Risk screening tools recommended by the United States Preventative Services Task Force (USPSTF) are used to screen potential BRCA1/2 pathogenic variant carriers. The purpose of this study was to identify an appropriate breast cancer risk-screening tool for genetic referral among women with a family history of breast cancer in Taiwan.

A cross-sectional design with convenience sampling was used in this study. Women with a family history of breast cancer but not diagnosed with breast cancer were recruited from surgical outpatient clinics. Sociodemographic and family cancer history were collected based on the screening tools. Both the Tyrer-Cuzick (IBIS) and BRCAPRO were used as a Gold standard to evaluate the accuracy of five screening tools. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and the areas under the receiver-operating curve (AUC) were compared to identify the most accurate one to determine women with elevated risk as defined by IBIS and BRCAPRO calculations with lifetime risk over 15%.

One hundred twenty-four women with a family history of breast cancer but not yet diagnosed as breast cancer were recruited in this study. When the Tyrer-Cuzick (IBIS) was used as the standard, the AUC for the tools ranged from 0.490 to 0.562. When the BRCAPRO was used as the standard, the p values of the Ontario Family History Assessment Tool (Ontario-FHAT) (p = 0.003) and Pedigree Assessment Tool (PAT) (p = 0.016) were significant, and the AUCs were 0.938 and 0.854 for Ontario-FHAT and PAT, respectively. Since the sensitivity of Ontario-FHAT was 100, which is higher than PAT, we considered that using Ontario-FHAT in Taiwanese women would be better than using PAT.

Ontario-FHAT would be an appropriate screening tool for identifying individuals in Taiwan who may need a genetic referral for further BRCA1/2 risk evaluation.

Breast cancer is the most commonly diagnosed neoplasm and one of the most widespread cancers among women. The research advanced the Mf-EIT hardware through analogue discovery, component assessment, hardware integration, software creation, and data reconstruction utilizing Gauss-Newton and GREIT approaches. The breast cancer phantom consisted of a gelatin and sodium chloride solution. The position and number of anomalies in the reconstructed image correspond with the phantom. Anomalies in the reconstructed image are illustrated in red, indicating that they exhibit higher conductivity than their environment. The smallest percentage difference in conductivity between the reconstructed image of the cancer abnormality and the phantom is 0.18 %, recorded at a current of 0.35 mA and a frequency of 150 kHz. The smallest percentage difference in size between cancer abnormalities 1 and 2 in the reconstructed image and the phantom is 0.14 %, observed at a current of 0.22 mA and a frequency of 80 kHz. In brief,•This study proposes an innovative Electrical Impedance Tomography (EIT)•The designed and built the Mf-EIT hardware based on data reconstruction using Gauss-Newton and GREIT•The Electrical Impedance Tomography designed to detect the anomalies in the reconstructed image of Breast Cancer.

Breast cancer is a leading cause of cancer-related mortality among women worldwide, characterized by its aggressive nature, propensity for metastasis, and resistance to standard treatment modalities. Traditional therapies, including surgery, chemotherapy, and radiation, often encounter significant limitations such as systemic toxicity and lack of specificity.

This review aims to evaluate the recent advancements in phage-based nanomedicines as a novel approach for targeted breast cancer therapy, focusing on their mechanisms of action, therapeutic benefits, and the challenges faced in clinical implementation.

A comprehensive literature review was conducted, analyzing studies that investigate the application of bacteriophages in cancer therapy, particularly in breast cancer. The review highlights the integration of nanotechnology with phage therapy, examining the potential for enhanced targeting and reduced side effects.

Phage-based nanomedicines have shown promise in selectively targeting breast cancer cells while sparing healthy tissues, thereby improving therapeutic efficacy and safety profiles. The unique properties of bacteriophages, including their ability to be engineered for specific targeting and their natural ability to induce immune responses, present significant advantages over conventional treatments.

The integration of phage therapy with nanotechnology represents a promising frontier in the fight against breast cancer. This review underscores the need for continued research to address existing challenges and to explore the full potential of phage-based nanomedicines in improving patient outcomes in breast cancer treatment.

Currently, breast cancer (BC) and ovarian cancer (OC) are the most prevalent forms of cancer among women worldwide. Even though BC has a favorable outlook when detected early and managed appropriately compared to OC, the spread of BC and OC to other parts of the body, known as metastasis, is a significant cause of death. A robust association exists between genetic and protein alterations and post-translational modifications (PTMs), significantly impacting tumor formation, advancement, and prognosis. Ubiquitination, a crucial PTM, regulates almost all aspects of cellular function, and E3-ligase-mediated ubiquitination is a pivotal process that controls the speed of the protein ubiquitination cascade. NEDD4-1, a neural developmentally downregulated protein 4-1, is a crucial E3 ligase that plays a significant role in regulating several proteins that have important functions in the development and progression of BC and OC, thus controlling BC and OC cells' movement, infiltration, and multiplication. This review discusses the latest developments in comprehending NEDD4-1 substrates and their involvement in signal transduction pathways in BC and OC. NEDD4-1 likely serves as a novel diagnostic indicator and a target for therapy in the battle against both cancers.

Growing evidence highlights the critical role of chromatin remodeling in tumor development and progression. This study explores the relationship between chromatin remodeling-related genes (CRRGs) and breast cancer (BRCA). Public databases were used to retrieve the TCGA-BRCA and GSE20685 datasets. CRRGs were sourced from prior studies. Prognosis-associated CRRGs were identified using univariate Cox regression analysis. TCGA-BRCA BRCA samples were grouped into CRRG-related subtypes through consensus clustering analysis. Differential expression analysis was conducted in TCGA-BRCA (BRAC vs. control) and among subtypes to identify differentially expressed genes (DEGs). Candidate genes were obtained through the intersection of these DEGs. Prognostic genes were selected using univariate Cox and least absolute shrinkage and selection operator (LASSO) regression analyses. Independent prognostic factors were identified, and a nomogram model was developed. Functional enrichment, immune infiltration, clinical relevance, and drug sensitivity analyses were subsequently performed. TCGA-BRCA BRCA samples were classified into two CRRG-related subtypes (clusters 1 and 2) based on prognosis-associated CRRGs. A total of 141 candidate genes were identified by intersecting 250 DEGs (cluster 1 vs. cluster 2) with 3,145 DEGs (BRCA vs. control). Five prognostic genes-LHX5, ZP2, GABRQ, APOA2, and CLCNKB-were selected, and a prognostic risk model was developed. In clinical samples, APOA2 (P = 0.0290) and GABRQ (P = 0.0132) expression were significantly up-regulated, CLCNKB (P < 0.0001) and ZP2 (P = 0.0445) expression were significantly down-regulated, while LHX5 (P = 0.1508) expression did not present a significant difference. A nomogram was created, and calibration and Receiver Operating Characteristic (ROC) curves demonstrated its superior predictive ability for BRCA. Gene Set Variation Analysis (GSVA) revealed 16 pathways, such as "mTORC1 signaling" and "E2F targets," were enriched in the high-risk group, while 9 pathways, including "estrogen response early" and "myogenesis," were enriched in the low-risk group. Additionally, significant differences in immune cell types, including CD8+ T cells and follicular helper T cells, were observed between the two risk groups. The risk score was also significantly associated with six drugs, including AZD1332 1463 and SB505124 1194. This study presents a prognostic model based on five genes (LHX5, ZP2, GABRQ, APOA2, and CLCNKB) for BRCA, offering a novel perspective on the link between CRRGs and BRCA.

Gene therapy has a strong potential to treat different cancer types cancers with high therapeutic outcomes. c-myc is believed to be responsible for more than 15% of all gene regulation and functions as a transcription factor for proteins essential for cell proliferation. This study aimed to develop niosome nanocarriers to knockdown c-myc expression using anti-c-myc short-interfering RNA (siRNA) in MCF-7 cells. Altering the activity of the c-myc proto-oncogene has been identified as an important element in minimizing cancer cell growth because anti-c-myc siRNA degrades c-myc mRNA.

Noisomes were prepared from Tween 85, cholesterol, and didodecyldimethylammonium bromide at 50:40:10 and 40:40:20 molar ratios. Anti-c-myc siRNA was loaded in the prepared niosomes and then applied on MCF-7 cells.

Niosomes had a total positive charge formed electrostatic interactions with siRNA. Niosomes were spherical with a size range of 70-100 nm. The prepared niosomes were nontoxic to MCF-7 cells, with IC50 values of >250 µg/ml for both formulations. After encapsulation of anti-c-myc siRNA, nioplexes reduced c-myc mRNA expression by more than 50% compared with the untreated cells. Empty niosomes did not affect c-myc mRNA expression levels, indicating that the effect was due to siRNA rather than the particles themselves.

This study provides evidence that niosomes can function as suitable carriers for siRNA delivery to knockdown the c-myc oncogene in MCF-7 cells, thus reducing cancer cell growth.

Breast cancer is the leading cause of cancer-related death and the most common cancer among women worldwide. It is crucial to identify potentially modifiable risk factors to intervene and prevent breast cancer effectively. Sleep factors have emerged as a potentially novel risk factor for female breast cancer. Current epidemiologic studies suggest a significant impact of sleep factors on breast cancer. Exposure to abnormal sleep duration, poor sleep quality, sleep disorders, sleep medication use, or night shift work can increase the risk of breast cancer by decreasing melatonin secretion, disrupting circadian rhythm, compromising immune function, or altering hormone levels. However, there are still controversies regarding the epidemiologic association, and the underlying mechanisms have yet to be fully elucidated. This paper summarizes the epidemiologic evidence on the associations between sleep factors, including sleep duration, sleep quality, sleep disorders, sleep medication use, sleep habits, and night shift work, and the development of breast cancer. The potential mechanisms underlying these associations were also reviewed.

Globally, breast cancer is the most common cancer to affect women. There are different molecular and pathological factors that are involved in the uncontrolled proliferation of breast cancer cells. FOXN3 that is member of Forkhead box family proteins is well recognized for having a crucial role in different biological processes and is reported to be dysregulated in various malignancies. The studies to evaluate the significance of the FOXN3 gene in progression of breast cancer are still under progress. We in the current study aim to examine the FOXN3 gene expression in Indian breast cancer patients and find its clinical relevance. FOXN3 expression analysis using RT-PCR, immunohistochemistry, and western blotting was performed in tumor and normal tissue collected from 142 sporadic breast cancer patients. To identify the genetic aberrations in FOXN3 gene automated DNA sequencing was done. FOXN3 expression study revealed the elevated expression of FOXN3 mRNA in 61.26% of the cases whereas FOXN3 protein was seen to be overexpressed in 59.15% cases. Further, it was found that the elevated expression of FOXN3 mRNA was significantly correlated with the post-menopausal (p = 0.003) status and positive lymph node status (p = 0.049) of the patients. The FOXN3 protein expression also exhibited the significant association with menopausal status (p = 0.008), lymph node status (p = 0.001) and clinical stage (p = 0.018) of the patients. However, we did not find any mutation in the DNA binding domain of the FOXN3 gene in the Indian breast cancer cases. Our findings indicates that overexpression of FOXN3 gene in Indian breast cancer cases can have a potential role in breast cancer progression especially in advanced clinical stages.

Mamary Paget's disease presents with subtle and insidious symptoms leading to late diagnosis that poses medical challenges. This uncommon pathology often has underlying ductal breast cancer, including in situ or invasive breast cancer, which makes early recognition crucial for better prognoses. A 78-year-old postmenopausal woman presented with progressive and persistent eczematous skin lesions of the nipple without breast lumps. Additional imaging procedures revealed subtle findings, but the histopathology and immunohistopathology confirmed Paget's disease. This case highlights the importance of the correlation between clinical findings and the chosen diagnostic method for establishing a definitive diagnosis of mammary Paget's disease.

Cancer participates in the immune response by releasing several factors, such as cytokines and chemokines, which can alter the ability of the immune system to identify and eradicate cancer. Notably, the role of thymic stromal lymphopoietin (TSLP) in breast cancer (BC) is currently controversial and unclear. The present study characterized the role of TSLP in BC and its interaction with peripheral blood mononuclear cells, focusing on the CD14+CD16+ monocyte population via the secretome released by BC cells. The UALCAN and Gene Expression Profiling Interactive Analysis tools were employed to define TSLP expression in BC, and its levels in different BC subtype cell lines were validated using reverse transcription-quantitative PCR and ELISA. In addition, TIMER 2.0 was used to determine the abundance of immune cell infiltration in BC. Subsequently, the effects of BC conditioned medium (CM) and TSLP were investigated on CD14+CD16+ monocytes via flow cytometry. A Cellular Reactive Oxygen Species (ROS) Assay Kit, Fluo-4 AM assay and ATPlite assay were used to explore the effects of TSLP on monocyte cellular metabolism. The results showed that a reduction in TSLP expression was associated with an unfavorable prognosis in BC. Furthermore, a higher expression of TSLP in CM from a non-tumoral cell line increased the percentage of CD14+CD16+ monocytes. Finally, it was revealed that TSLP decreased intracellular ATP levels, while increasing intracellular calcium levels and producing ROS in THP-1 cells. Therefore, TSLP may be considered a novel biomarker in the BC microenvironment, where it could regulate cellular metabolism through the expansion of CD14+CD16+ monocytes.

Despite a high burden of osteoporosis and minimal trauma fractures worldwide, there is still a treatment gap in timely diagnosis and optimal treatment. There is also a lack of international consensus and guidelines on the management of bone fragility in premenopausal women. This review article provides an overview of the current understanding of factors impacting women's bone health across the adult lifespan, as well as dilemmas in the diagnosis, assessment and management of osteoporosis in premenopausal and postmenopausal women, premature ovarian insufficiency and bone health following breast cancer.

Breast cancer is a significant healthcare challenge, and despite advancements in treatment, the risk of recurrence remains a critical concern, particularly for postmenopausal women. Understanding the factors that contribute to this risk is essential for improving monitoring and prevention strategies, ultimately enhancing long-term care and disease management for this patient population. The study analyzes scholarly literature on recurrence patterns in postmenopausal Caucasian women with prior breast cancer, highlighting the potential for innovative insights to reduce breast cancer mortality and improve long-term survival. We used R software and the "R-Bibliometrix" package to analyze postmenopausal breast cancer recurrence. Data was collected from the Web of Science Core Collection database to identify relevant documents and highlight significant collaborative efforts and commonly used terminology. The extensive analysis included 500 articles authored by 3,204 individuals from 195 distinct sources, all published between 2010 and 2024. It specifically focused on assessing the risk of breast cancer recurrence in postmenopausal women. The results underscored several critical factors influencing the risk of recurrence, encompassing hormonal factors, lifestyle influences, the effectiveness of various types of adjuvant therapy, and the role of genetic factors. In conclusion, the research highlights the multifaceted nature of factors contributing to breast cancer recurrence in postmenopausal women. We believe that this study not only enhances the current understanding of the risk of breast cancer recurrence in postmenopausal women but also provides clear directions for future research and improvements in clinical practice and health policy.

TikTok is one of the biggest social media platforms where people look for support, seek advice, and educate themselves through videos created by other users. In today's world, people frequently turn to the internet for easy access to health and medical information; it is no surprise that TikTok has helped facilitate the creation of online support groups for those who are overcoming various illnesses and diseases. Breast cancer (BRCA) is worldwide the most common cancer in women, and while BRCA discussions on TikTok have been researched previously, discussions surrounding the BRCA susceptibility gene mutations have not. This study aims to explore content on TikTok related to BRCA mutations and assess its impact on public awareness and physician involvement. One hundred videos were watched on TikTok after searching "BRCA", BRCA1", or "BRCA2". These videos were categorized into groups based on content creator and type of content. The content included discussion regarding preventative measures with BRCA mutations, BRCA and BRCA mutation, ovarian cancer and BRCA mutation, and various treatment options. The videos were also evaluated based on the number of views each video received. This study found that healthcare workers participated in BRCA-related TikTok videos at only 2.3% of all evaluated videos; 97.4% were created by laypersons. Of those videos created by non-medical personnel, 17.3% were educational. The majority (49.3%) were centered around preventative measures and treatments undergone after a BRCA mutation diagnosis. The treatment modality most discussed was double mastectomy at 68%, with 41.3% of those videos being preventative double mastectomies without a current cancer diagnosis. The video with the most views was with regard to motherhood and BRCA prevention at 2.3 million views; 10.4% of the videos discussed difficulties with BRCA in motherhood. Overall, this study highlights the importance of physician involvement in social media platforms. It also showcases how medical providers can use TikTok to better understand patients' needs and discussions outside of the office with regard to their diagnosis.

Breast cancer (BC) is the most common malignancy among Iranian females, accounting for 24.4% of all malignancies. Germ line mutations in DNA repair system-related genes are associated with an increased risk of BC. This study aims to evaluate the frequencies of single nucleotide polymorphisms (SNPs) in the BRCA1, BRCA2, and PALB2 genes in patients with BC from a subset of the Iranian population in the western part of Iran.

Blood samples were collected from 335 patients with BC and 354 healthy matched volunteers. Genomic DNA was extracted using the salting-out method and, after quality control, was genotyped using the multiplex TaqMan allelic discrimination assay for three SNPs: rs80359550 (6174 delT) in the BRCA2 gene, rs180177102 in the PALB2 gene, and rs386833395 (185delAG) in the BRCA1 gene. Statistical analysis was performed to examine allele frequency, odds ratio, and relative risk (genetic association) in a retrospective case-control study.

The data showed no association between rs386833395 and BC risk in the studied population (odds ratio = 1), whereas rs80359550 and rs180177102 polymorphisms were strongly associated with BC risk in patients (odds ratio = 0.01 for both, with p-values of 0.011 and 0.021, respectively).

Our findings suggest no significant association between the rs386833395 polymorphism and BC risk in the Iranian Kurdish population, while rs80359550 and rs180177102 polymorphisms were strongly associated with BC. However, the study has several limitations, including its retrospective design, a relatively small sample size, and the potential lack of generalizability to other ethnic groups within Iran. Future studies involving larger cohorts and more diverse populations are needed to confirm these results.

Breast cancer is the most common malignancy among women globally, with incidence rates continuing to rise. A comprehensive understanding of its risk factors and the underlying biological mechanisms that drive tumor initiation is essential for developing effective prevention strategies. This review examines key non-modifiable risk factors, such as genetic predisposition, demographic characteristics, family history, mammographic density, and reproductive milestones, as well as modifiable risk factors like exogenous hormone exposure, obesity, diet, and physical inactivity. Importantly, reproductive history plays a dual role, providing long-term protection while temporarily increasing breast cancer risk shortly after pregnancy. Current chemoprevention strategies primarily depend on selective estrogen receptor modulators (SERMs), including tamoxifen and raloxifene, which have demonstrated efficacy in reducing the incidence of estrogen receptor-positive breast cancer but remain underutilized due to adverse effects. Emerging approaches such as aromatase inhibitors, RANKL inhibitors, progesterone antagonists, PI3K inhibitors, and immunoprevention strategies show promise for expanding preventive options. Understanding the interactions between risk factors, hormonal influences, and tumorigenesis is critical for optimizing breast cancer prevention and advancing safer, more targeted chemopreventive interventions.

Breast cancer is the most common cancer among females, and early detection plays a crucial role in disease management. This study aimed to assess the knowledge, practices, and barriers related to breast self-examination (BSE) and mammography among Saudi women in Arar City, Saudi Arabia.

A cross-sectional observational study was conducted using an online Google Form distributed to women in Arar City. The survey collected sociodemographic data and assessed knowledge, practices, and barriers related to BSE and mammography. Statistical analyses were performed using IBM SPSS Statistics version 27.0.1, with significance set at p < 0.05.

The study included 385 females, with women aged 19-25 constituting nearly one-third of the population (n = 118; 30.6%). Most participants were married (n = 217; 56.4%) and held a bachelor's degree (n = 281; 73%). While 84.2% (n = 324) had heard of BSE and 80% (n = 308) demonstrated good knowledge, only 33.5% (n = 129) reported performing BSE. Regarding mammography, only 19.5% (n = 75) reported undergoing screening, despite 65.1% (n = 247) recognizing it as a safe procedure. Educational level (p = 0.018), prior knowledge of BSE (p = 0.009), and history of breast problems (p = 0.027) were significantly associated with higher knowledge scores.

While women demonstrated good awareness and knowledge of BSE, its practice remains low, with many unaware of proper techniques, timing, and frequency. Mammography awareness and utilization were also limited, emphasizing the need for targeted educational campaigns to promote early detection and improve screening behaviours.

Breast cancer is the second leading cause of cancer-related mortality among women worldwide, with its progression closely tied to the tumor microenvironment. To address the limitations and adverse effects of conventional therapies, algal polysaccharides and their nanoparticle derivatives have emerged as promising and effective anti-breast cancer agents. These bioactive compounds, derived from algae, are distinguished by their natural origin, non-toxicity, and significant medical relevance. Notably, algal polysaccharide-based nanoparticles exhibit advantageous properties such as hydrophilicity, biodegradability, prolonged circulation, and selective accumulation in tumor tissues. This review explores the relationship between the structural attributes of algal polysaccharides and their therapeutic efficacy. It further highlights the advantages of algal polysaccharide-based nanoparticles as drug delivery systems, particularly their potential in tumor targeting and overcoming multidrug resistance, thereby providing a theoretical foundation for their application in breast cancer treatment.

IntroductionBreast cancer is the most common cancer among women, and metabolic syndrome (MetS) is a risk factor for breast cancer, especially postmenopausal breast cancer. We evaluated the role of the advanced glycated end products (AGEs) levels contributing to the association between MetS and breast cancer risk.MethodsPlasma AGEs were measured in a case-control study nested within the Hormones and Diet in the Etiology of Breast Tumors (ORDET) cohort, including 40 incident postmenopausal breast cancer cases (20 with MetS and 20 without) and 40 postmenopausal controls (20 with MetS and 20 without). The association between AGEs and breast cancer was analyzed using Bayesian logistic regression models. An informative prior for the exposure coefficient, modeled as a normal distribution, centered on the natural logarithm of an odds ratio ((OR)=1.635) derived from prior evidence, was employed alongside weakly informative priors (WIPs). Bayesian linear regression with WIPs was used to examine the association between MetS and AGEs. Estimates were reported with SDs and 90% and 95% credible intervals (CI).ResultsAGEs were associated with higher breast cancer risk both with the informative prior (OR = 1.745, SD):0.362; 90% CI:1.218-2.390; 95% CI:1.137-2.548) and the WIP (OR = 1.861, SD = 0.661; 90% CI:1.026-3.082; 95% CI:0.924-3.528) specification. Although the difference in plasma AGEs in women with and without MetS was not significant, we found a suggestion of higher levels in women with MetS (mean difference in standardized AGEs between individuals with and without MetS = 0.155, SD = 0.245; 90% CI:-0.246 to 0.553; 95% CI:-0.322 to 0.625).ConclusionsThese data, although from a small sample of women, support a role of endogenous AGEs in the pathological pathways underlying the association between MetS and breast cancer development.

Among women worldwide, breast cancer is one of the most common cancers results from the growth of cancerous cells. This work investigates 87 patients using polarimetry in the visible spectral range (400-800 nm). Polarimetry is used for tissue characterization, particularly to prognosis cancer and biochemical quantification. Nine derived polarization properties were compared for both malignant and benign breast tissue. All nine polarimetric properties have high values for Grade III as compared to grade II and fibroadenoma. Benign tumours have higher anisotropy than malignant tumors. Ellipticity and orientation exhibit an inverse tendency. Hematology shows that moringa significantly improves the blood components of breast cancer. Pearson & Spearman correlation analysis was used with level of significance p < 0.05 where' p' is probability that the observed effect within the study would have occurred by chance. All parameters and components show significance level expect Leukocytes, Urea, Creatinine, SGOT and Bilirubin Total. Model training is a difficult procedure that determines the quality of application upon which it is deployed. Our data produces the accuracy 82.8%, with 1360 observations and 38 predictors. Thus a framework for breast cancer prognosis is provided by the combination of polarisation analysis, math and classification techniques.

Breast cancer is the most common type of cancer in women and the second leading cause of death by cancer. Despite recent advances, the mortality rate remains high, underlining the need to develop new therapeutic approaches. The complex interaction between cancer cells and the tumor microenvironment (TME) is crucial in determining tumor progression, therapy response, and patient prognosis. Understanding the role of immune cells in carcinogenesis and tumor progression can help improve targeted therapeutic options, increasing the likelihood of a favorable prognosis. Therefore, this review aims to critically analyze the complex interaction between tumor cells and immune cells, emphasizing the clinical and therapeutic implications. Additionally, we explore advances in immunotherapies, with a focus on immune checkpoint inhibitors.

Background/Objectives: The primary purpose of this study is to provide a more in-depth insight into various demographic, clinical, and lifestyle factors in relation to breast cancer and to predict the extent to which certain variables described as "predictors" might lead to further investigation. By analyzing a large cohort, we are able to provide valuable and up-to-date information on breast cancer screening, support breast specialists, and further enhance international screening guidelines. Methods: We screened for breast cancer in a population of women aged 50 to 69 years by using the standardized breast cancer imaging screening method (breast mammography) and ultrasonography as a complementary imagistic tool, and we compared the results with the gold standard, breast biopsy. For this, 58,760 women with no known history of breast cancer coming from 4 major regions of Romania (North-East, North-West, South-East, and West) were first evaluated through mammography. Out of these, 3197 women with positive mammograms subsequently underwent a breast ultrasound examination. The remaining 688 patients with positive breast ultrasound were further referred for a breast biopsy. Results: The statistical analysis revealed several predictors such as the body mass index (BMI), positive family medical history of breast cancer, age at first birth, and age at menopause that influenced the progression from mammography (first stage of the screening program) towards echography (additional imaging modality). Furthermore, we established that age, age at first birth, and BMI are significant predictors of progression from echography towards biopsy (the last stage of the screening program). Furthermore, by analyzing the number of positive biopsies (688) out of the total number of patients in the study (58,760), we calculated a total breast cancer detection rate of 8 per 1000 patients. Lastly, by studying the patient demographics in the context of breast cancer (BC) screening, we observed that participants coming from an urban environment presented a higher rate of positive mammographic results as compared to ones of rural provenience. Conclusions: Our study analyzed a large cohort of patients and offers real world data which shows that multiple factors were positively associated with an increased risk of BC. Older age, older age at first birth, and an older menopausal age are all estrogen-dependent risk factors that were linked with an increased breast cancer risk in our study. Furthermore, our findings concerning the rural/urban disparities and regional differences highlight the need for region-specific interventions to address lifestyle risk factors, improve healthcare access, and enhance breast cancer screening and follow-up protocols, particularly in underserved areas like the North-East and South-East regions.

Physical activity (PA) has been associated with remarkable benefits in breast cancer (BC) survivors. However, the physiological mechanisms that underlie these benefits are not well understood and the published results are inconsistent and weak. Some authors suggest that some biomarkers, particularly those related with inflammation, insulin resistance, or sexual hormones may account for some of these benefits. Most studies have used self-reported tools to assess PA.

To explore the association between objectively assessed PA and potentially related biomarkers.

A cross-sectional study was performed in a single hospital in Madrid, Spain. Candidates were BC survivors older than 18, who had finished their treatments. PA was assessed through accelerometers. Biomarkers related with insulin resistance (glucose, insulin, IGF-1, IGFBP-3), inflammation (C-reactive protein (CRP), neutrophil-lymphocyte ratio (NLR), interleukin (IL) 1, IL-6, IL-8, IL-10, TNF, sexual hormones (progesterone, testosterone, estrogens, androsterone), hypothalamic-pituitary axis (HPA) (cortisol), autonomic nervous system (ANS) (noradrenaline), and oxidative stress (8-hydroxy-2'-deoxyguanosine, 8-OHdG) were assessed.

Data of 91 women (mean age: 51.4 ± 8.1 years, mean BMI (kg/m2): 25.9 ± 4.5) were analyzed. Sedentary time (β (SE): - 0.001 (0.001), p-value 0.040) and vigorous PA time (β (SE): 0.010 (0.004), p-value 0.026) were significantly associated with NLR, but not with other biomarkers.

PA was not associated with biomarkers related to insulin resistance, sexual hormones, HPA, ANS, and oxidative stress. Neither was it associated with typical biomarkers of inflammation. An unexpected but consistent direct association with NLR was found. This relationship deserves further confirmation.

The aim of this study was to identify the women's experiences of intimate partner violence (IPV) after breast cancer.

This is a qualitative descriptive study. Semi-structured interviews were carried out with 11 women with breast cancer, all participants referred to the outpatient Oncology Clinic in IRAN. Data were analyzed using conventional content analysis approach.

The results revealed the essential category of "pervasive violence" which was manifested through six subcategories: 1) psychological violence, 2) physical violence, 3) sexual violence, 4) economic violence, 5) controlling behaviors, and 6) neglect.

Women with breast cancer are more vulnerable to IPV and experience a wide range of IPV forms. Healthcare providers should monitor women with breast cancer in terms of IPV to prevent the consequences of IPV on the cancer treatment process.

Carob, Ceratonia siliqua L. (CS), is a legume well-known for its edible pod pulp. Its seeds are used almost exclusively as a source of the food additive E410. Although a variety of metabolites have been identified by HPLC and LC-MS analysis in CS, reports concerned with their isolation are scarce. In this study, two flavonoid derivatives were isolated from the methanolic extract of CS seeds, namely, quercetin-3-O-rhamnoside and 4'-p-hydroxybenzoylisorhamnetin-3,7-di-O-rhamnoside. Network pharmacology was unusually used as a guide for estimation of the biological potential of the isolated compounds. Finally, the methanolic extract of CS seeds and its ethyl acetate fraction were standardized for their 4'-p-hydroxybenzoylisorhamnetin-3,7-di-O-rhamnoside content by HPLC. The identified isolates displayed the ability to interfere with the activity of several target proteins associated with renal and colon cancers. Their cytotoxic effect on renal and colorectal cancer cell lines was investigated in comparison to Doxorubicin. The selectivity of the isolated compounds was evaluated on normal human fetal fibroblast cell lines. The isolated 4'-p-hydroxybenzoylisorhamnetin-3,7-di-O-rhamnoside showed very potent cytotoxic activity against the tested cell lines with the highest selectivity. CS seeds can be used as a source of bioactive flavonoid derivatives that can be incorporated in pharmaceutical industries.

The incidence rate and mortality rate of breast cancer remain high, and there is an urgent need for safe and effective drugs. The excellent biological activity of hesperidin (HE) is a potential drug for the treatment of breast cancer. In this study, silk fibroin peptides (SFP) were used as delivery carriers and HE loaded SFP nanofibers (SFP/HE NFs) was prepared. The in vitro results showed that SFP/HE NFs significantly inhibited the proliferation and migration of breast cancer cell MDA-MB-231 compared with free HE. The mechanism results demonstrated that SFP/HE NFs induced apoptosis and DNA double stranded damage (DSBs) and further activated the cyclic monophosphate guanosine adenosine monophosphate synthase- stimulator of interferon gene (cGAS-STING) pathway. The in vivo studies showed that SFP/HE NFs treatment significantly inhibited the growth of breast cancer, with an inhibition rate of 65.9 % (100 mg/kg). In vivo mechanism studies also demonstrated that the anti-tumor activity of SFP/HE NFs was related to the activation of the cGAS-STING pathway. Interestingly, we found that the combination of SFP/HE NFs and cisplatin not only enhanced the anti-tumor activity of cisplatin, but also alleviated cisplatin induced nephrotoxicity. In conclusion, our results demonstrate the benefits of activating the cGAS-STING pathway in the treatment of breast cancer, which is expected to provide potential candidates for combined treatment of breast cancer.

Platycodin D2 (PD2) is a triterpenoid saponin extracted from the root of Platycodon grandiflorum , a common source of medicine and food. Platycodon grandiflorum saponins have anti-inflammatory, antioxidative, antitumor, and immunity-promoting effects. However, the effect of PD2 on breast cancer cells has not been reported. The purpose of this study is to explore the molecular mechanism underlying the effect of PD2 on breast cancer cells. We analyzed the inhibitory effects and pathways of PD2 on breast cancer by CCK-8 assay, WB assay, and immunofluorescence assay. Subsequently, autophagy and ferroptosis were analyzed using different inhibitors. It was found that PD2 caused mitochondrial damage and promoted mitochondrial reactive oxygen species (mtROS) production, leading to autophagy flux inhibition and ferroptosis. Blockage of autophagy flux and ferroptosis promoted each other, resulting in the inhibition of breast cancer cell proliferation. Similar results were obtained in the tumor-bearing model in vivo. PD2 promoted autophagy flux blockage and ferroptosis in breast cancer cells, which induced each other under the action of mtROS, thus inhibiting the proliferation of breast cancer cells. PD2 is a potential new strategy for the treatment of breast cancer.

Breast cancer is one of the most aggressive types of cancer, and its early diagnosis is crucial for reducing mortality rates and ensuring timely treatment. Computer-aided diagnosis systems provide automated mammography image processing, interpretation, and grading. However, since the currently existing methods suffer from such issues as overfitting, lack of adaptability, and dependence on massive annotated datasets, the present work introduces a hybrid approach to enhance breast cancer classification accuracy. The proposed Q-BGWO-SQSVM approach utilizes an improved quantum-inspired binary Grey Wolf Optimizer and combines it with SqueezeNet and Support Vector Machines to exhibit sophisticated performance. SqueezeNet's fire modules and complex bypass mechanisms extract distinct features from mammography images. Then, these features are optimized by the Q-BGWO for determining the best SVM parameters. Since the current CAD system is more reliable, accurate, and sensitive, its application is advantageous for healthcare. The proposed Q-BGWO-SQSVM was evaluated using diverse databases: MIAS, INbreast, DDSM, and CBIS-DDSM, analyzing its performance regarding accuracy, sensitivity, specificity, precision, F1 score, and MCC. Notably, on the CBIS-DDSM dataset, the Q-BGWO-SQSVM achieved remarkable results at 99% accuracy, 98% sensitivity, and 100% specificity in 15-fold cross-validation. Finally, it can be observed that the performance of the designed Q-BGWO-SQSVM model is excellent, and its potential realization in other datasets and imaging conditions is promising. The novel Q-BGWO-SQSVM model outperforms the state-of-the-art classification methods and offers accurate and reliable early breast cancer detection, which is essential for further healthcare development.

Purpose: Collagen type XI alpha 1 (COL11A1), a critical member of the collagen superfamily, is essential for tissue structure and integrity. This study aimed to validate previously identified variations in COL11A1 expression during breast cancer carcinogenesis and progression, as well as elucidate their clinical implications. Methods: COL11A1 mRNA expression levels were assessed using real-time reverse transcription-PCR (RT-PCR) in 30 pairs of normal breast tissue and primary breast cancer, 30 pairs of primary breast cancer and lymph node metastases, 30 benign tumors, and 107 primary breast cancers. COL11A1 protein expression was evaluated by Western blot in six matched trios of normal tissue, primary cancer, and lymph node metastasis. Results: COL11A1 mRNA levels were significantly higher in primary breast cancer tissues (n = 30) than in adjacent normal breast tissues (p < 0.001). Conversely, lymph node metastases (n = 30) showed significantly lower COL11A1 mRNA levels compared to their primary breast cancer counterparts (p=0.005). In a larger cohort, primary breast cancers (n = 107) had significantly elevated COL11A1 mRNA levels relative to adjacent normal tissues (n = 30) and benign tumors (n = 30) (p < 0.001). Benign tumors also demonstrated higher levels compared to normal tissues (p=0.012). The protein expression patterns were consistent with the mRNA findings. Receiver operating characteristic (ROC) curve analysis confirmed the diagnostic relevance of COL11A1 expression levels. Significant associations were found between COL11A1 mRNA levels and clinical parameters including lymph node involvement (p=0.046), clinical stage (p=0.004), and progesterone receptor status (p=0.048). Overexpression of COL11A1 was correlated with poor prognosis. Conclusions: COL11A1 expression varies during breast tumor initiation and progression, with elevated levels linked to worse prognoses. These findings underscore COL11A1's potential as a biomarker in breast cancer, suggesting its assessment could enhance diagnostic and prognostic strategies for more personalized patient management.

Cancer is one of the major causes of morbidity and mortality worldwide. Current treatments for both solid and hematological tumors are associated with severe adverse effects and drug resistance, necessitating the development of novel selective antineoplastic drugs.

The present study describes the antitumor activity of the imidazacridine derivative 5- acridin-9-ylmethylidene-2-thioxoimidazolidin-4-one (LPSF/AC05) in breast cancer, leukemia, and lymphoma cells. Cytotoxicity assays were performed in PBMC and in breast cancer, leukemia, and lymphoma cell lines using the MTT method. Changes in cell cycle progression and apoptosis were assessed using flow cytometry. Moreover, topoisomerase II inhibition assays were performed. LPSF/AC05 exhibited cytotoxicity in six of the nine cell lines tested.

The best results for leukemia and lymphoma were observed in the Toledo, Jurkat, and Raji cell lines (IC50 = 27.18, 31.04, and 33.36 µM, respectively). For breast cancer, the best results were observed in the triple-negative cell line MDA-MB-231 (IC50 = 27.54 μM). The compound showed good selectivity, with no toxicity to normal human cells (IC50 > 100µM; selectivity index > 3). Cell death was primarily induced by apoptosis in all cell lines. Furthermore, LPSF/AC05 treatment induced cell cycle arrest at the G0/G1 phase in leukemia/lymphoma and at the G2/M phase in breast cancer. Finally, topoisomerase II was inhibited.

These results indicate the potential application of LPSF/AC05 in cancer therapy.

Breast and ovarian cancers are significant global health challenges, with inherited variations in breast cancer gene 1 (BRCA1) and breast cancer gene 2 (BRCA2) substantially increasing the risk, aggressiveness, and early onset of these diseases. This work aimed to examine pathogenic variants (PVs) in BRCA1 and BRCA2 databases that include Mexican populations. A systematic review of literature and data mining spanning from 2002 to 2023 was conducted. Articles published in journals indexed in SCImago quartiles Q1 to Q4 were screened. Databases were paired, standardized, and enriched with data from reputable global platforms: Genome Data Viewer, dbSNP, ClinVar, gnomAD browser, Breast Cancer Information Core (BIC), ClinGen, Varsome, Human Genome Variation Society (HGVS), Bioproject, Ensembl, Gene NIH NCIB, UniProt, and BRCA Exchange. Outcomes included data from 9,026 Mexican genotypes, identifying 657 PVs. Genetic mapping revealed certain exons, notably exon 10 of BRCA1 and exon 11 of BRCA2, as highly mutagenic hot spots. The most frequent alteration was a large deletion in BRCA1 (ex9-12del), associated with a founder effect originating from a common Mexican ancestor. Finally, we constructed a genetic map containing all the single nucleotide variants (SNVs) and large rearrangements presented in the analyzed databases.

The incidence of triple-negative breast cancer (TNBC) in India is higher compared to Western populations. The objective of this study is to identify novel and less reported variants in TNBC in Mizoram, a state with a high cancer incidence in India.

We analysed whole exome sequencing data from triple-negative breast cancer (TNBC) patients in the Mizo population to identify key and novel variants. Moreover, we analysed reported breast cancer-related genes and pathway alterations.

Somatic mutation analysis revealed that TP53 was the most frequently mutated gene and TP53, CACNA1E, IGSF3, RYR1, and FAM155A as significantly mutated driver genes. Based on the ACMG guidelines, we identified a rare pathogenic germline variant of BRCA1 (p.C1697R) in 13% and a likely pathogenic frameshift insertion in RBMX (p.P106Ffs) in 73% of the patients. We also found that the ATM, STK11, and CDKN2A genes were significantly mutated in germline TNBC samples compared to healthy samples. Moreover, we identified novel somatic variants in CHEK2 (p.K182M) and NF1 (p.C245X), and novel germline variants RB1 (p.D111G), CDH1 (p.A10Gfs), CDKN2A (p.V96G), CDKN2A (p.S12Afs*22), MAP3K1 (CAAdelins0), MSH6 (p.L1226_L1230del), and PMS2 (TTCdelins0). Pathway analysis revealed that most somatic mutations were highly associated with PI3K-Akt signalling pathway and MAPK signalling pathways in TNBC.

These findings identified novel variants and key genes contributing to disease development and progression. Further analysis of less studied genes, including RBMX, MRC1, ATM, CTNNB1, and CDKN2A, in TNBC may reveal new potential genes for targeted therapeutic strategies and contribute to clinical advancements in the treatment of TNBC.

Although humans are frequently exposed to multiple pollutants simultaneously, research on their harmful effects on health has typically focused on studying each pollutant individually. Inorganic arsenic (As) and benzo[a]pyrene (BaP) are well-known pollutants with carcinogenic potential, but their co-exposure effects on breast cancer cell progression remain incompletely understood. This study aimed to assess the combined impact of BaP and As on the viability and migration of MDA-MB-231 cells. The results indicated that even at low levels, both inorganic As (0.01 μM, 0.1 μM, and 1 μM) and BaP (1 μM, 2.5 μM), individually or in combination, enhanced the viability and migration of the cells. However, the cell cycle analysis revealed no significant differences between the control group and the cells exposed to BaP and As. Specifically, exposure to BaP alone or in combination with As (As 0.01 μM + BaP 1 μM) for 24 h led to a significant increase in vimentin gene expression. Interestingly, short-term exposure to As not only did not induce EMT but also modulated the effects of BaP on vimentin gene expression. However, there were no observable changes in the expression of E-cadherin mRNA. Consequently, additional research is required to evaluate the prolonged effects of co-exposure to As and BaP on the initiation of EMT and the progression of breast cancer.

Breast cancer is the most common malignancy among women worldwide, characterized by complex molecular and cellular heterogeneity. Despite advances in diagnosis and treatment, there is an urgent need to identify reliable biomarkers and therapeutic targets to improve early detection and personalized therapy. The OAS (2'-5'-oligoadenylate synthetase) family genes, known for their roles in antiviral immunity, have emerged as potential regulators in cancer biology. This study aimed to explore the diagnostic and functional relevance of OAS family genes in breast cancer.

Breast cancer cell lines and controls were cultured under specific conditions, and DNA and RNA were extracted for downstream analyses. RT-qPCR, bisulfite sequencing, and Western blotting were employed to assess gene expression, promoter methylation, and knockdown efficiency of OAS family genes. Functional assays, including CCK-8, colony formation, and wound healing, evaluated cellular behaviors, while bioinformatics tools (UALCAN, GEPIA, HPA, OncoDB, cBioPortal, and others) validated findings and explored correlations with clinical data.

The OAS family genes (OAS1, OAS2, OAS3, and OASL) were found to be significantly upregulated in breast cancer cell lines and tissues compared to normal controls. This overexpression was strongly associated with reduced promoter methylation. Receiver operating characteristic (ROC) analysis demonstrated high diagnostic accuracy, with area under the curve (AUC) values exceeding 0.93 for all four genes. Increased OAS expression correlated with advanced cancer stages and poor overall survival in breast cancer patients. Functional analysis revealed their involvement in critical biological processes, including immune modulation and oncogenic pathways. Silencing OAS genes in breast cancer cells significantly inhibited cell proliferation and colony formation, while unexpectedly enhancing migratory capacity. Additionally, correlations with immune cell infiltration, molecular subtypes, and drug sensitivity highlighted their potential roles in the tumor microenvironment and therapeutic response.

The findings of this study established OAS family genes as potential biomarkers and key players in breast cancer progression, offering promise as diagnostic biomarkers and therapeutic targets to address unmet clinical needs.

Fibulin-2 (FBLN2) is a secreted extracellular matrix (ECM) glycoprotein and has been identified in the mouse mammary gland, in cap cells of terminal end buds (TEBs) during puberty, and around myoepithelial cells during early pregnancy. It is required for basement membrane (BM) integrity in mammary epithelium, and its loss has been associated with human breast cancer invasion. Herein, we attempted to confirm the relevance of FBLN2 to myoepithelial phenotype in mammary epithelium and to assess its expression in molecular subtypes of human breast cancer.

The relationship between FBLN2 expression and epithelial markers was investigated in pubertal mouse mammary glands and the EpH4 mouse mammary epithelial cell line using immunohistochemistry, immunocytochemistry, and immunoblotting. Human breast cancer mRNA data from the METABRIC and TCGA datasets from Bioportal were analyzed to assess the association of Fbln2 expression with epithelial markers, and with molecular subtypes. Survival curves were generated using data from the METABRIC dataset and the KM databases.

FBLN2 knockdown in mouse mammary epithelial cells was associated with a reduction in KRT14 and an increase in KRT18. Further, TGFβ3 treatment resulted in the upregulation of FBLN2 in vitro. Meta-analyses of human breast cancer datasets from Bioportal showed a higher expression of Fbln2 mRNA in claudin-low, LumA, and normal-like breast cancers compared to LumB, Her2 +, and Basal-like subgroups. Fbln2 mRNA levels were positively associated with mesenchymal markers, myoepithelial markers, and markers of epithelial-mesenchymal transition. Higher expression of Fbln2 mRNA was associated with better prognosis in less advanced breast cancer and this pattern was reversed in more advanced lesions.

With further validation, these observations may offer a molecular prognostic tool for human breast cancer for more personalized therapeutic approaches.

Breast cancer development and progression are driven by intricate networks involving receptor tyrosine kinases (RTKs) and steroid hormone receptors specifically estrogen receptor (ER) and progesterone receptor (PR). This review examined roles of each receptor under normal physiology and in breast cancer, and explored their multifaceted interactions via signaling pathways, focusing on their contributions to breast cancer progression. Since defining the mechanism by which these two-receptor mediated signaling pathways cooperate is essential for understanding breast cancer progression, we discussed the mechanisms of cross-talk between RTKs and ER and PR and their potential therapeutic implications as well. The crosstalk between RTKs and steroid hormone receptors (ER and PR) in breast cancer can influence the disease's progression and treatment outcomes. Therefore, understanding the functions of the aforementioned receptors and their interactions is crucial for developing effective therapies.

Breast cancer (BC) is the most prevalent cancer among women worldwide and poses significant treatment challenges. Traditional therapies often lead to adverse side effects and resistance, necessitating innovative approaches for effective management.

This review aims to explore the potential of copper nanoparticles (CuNPs) in enhancing breast cancer therapy through targeted drug delivery, improved imaging, and their antiangiogenic properties.

The review synthesizes existing literature on the efficacy of CuNPs in breast cancer treatment, addressing common challenges in nanotechnology, such as nanoparticle toxicity, scalability, and regulatory hurdles. It proposes a novel hybrid method that combines CuNPs with existing therapeutic modalities to optimize treatment outcomes.

CuNPs demonstrate the ability to selectively target cancer cells while sparing healthy tissues, leading to improved therapeutic efficacy. Their unique physicochemical properties facilitate efficient biodistribution and enhanced imaging capabilities. Additionally, CuNPs exhibit antiangiogenic activity, which can inhibit tumor growth by preventing the formation of new blood vessels.

The findings suggest that CuNPs represent a promising avenue for advancing breast cancer treatment. By addressing the limitations of current therapies and proposing innovative solutions, this review contributes valuable insights into the future of nanotechnology in oncology.

Transportation noise has been linked with breast cancer, but existing literature is conflicting. One proposed mechanism is that transportation noise disrupts sleep and the circadian rhythm. We investigated the relationships between road traffic noise, DNA methylation in circadian rhythm genes, and breast cancer. We selected 610 female participants (318 breast cancer cases and 292 controls) enrolled into the Malmö, Diet, and Cancer cohort. DNA methylation of CpGs (N = 29) in regulatory regions of circadian rhythm genes (CRY1, BMAL1, CLOCK, and PER1) was assessed by pyrosequencing of DNA from lymphocytes collected at enrollment. To assess associations between modeled 5-year mean residential road traffic noise and differentially methylated CpG positions, we used linear regression models adjusting for potential confounders, including sociodemographics, shiftwork, and air pollution. Linear mixed effects models were used to evaluate road traffic noise and differentially methylated regions. Unconditional logistic regression was used to investigate CpG methylation and breast cancer.

We found that higher mean road traffic noise was associated with lower DNA methylation of three CRY1 CpGs (CpG1, CpG2, and CpG12) and three BMAL1 CpGs (CpG2, CpG6, and CpG7). Road traffic noise was also associated with differential methylation of CRY1 and BMAL1 promoters. In CRY1 CpG2 and CpG5 and in CLOCK CpG1, increasing levels of methylation tended to be associated with lower odds of breast cancer, with odds ratios (OR) of 0.88 (95% confidence interval (CI) 0.76-1.02), 0.84 (95% CI 0.74-0.96), and 0.80 (95% CI 0.68-0.94), respectively.

In summary, our data suggest that DNA hypomethylation in CRY1 and BMAL1 could be part of a causal chain from road traffic noise to breast cancer. This is consistent with the hypothesis that disruption of the circadian rhythm, e.g., from road traffic noise exposure, increases the risk of breast cancer. Since no prior studies have explored this association, it is essential to replicate our results.

Gestational diabetes mellitus (GDM) is a common pregnancy complication characterized by insulin resistance. A link has been suggested between insulin resistance and breast cancer, which is the most common cancer in women. Hence, women with previous GDM may be at increased risk of developing breast cancer, yet, the existing evidence is conflicting. This study explored the association between GDM and incident breast cancer, including age at cancer diagnosis. Additionally, we investigated the potential impact of severity of insulin resistance during pregnancy and of subsequent diabetes development on the breast cancer risk.

We conducted a nationwide, register-based cohort study including all women giving birth in Denmark from 1997 to 2018. We defined GDM and breast cancer based on ICD-10 codes. Premenopausal and postmenopausal breast cancer was pragmatically defined as age at outcome < 50 years and ≥ 50 years, respectively. A proxy for severity of insulin resistance during pregnancy was based on insulin treatment; subsequent diabetes was defined as presence of ICD-10 codes and/or antidiabetic medication after pregnancy. The statistical analyses included Cox regression, logistic regression and t-test.

Of 708,121 women, 3.4% had GDM. The median follow-up period was 11.9 years (range 0-21.9). The overall breast cancer risk was comparable in women with and without previous GDM (adjusted hazard ratio 0.96 [95% CI 0.83-1.12]). Premenopausal and postmenopausal breast cancer risk also did not differ; however, women with previous GDM had a breast cancer diagnosis at younger age (42.6 vs. 43.5 years, p-value 0.01). All-cause mortality was similar regardless of GDM history. Severity of insulin resistance during pregnancy and subsequent diabetes did not affect breast cancer risk.

This large, population-based cohort study showed no higher risk of incident breast cancer in women with previous GDM compared to women without previous GDM after a median of almost 12 years of follow-up. This was evident irrespective of menopausal state. The breast cancer risk was not influenced by the severity of insulin resistance during pregnancy and by subsequent diabetes development. Regardless of GDM history, attention towards prevention, early detection and treatment of breast cancer should be prioritized.

The adult mammary gland is maintained by lineage-restricted progenitor cells through pregnancy, lactation, involution, and menopause. Injury resolution, transplantation-associated mammary gland reconstitution, and tumorigenesis are unique exceptions, wherein mammary basal cells gain the ability to reprogram to a luminal state. Here, we leverage newly developed cell-identity reporter mouse strains, and time-resolved single-cell epigenetic and transcriptomic analyses to decipher the molecular programs underlying basal-to-luminal fate switching in vivo. We demonstrate that basal cells rapidly reprogram toward plastic cycling intermediates that appear to hijack molecular programs we find in bipotent fetal mammary stem cells and puberty-associatiated cap cells. Loss of basal-cell specifiers early in dedifferentiation coincides with activation of Notch and BMP, among others. Pharmacologic blockade of each pathway disrupts basal-to-luminal transdifferentiation. Our studies provide a comprehensive map and resource for understanding the coordinated molecular changes enabling terminally differentiated epithelial cells to transition between cell lineages and highlights the stunning rapidity by which epigenetic reprogramming can occur in response to disruption of tissue structure.

Research on breast cancer risk factors and mortality is gaining recognition and attention globally; there is need to add more information on its determinants among patients admitted in hospital. Some studies on risk factors and mortality of breast cancer in Nigeria hospitals conducted in the urban and suburban areas have been documented. Therefore, an addition of a study conducted in the setting of a rural health institution is necessary. This study assessed the risk factors and determinants of mortality among patients admitted for breast cancer in rural Southwestern Nigeria.

A retrospective observational study was conducted on 260 patients who were admitted for breast cancer between January 2010 and December 2023 using a data form and a standardized information form. The data were analyzed using SPSS version 22.0. The risk factors and the determinants of mortality of patients with breast cancer were identified using multivariate regression model.

The breast cancer risk factors were old age, family history, tobacco smoking, combined oral contraceptives, and hormonal therapy use. The case fatality rate was 38.1%, and its determinants of mortality were patients who were older (adjusted odds ratio [AOR], 1.956; 95% confidence interval [CI]:1.341-4.333), obese (AOR, 2.635; 95% CI: 1.485-6.778), stage IV (AOR, 1.895; 95% CI: 1.146-8.9742), mastectomy (AOR, 2.512; 95% CI: 1.003-6.569), discontinued adjuvant chemotherapy (AOR, 1.785; 95% CI: 1.092-4.6311), and yet to commence adjuvant chemotherapy (AOR, 2.568; 95% CI: 1.367-5.002).

The study revealed that patients with breast cancer were associated with high mortality. Sustained health education to promote early diagnosis, managed co-morbidities, and access to treatment may contribute to reduction in breast cancer mortality in rural Nigeria.