distribution consistent with higher BC risk was observed in our cohort compared to the general population. Higher PRS-based BC risks were detected in younger patients and in those with FH of cancers. Among patients with a pathogenic germline variant detected, reduced PRS values were observed, while the BC risk was mainly determined by a monogenic etiology. Upon comprehensive analysis encompassing FH, gene status, and PRS, it was determined that 41.90% (44/105) of the patients demonstrated an elevated susceptibility for BC. Moreover, 63.63% of the patients with FH of BC and without an inherited pathogenic genetic variant detected showed increased BC risk by incorporating the PRS result. Our results indicate a major utility of PRS calculation in women with FH in the absence of a monogenic etiology detected by NGS. By combining high-risk strategies, such as inherited disease analysis, with low-risk screening strategies, such as FH and PRS, breast cancer risk stratification can be improved. This would facilitate the development of more effective preventive measures and optimize the allocation of healthcare resources. [ABSTRACT FROM AUTHOR]

Assessing a woman's risk of breast cancer is important for personalized screening. Mammographic density is a strong risk factor for breast cancer, but parenchymal texture patterns offer additional information which cannot be captured by density. We aimed to combine BI-RADS density score 4th Edition and a deep-learning-based texture score to stratify women in screening and compare rates among the combinations. This retrospective study cohort study included 216,564 women from a Danish populations-based screening program. Baseline mammograms were evaluated using BI-RADS density scores (1–4) and a deep-learning texture risk model, with scores categorized into four quartiles (1–4). The incidence rate ratio (IRR) for screen-detected, interval, and long-term cancer were adjusted for age, year of screening and screening clinic. Compared with subgroup B1-T1, the highest IRR for screen-detected cancer were within the T4 category (3.44 (95% CI: 2.43–4.82)−4.57 (95% CI: 3.66–5.76)). IRR for interval cancer was highest in the BI-RADS 4 category (95% CI: 5.36 (1.77–13.45)−16.94 (95% CI: 9.93–30.15)). IRR for long-term cancer increased both with increasing BI-RADS and increasing texture reaching 5.15 (4.31–6.16) for the combination of B4-T4 compared with B1-T1. Deep-learning-based texture analysis combined with BI-RADS density categories can reveal subgroups with increased rates beyond what density alone can ascertain, suggesting the potential of combining texture and density to improve risk stratification in breast cancer screening. [ABSTRACT FROM AUTHOR]

(1) Background: Atherosclerosis is a leading cause of vascular death worldwide. High urinary phosphate has recently been identified as a cardiovascular risk factor, but its role has not been fully established. The aim of this study was to investigate the association between urinary phosphate and subclinical atherosclerosis in the carotid, femoral as well as coronary territories; (2) Methods: We performed a cross-sectional analysis of a sample of 1169 middle-aged men, aged 50.9 years (SD 3.7), without previous cardiovascular disease, belonging to the Aragon Workers Health Study (AWHS). Urinary phosphate was analyzed in urine samples using the Fiske-Subbarow method. The presence of carotid plaque and femoral plaque was assessed by ultrasound and coronary artery calcium score (CACS) by computed tomography. Demographic, anthropometric and clinical data were collected at annual medical examinations. Logistic regression models were used to estimate the prevalence of adjusted atherosclerosis in the different vascular arteries; (3) Results: A significant inverse association was observed between urinary phosphate and subclinical atherosclerosis in the carotid [OR 95% CI 0.69 (0.49–0.99)] and coronary (CACS > 200) [OR 95% CI 0.46 (0.23–0.88)] arteries; however, no statistically significant association was found between urinary phosphate and the presence of atheroma plaques in the femoral territory [OR 1.02 (0.72–1.45)]; (4) Conclusions: In middle-aged men, a higher urinary phosphate concentration is associated with a lower prevalence of subclinical carotid and coronary atherosclerosis compared with those with a lower urinary phosphate concentration. [ABSTRACT FROM AUTHOR]

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]

Open burning poses a significant threat to human health and the environment by releasing hazardous chemicals and exacerbating plastic pollution. Urgent action is required to address its pervasive impact and the substantial release of gaseous pollutants. Limited research has explored the demographic aspect of open burning behavior, with none specifically conducted in Kentucky. An analysis of open burning complaints reported to the Kentucky Division for Air Quality in 2015, 2019, and 2021 revealed no significant differences in reported incidents by month and county. Binary logistic regression analyses identified the urban vs rural divide as significant predictors of open burning incidents, while violations were influenced by both urban and rural factors and average household income. Unemployment rates and the percentage of individuals with less than a high school diploma did not significantly predict open burning violations. Targeted interventions at the state and local level, focusing on rural areas and economically disadvantaged communities, can effectively address and mitigate open burning issues. [ABSTRACT FROM AUTHOR]

(1) Background: Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. The aim of the study was to examine the existing published results of the association between elevated serum phosphate concentrations and cardiovascular mortality, along with the CVD incidence and subclinical coronary atherosclerosis, in primary prevention among non-selected samples of the general population. (2) Methods: A systematic review and meta-analysis were carried out using literature obtained from PubMed, SCOPUS, and the Web Of Science until March 2024 and following the PRISMA guidelines. Relevant information was extracted and presented. Random and fixed effects models were used to estimate the pooled odds ratio (OR) and hazard ratio (HR) with their 95% coefficient interval (CI), and I2 was used to assess heterogeneity. (3) Results: Twenty-five studies met our inclusion criteria and were included in the meta-analysis (11 cross-sectional and 14 cohort studies). For cardiovascular mortality, which included 7 cohort studies and 41,764 adults, the pooled HR was 1.44 (95% CIs 1.28, 1.61; I2 0%) when the highest versus the reference level of serum phosphate concentrations were compared. For CVDs, which included 8 cohort studies and 61,723 adults, the pooled HR was 1.12 (95% CIs 0.99, 1.27; I2 51%). For subclinical coronary atherosclerosis, which included 11 cross-sectional studies and 24,820 adults, the pooled OR was 1.44 (95% CIs 1.15, 1.79; I2 88%). (4) Conclusions: The highest serum phosphate concentrations were positively associated with a 44% increased risk of cardiovascular mortality and subclinical coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Periodontitis is a common oral condition that can have a significant impact on the overall health of the body. In recent years, attention has been paid to potential relationships between periodontitis and various hematological disorders. This publication aims to present information available in the literature on this relationship, focusing on examples of red blood cell disorders (such as aplastic anemia and sickle cell anemia) and white blood cell disorders (such as cyclic neutropenia, maladaptive trained immunity, clonal hematopoiesis, leukemia, and multiple myeloma). Understanding these associations can help physicians and dentists better diagnose, monitor, and treat patients associated with both groups of conditions, highlighting the need for interdisciplinary care for patients with oral disorders and hematologic diseases. [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]

Cannabinoid use has surged in the past decade, with a growing interest in expanding cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC) applications into special populations. Consequently, the increased use of CBD and THC raises the risk of drug–drug interactions (DDIs). Nevertheless, DDIs for cannabinoids, especially in special populations, remain inadequately investigated. While some clinical trials have explored DDIs between therapeutic drugs like antiepileptic drugs and CBD/THC, more potential interactions remain to be examined. This review summarizes the published studies on CBD and THC–drug interactions, outlines the mechanisms involved, discusses the physiological considerations in pharmacokinetics (PK) and DDI studies in special populations (including pregnant and lactating women, pediatrics, older adults, patients with hepatic or renal impairments, and others), and presents modeling approaches that can describe the DDIs associated with CBD and THC in special populations. The PK of CBD and THC in special populations remain poorly characterized, with limited studies investigating DDIs involving CBD/THC in these populations. Therefore, it is critical to evaluate potential DDIs between CBD/THC and medications that are commonly used in special populations. Modeling approaches can aid in understanding these interactions. [ABSTRACT FROM AUTHOR]

Background: The identification of vitamin D (VitD) deficiency in pediatric populations is essential for preventive healthcare. We refined and tested the Evaluation of Deficiency Questionnaire (EVIDENCe-Q) for its utility in detecting VitD insufficiency among children. Patients and methods: We enrolled 201 pediatric patients (aged between 3 and 18 years). Clinical evaluation and serum vitamin D levels were assessed in all subjects. The EVIDENCe-Q was updated to incorporate factors influencing VitD biosynthesis, intake, assimilation, and metabolism, with scores spanning from 0 (optimal) to 36 (poor). Results: We established scores for severe deficiency (<10 mg/dL) at 20, deficiency (<20 mg/dL) at 22, and insufficiency (<30 mg/dL) at 28. A score of 20 or greater was determined as the optimal cut-off for distinguishing VitD deficient from sufficient statuses, as evidenced by ROC curve analysis AUC = 0.7066; SE = 0.0841; sensitivity 100%, 95% CI 0.561–1. The most accurate alignment was seen with VitD insufficiency, defined as 25-OH-D3 < 20 ng/mL. Conclusions: This study confirms that the EVIDENCe-Q is a valid instrument for assessing the risk of vitamin D deficiency and insufficiency in children. It offers a practical approach for determining the need for clinical intervention and dietary supplementation of VitD in the pediatric population. [ABSTRACT FROM AUTHOR]

The aryl hydrocarbon receptor (AHR) serves as a ligand-activated transcription factor crucial for regulating fundamental cellular and molecular processes, such as xenobiotic metabolism, immune responses, and cancer development. Notably, a spectrum of endocrine-disrupting chemicals (EDCs) act as agonists or antagonists of AHR, leading to the dysregulation of pivotal cellular and molecular processes and endocrine system disruption. Accumulating evidence suggests a correlation between EDC exposure and the onset of diverse pancreatic diseases, including diabetes, pancreatitis, and pancreatic cancer. Despite this association, the mechanistic role of AHR as a linchpin molecule in EDC exposure-related pathogenesis of pancreatic diseases and cancer remains unexplored. This review comprehensively examines the involvement of AHR in EDC exposure-mediated regulation of pancreatic pathogenesis, emphasizing AHR as a potential therapeutic target for the pathogenesis of pancreatic diseases and cancer. [ABSTRACT FROM AUTHOR]

We are exposed to a mixture of environmental man-made and natural xenobiotics. We experience a wide spectrum of environmental exposure in our lifetime, including the effects of xenobiotics on gametogenesis and gametes that undergo fertilization as the starting point of individual development and, moreover, in utero exposure, which can itself cause the first somatic or germline mutation necessary for breast cancer (BC) initiation. Most xenobiotics are metabolized or/and bioaccumulate and biomagnify in our tissues and cells, including breast tissues, so the xenobiotic metabolism plays an important role in BC initiation and progression. Many considerations necessitate a more valuable explanation regarding the molecular mechanisms of action of xenobiotics which act as genotoxic and epigenetic carcinogens. Thus, exposomics and the exposome concept are based on the diversity and range of exposures to physical factors, synthetic chemicals, dietary components, and psychosocial stressors, as well as their associated biologic processes and molecular pathways. Existing evidence for BC risk (BCR) suggests that food-borne chemical carcinogens, air pollution, ionizing radiation, and socioeconomic status are closely related to breast carcinogenesis. The aim of this review was to depict the dynamics and kinetics of several xenobiotics involved in BC development, emphasizing the role of new omics fields related to BC exposomics, such as environmental toxicogenomics, epigenomics and interactomics, metagenomics, nutrigenomics, nutriproteomics, and nutrimiRomics. We are mainly focused on food and nutrition, as well as endocrine-disrupting chemicals (EDCs), involved in BC development. Overall, cell and tissue accumulation and xenobiotic metabolism or biotransformation can lead to modifications in breast tissue composition and breast cell morphology, DNA damage and genomic instability, epimutations, RNA-mediated and extracellular vesicle effects, aberrant blood methylation, stimulation of epithelial–mesenchymal transition (EMT), disruption of cell–cell junctions, reorganization of the actin cytoskeleton, metabolic reprogramming, and overexpression of mesenchymal genes. Moreover, the metabolism of xenobiotics into BC cells impacts almost all known carcinogenic pathways. Conversely, in our food, there are many bioactive compounds with anti-cancer potential, exerting pro-apoptotic roles, inhibiting cell cycle progression and proliferation, migration, invasion, DNA damage, and cell stress conditions. We can conclude that exposomics has a high potential to demonstrate how environmental exposure to xenobiotics acts as a double-edged sword, promoting or suppressing tumorigenesis in BC. [ABSTRACT FROM AUTHOR]

Simple Summary: This exploratory narrative review investigates the association between exposure to per- and polyfluoroalkyl substances (PFAS), sociodemographic factors, stressors, and endometrial cancer risk. It explores the diverse sources of PFAS exposure and examines the role of income, education, occupation, ethnicity, and geographic location in influencing exposure levels and cancer risk. The review finds significant correlations between these sociodemographic factors and both PFAS exposure and endometrial cancer risk. It emphasizes the need for further interdisciplinary research and targeted interventions to understand and address these complex relationships, highlighting the importance of addressing health disparities for effective disease prevention and management. This exploratory narrative review paper delves into the intricate interplay between per- and polyfluoroalkyl substances (PFAS) exposure, sociodemographic factors, and the influence of stressors in the context of endometrial cancer. PFAS, ubiquitous environmental contaminants notorious for their persistence in the ecosystem, have garnered attention for their potential to disrupt endocrine systems and provoke immune responses. We comprehensively examine the various sources of PFAS exposure, encompassing household items, water, air, and soil, thus shedding light on the multifaceted routes through which individuals encounter these compounds. Furthermore, we explore the influence of sociodemographic factors, such as income, education, occupation, ethnicity/race, and geographical location and their relationship to endometrial cancer risk. We also investigated the role of stress on PFAS exposure and endometrial cancer risk. The results revealed a significant impact of sociodemographic factors on both PFAS levels and endometrial cancer risk. Stress emerged as a notable contributing factor influencing PFAS exposure and the development of endometrial cancer, further emphasizing the importance of stress management practices for overall well-being. By synthesizing evidence from diverse fields, this review underscores the need for interdisciplinary research and targeted interventions to comprehensively address the complex relationship between PFAS, sociodemographic factors, stressors, and endometrial cancer. [ABSTRACT FROM AUTHOR]

Breast cancer survival has increased significantly over the last few decades due to more effective strategies for prevention and risk modification, advancements in imaging detection, screening, and multimodal treatment algorithms. However, many have observed disparities in benefits derived from such improvements across populations and demographic groups. This review summarizes published works that contextualize modern disparities in breast cancer prevention, diagnosis, and treatment and presents potential strategies for reducing disparities. We conducted searches for studies that directly investigated and/or reported disparities in breast cancer prevention, detection, or treatment. Demographic factors, social determinants of health, and inequitable healthcare delivery may impede the ability of individuals and communities to employ risk-mitigating behaviors and prevention strategies. The disparate access to quality screening and timely diagnosis experienced by various groups poses significant hurdles to optimal care and survival. Finally, barriers to access and inequitable healthcare delivery patterns reinforce inequitable application of standards of care. Cumulatively, these disparities underlie notable differences in the incidence, severity, and survival of breast cancers. Efforts toward mitigation will require collaborative approaches and partnerships between communities, governments, and healthcare organizations, which must be considered equal stakeholders in the fight for equity in breast cancer care and outcomes. [ABSTRACT FROM AUTHOR]

Background: Studies have shown lower rates of cancer screening and high mortality rates among all Asian Americans than among non-Hispanic White populations. However, most of these studies often confound diverse Asian American subgroups with limited data on cancer screening for Indian Americans, with this group being particularly interesting because of their counterintuitive socioeconomic status. For this reason, the objective of this study is to evaluate knowledge of the United States Preventive Services Task Force (USPSTF) cancer screening guidelines and compliance among South Indian Americans residing in Southern California. Methods: This was a cross-sectional study gathering community responses through an electronic survey. The survey reports knowledge of USPSTF screening guidelines and participant compliance rates. Rates were further compared to non-Hispanic White populations from official sources. Results: South Indian Americans residing in California had lower rates of compliance for colorectal, lung, and breast cancer screening when compared to that of non-Hispanic White populations in the same region, with the exception of cervical cancer screening rates. Conclusion: Understanding the cultural characteristics of special populations, such as Indian Americans, can help communities adhere to more effective screening practices that can improve outcomes. [ABSTRACT FROM AUTHOR]

Serum 25(OH)D deficiency consistently demonstrated molecular mechanisms through which chronic inflammation is associated with the risk of nasopharyngeal carcinoma (NPC). This study aimed to determine the association between serum 25(OH)D and NPC. A matched case–control study was conducted at two local hospitals. A total of 300 histologically confirmed NPC cases were matched with controls for age, gender, and ethnicity, and assessed for vitamin D status and other nutritional factors. Mean Vitamin D concentration was significantly lower among cases compared to controls (63.17 ± 19.15 nmol/L and 67.34 ± 23.06 nmol/L) (t = −2.41, p = 0.016). Multiple conditional logistic regression analysis indicated that higher levels of serum 25(OH)D were associated with reduced odds of NPC (AOR = 0.73, 95% CI = 0.57–0.94, p = 0.016) controlling for confounders including BMI, physical activity, smoking status, alcohol consumption, consumption of food high in vitamin D, salted fish consumption, and family history of NPC. There was a significant association between inadequate serum 25(OH)D status with accumulation of four risk factors and increased odds of getting NPC using polynomial regression analysis. Increased NPC odds ratios were observed after sequential accumulation of additional risk factors with the presence of inadequate serum 25(OH)D status (OR = 0.54, 95% CI = 0.27, 4.77, p = 0.322, OR = 1.04, 95% CI = 0.64, 1.72, p = 0.267, OR = 1.15, 95% CI = 0.73, 1.80, p = 0.067, OR = 1.93, 95% CI = 1.13, 3.31, p = 0.022, and OR = 5.55, 95% CI = 1.67, 10.3, p < 0.001 respectively). Future research in Malaysia should involve both prospective cohort studies and randomized controlled trials to confirm and further clarify the role of vitamin D in NPC outcomes. [ABSTRACT FROM AUTHOR]

Known as a diverse collection of neoplastic diseases, breast cancer (BC) can be hyperbolically characterized as a dynamic pseudo-organ, a living organism able to build a complex, open, hierarchically organized, self-sustainable, and self-renewable tumor system, a population, a species, a local community, a biocenosis, or an evolving dynamical ecosystem (i.e., immune or metabolic ecosystem) that emphasizes both developmental continuity and spatio-temporal change. Moreover, a cancer cell community, also known as an oncobiota, has been described as non-sexually reproducing species, as well as a migratory or invasive species that expresses intelligent behavior, or an endangered or parasite species that fights to survive, to optimize its features inside the host's ecosystem, or that is able to exploit or to disrupt its host circadian cycle for improving the own proliferation and spreading. BC tumorigenesis has also been compared with the early embryo and placenta development that may suggest new strategies for research and therapy. Furthermore, BC has also been characterized as an environmental disease or as an ecological disorder. Many mechanisms of cancer progression have been explained by principles of ecology, developmental biology, and evolutionary paradigms. Many authors have discussed ecological, developmental, and evolutionary strategies for more successful anti-cancer therapies, or for understanding the ecological, developmental, and evolutionary bases of BC exploitable vulnerabilities. Herein, we used the integrated framework of three well known ecological theories: the Bronfenbrenner's theory of human development, the Vannote's River Continuum Concept (RCC), and the Ecological Evolutionary Developmental Biology (Eco-Evo-Devo) theory, to explain and understand several eco-evo-devo-based principles that govern BC progression. Multi-omics fields, taken together as onco-breastomics, offer better opportunities to integrate, analyze, and interpret large amounts of complex heterogeneous data, such as various and big-omics data obtained by multiple investigative modalities, for understanding the eco-evo-devo-based principles that drive BC progression and treatment. These integrative eco-evo-devo theories can help clinicians better diagnose and treat BC, for example, by using non-invasive biomarkers in liquid-biopsies that have emerged from integrated omics-based data that accurately reflect the biomolecular landscape of the primary tumor in order to avoid mutilating preventive surgery, like bilateral mastectomy. From the perspective of preventive, personalized, and participatory medicine, these hypotheses may help patients to think about this disease as a process governed by natural rules, to understand the possible causes of the disease, and to gain control on their own health. [ABSTRACT FROM AUTHOR]

It has been found that the development of some cancers can be attributed to obesity, which is associated with the excessive intake of lipids. Cancer cells undergo metabolic reprogramming, shifting from utilizing glucose to fatty acids (FAs) for energy. CD36, a lipid transporter, is highly expressed in certain kinds of cancer cells. High expressions of CD36 in tumor cells triggers FA uptake and lipid accumulation, promoting rapid tumor growth and initiating metastasis. Meanwhile, immune cells in the tumor microenvironment overexpress CD36 and undergo metabolic reprogramming. CD36-mediated FA uptake leads to lipid accumulation and has immunosuppressive effects. This paper reviews the types of FAs associated with cancer, high expressions of CD36 that promote cancer development and progression, effects of CD36 on different immune cells in the tumor microenvironment, and the current status of CD36 as a therapeutic target for the treatment of tumors with high CD36 expression. [ABSTRACT FROM AUTHOR]

Chicoric acid (CA) has been reported to exhibit biological activities; it remains unclear, however, whether CA could regulate colitis via modulation of the gut microbiota and metabolites. This study aimed to assess CA's impact on dextran sulfate sodium (DSS)-induced colitis, the gut microbiota, and metabolites. Mice were induced with 2.5% DSS to develop colitis over a 7-day period. CA was administered intragastrically one week prior to DSS treatment and continued for 14 days. The microbial composition in the stool was determined using 16S rRNA sequencing, while non-targeted metabolomics was employed to analyze the metabolic profiles of each mouse group. The results show that CA effectively alleviated colitis, as evidenced by an increased colon length, lowered disease activity index (DAI) and histological scores, and decreased tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) expression levels. CA intervention restored the structure of gut microbiota. Specifically, it decreased the abundance of Bacteroidetes and Cyanobacteria at the phylum level and Bacteroides, Rosiarcus, and unclassified Xanthobacteraceae at the genus level, and increased the abundance of unclassified Lachnospiraceae at the genus level. Metabolomic analysis revealed that CA supplementation reversed the up-regulation of asymmetric dimethylarginine, N-glycolylneuraminic acid, and N-acetylneuraminic acid, as well as the down-regulation of phloroglucinol, thiamine, 4-methyl-5-thiazoleethanol, lithocholic acid, and oxymatrine induced by DSS. Our current research provides scientific evidence for developing CA into an anti-colitis functional food ingredient. Further clinical trials are warranted to elucidate the efficacy and mechanism of CA in treating human inflammatory bowel disease (IBD). [ABSTRACT FROM AUTHOR]

The study of liquid biopsy with plasma samples is being conducted to identify biomarkers for clinical use. Exosomes, containing nucleic acids and metabolites, have emerged as possible sources for biomarkers. To evaluate the effectiveness of exosomes over plasma, we analyzed the small non-coding RNAs (sncRNAs) and metabolites extracted from exosomes in comparison to those directly extracted from whole plasma under both fasting and non-fasting conditions. We found that sncRNA profiles were not affected by fasting in either exosome or plasma samples. Our results showed that exosomal sncRNAs were found to have more consistent profiles. The plasma miRNA profiles contained high concentrations of cell-derived miRNAs that were likely due to hemolysis. We determined that certain metabolites in whole plasma exhibited noteworthy concentration shifts in relation to fasting status, while others did not. Here, we propose that (1) fasting is not required for a liquid biopsy study that involves both sncRNA and metabolomic profiling, as long as metabolites that are not influenced by fasting status are selected, and (2) the utilization of exosomal RNAs promotes robust and consistent findings in plasma samples, mitigating the impact of batch effects derived from hemolysis. These findings advance the optimization of liquid biopsy methodologies for clinical applications. [ABSTRACT FROM AUTHOR]

(1) Background: Breast cancer is the most prevalent cancer found in women in Mali. The aim of the current study was to determine the association between metabolites circulating in the blood, 25(OH)D and 1,25(OH)2D, and vitamin D levels with the risk of breast cancer in Malian women. (2) Methods: We conducted a prospective case–control study from August 2021 to March 2022. Control subjects were matched to cases according to age (within 5 years). The patients' clinical stage was determined by the oncologist according to the tumour–nodes–metastasis (TNM) classification system. (3) Results: We observed no differences in the mean 25(OH)D (p = 0.221) and 1,25(OH)2D (p = 0.285) between cases and controls. However, our findings indicate a more pronounced inverse association in the first level of plasma 25(OH)D, while the risk function decreases at higher levels. This observation takes strength with 1,25(OH)2D by a significant association between the first quartile and breast cancer as a risk factor (p = 0.03; OR = 71.84; CI: 1.36–3785.34). (4) Conclusions: These outcomes showed a possible association between 25(OH)D and 1,25(OH)2D in decreasing the risk of breast cancer. [ABSTRACT FROM AUTHOR]

Given the need to improve the sensitivity of non-invasive methods to detect colorectal neoplasia, particularly adenomas, we compared a fecal test using a monoclonal antibody (Mab) raised against constituents of colonic adenomas designated Adnab-9 (Adenoma Antibody 9), recognizing an N-linked 87 kDa glycoprotein, to gFOBT, which is shown to reduce CRC mortality. p87 immunohistochemistry testing is significantly more sensitive (OR 3.64[CI 2.37–5.58]) than gFOBT (guaiac-based fecal occult blood test) for adenomas (<3 in number), advanced adenomas (OR 4.21[CI 2.47–7.15]), or a combination of the two (OR 3.35[CI 2.47–4.53]). p87 immunohistochemistry shows regional Paneth cell (PC) expression mainly in the right-sided colon and is significantly reduced in the ceca of African Americans (p < 0.0001). In a subset of patients, we obtained other body fluids such as urine, colonic effluent, and saliva. Urine tests (organ-specific neoantigen) showed a significant difference for advanced adenomas (p < 0.047). We conclude that fecal p87 testing is more sensitive than gFOBT and Adnab-9 and could be used to better direct the colonoscopy screening effort. [ABSTRACT FROM AUTHOR]

Mammography is the primary breast cancer screening strategy. Recent methods have been developed using the mammogram image to improve breast cancer risk prediction. However, it is unclear on the extent to which the effect of risk factors on breast cancer risk is mediated through tissue features summarized in mammogram images and the extent to which it is through other pathways. While mediation analysis has been conducted using mammographic density (a summary measure within the image), the mammogram image is not necessarily well described by a single summary measure and, in addition, such a measure provides no spatial information about the relationship between the exposure risk factor and the risk of breast cancer. Thus, to better understand the role of the mammogram images that provide spatial information about the state of the breast tissue that is causally predictive of the future occurrence of breast cancer, we propose a novel method of causal mediation analysis using mammogram image mediator while accommodating the irregular shape of the breast. We apply the proposed method to data from the Joanne Knight Breast Health Cohort and leverage new insights on the decomposition of the total association between risk factor and breast cancer risk that was mediated by the texture of the underlying breast tissue summarized in the mammogram image. [ABSTRACT FROM AUTHOR]

Monoclonal gammopathy of undetermined significance (MGUS) is a pre-malignant plasma cell disorder with an etiology that is incompletely understood. Modifiable risk factors and genetic predispositions likely interact to increase MGUS risk in specific individuals and populations. Identifying geographic prevalence patterns and modifiable risk factors is critical for understanding the etiology of MGUS. The aim of this review was to outline original research on MGUS prevalence across geographic locations and modifiable risk factors. We conducted a systematic review of 39 eligible studies from PubMed®, Embase®, and Web of Science® written in English and published by February 2023. Our protocol was registered in accordance with PROSPERO guidelines. Studies were synthesized using Research Electronic Data Capture and appraised using the National Heart, Lung, and Blood Institute study quality assessment tools. The prevalence of MGUS ranged from 0.24% to 9% across geographic locations. Modifiable risk factors for MGUS include infections, autoimmune diseases, chronic inflammatory conditions, lifestyle factors, environmental exposures, and ionizing radiation. Therefore, the development of MGUS may be related to chronic antigenic stimulation and genetic aberrations that promote clonal proliferation of plasma cells. Prospective studies assessing gene–environment interactions are needed to further define risk factors for MGUS and inform screening and preventative strategies. [ABSTRACT FROM AUTHOR]

Simple Summary: Hepatocellular carcinoma (HCC) is a severe global health concern, and it is increasingly jeopardizing younger individuals. Despite this, there is a lack of available tools for the prognosis estimation of early-onset HCC. In our study, we conducted a retrospective analysis of early-onset HCC (EO-LIHC) using data of the period from 2004 to 2018. We identified independent risk factors using a Cox regression analysis, including age, sex, AFP level, the grading and staging of the tumor, the size of the tumor, and whether the patient was receiving therapy like surgery and chemotherapy. We developed a predictive nomogram to estimate 1-, 3-, and 5-year survival rates of EO-LIHC patients and a user-friendly web-based survival prediction model tailored for these patients. These findings provide valuable insights for personalized care and treatment decisions for individuals with EO-LIHC. Hepatocellular carcinoma (HCC) is a widespread and impactful cancer which has pertinent implications worldwide. Although most cases of HCC are typically diagnosed in individuals aged ≥60 years, there has been a notable rise in the occurrence of HCC among younger patients. However, there is a scarcity of precise prognostic models available for predicting outcomes in these younger patients. A retrospective analysis was conducted to investigate early-onset hepatocellular carcinoma (EO-LIHC) using data from the Surveillance, Epidemiology, and End Results (SEER) database from 2004 to 2018. The analysis included 1392 patients from the SEER database and our hospital. Among them, 1287 patients from the SEER database were assigned to the training cohort (n = 899) and validation cohort 1 (n = 388), while 105 patients from our hospital were assigned to validation cohort 2. A Cox regression analysis showed that age, sex, AFP, grade, stage, tumor size, surgery, and chemotherapy were independent risk factors. The nomogram developed in this study demonstrated its discriminatory ability to predict the 1-, 3-, and 5-year overall survival (OS) rates in EO-LIHC patients based on individual characteristics. Additionally, a web-based OS prediction model specifically tailored for EO-LIHC patients was created and validated. Overall, these advancements contribute to improved decision-making and personalized care for individuals with EO-LIHC. [ABSTRACT FROM AUTHOR]