Breast Cancer Prevention Research Articles

Assessing the causal relationships between circulating metabolic biomarkers and breast cancer by using mendelian randomization

ObjectivePrevious studies have established a causal relationship between metabolites and breast cancer (BC), but the underlying mechanisms remain unclear. Thus, we aimed to investigate the genetic relationship between metabolites and BC, including its subtypes, using Mendelian randomization (MR) analysis.MethodsUtilizing the latest and most comprehensive summary statistics from genome-wide association studies we conducted an Mendelian randomization study. Data on 233 metabolites, used as exposure variables, were obtained from a study involving 136,016 participants. BC data, used as outcome variables, were sourced from a study comprising 122,977 cases and 105,974 controls. We used the inverse-variance weighted method as the primary approach, along with three supplementary methods, to assess the causal relationship. We also used Cochran’s Q test to detect heterogeneity and MR-Egger regression to examine the presence of horizontal pleiotropy.ResultsUpon analyzing 233 metabolites across 11 classes in relation to BC, we found six classes of metabolites (fatty acids glycerides and phospholipids, lipoprotein subclasses, lipids, apolipoproteins, and lipoprotein particle size) associated with overall BC. Five classes of metabolites (fatty acids glycerides and phospholipids, lipoprotein subclasses, lipids, and lipoprotein particle size) were related to estrogen receptor (ER) + BC, and eight classes of metabolites (fatty acids, amino acids, glycerides and phospholipids, lipoprotein subclasses, lipids, apolipoproteins, glycolysis-related metabolites, and lipoprotein particle size) were linked to ER- BC.ConclusionOur study demonstrates a genetic causal relationship between most metabolites and BC, confirming the link between these factors. This research provides a significant foundation for the prevention and treatment of BC.

Swedish Genome-Wide Haplotype Association Analysis Suggests Breast Cancer Loci with Varying Risk-Modifying Effects

Background: To find support for risk-modifying genes in breast cancer, a haplotype GWAS in sporadic breast cancer cases was undertaken. The results were compared with the results from previous analyses in familial cases and all cases from the same Swedish cohort. Methods: In total, 2550 women with sporadic invasive breast cancer and 5021 healthy controls were included in a sliding-window haplotype GWAS using PLINK 1.07. Results: The analysis of sporadic cases confirmed the loci on chromosomes 10q26.13, 11q13.3, and 16q12.1 and suggested one novel locus on chromosome 12p11.21 (OR = 1.42 p = 4.55 × 10−8). A comparison between these loci and the same loci in the analyses of familial cases and all breast cancer cases was undertaken. Conclusions: Haplotype GWAS in sporadic cases of Swedish breast cancer cases supported known risk loci and suggested another risk locus. The loci identified in the analysis of sporadic and all breast cancer cases were suggested to act as modifiers of the risk of breast cancer. Haplotype analysis identified other loci with higher odds ratios than single-variant analysis. Further studies are needed to find out how to best include the findings in breast cancer prevention.

Causality between gut microbiota, immune cells, and breast cancer: Mendelian randomization analysis.

The association between gut microbiota (GM) and breast cancer (BC) has been studied. Nevertheless, the causal relationship between them and the potential mediating factors have not been clearly defined. Therefore, in this study, Mendelian randomization analysis (MR) was employed to explore the causal relationship between 473 GM and BC, as well as the mediating effect of potential immune cells. In this investigation, we availed ourselves of the publicly accessible summary statistics from the genome-wide association study to undertake two-sample and reverse Mendelian randomization analyses on GM and BC, with the intention of clarifying the causal association between GM and BC. Subsequently, through the application of the two-step Mendelian randomization analysis, it was revealed that the relationship between GM and BC was mediated by immune cells. The stability of the research outcomes was verified via sensitivity analysis. Mendelian randomization analysis elucidated the protective impacts of 8 genera on BC (such as Phylum Actinobacteriota, Species Bacteroides A plebeius A, Species Bifidobacterium adolescentis, Species CAG-841 sp002479075, Family Fibrobacteraceae, Order Fibrobacterales, Class Fibrobacteria, and Species Phascolarctobacterium sp003150755). Additionally, there are 23 immune cell traits related to BC. Our research findings showed that the species Megamonas funiformis was associated with an increased risk of BC, and 11.20% of this effect was mediated by CD38 on IgD+ CD24-. Likewise, HLA DR on CD33br HLA DR+ CD14- mediated the causal relationship between Species Prevotellamassilia and BC, having a mediating ratio of 7.89%. This study clarifies a potential causal relationship between GM, immune cells, and BC and provides genetic evidence for this causal connection. It offers research directions for the subsequent prevention and treatment of BC through the interaction between GM and immune cells, and provides a reference for future mechanistic and clinical studies in this field.

DNA-methylation age and accelerated epigenetic aging in blood as a tumor marker for predicting breast cancer susceptibility.

DNA methylation (DNAm)-based marker of aging, referred to as 'epigenetic age' or 'DNAm age' is a highly accurate multi-tissue biomarker for aging, associated with age-related disease risk, including cancer. Breast cancer (BC), an age-associated disease, is associated with older DNAm age and epigenetic age acceleration (age accel) at tissue levels. But this raises a question on the predictability of DNAm age/age accel in BC development, emphasizing the importance of studying DNAm age in pre-diagnostic peripheral blood (PB) in BC etiology and prevention. We included postmenopausal women from the largest study cohort and prospectively investigated BC development with their pre-diagnostic DNAm in PB leukocytes (PBLs). We estimated Horvath's pan-tissue DNAm age and investigated whether DNAm age/age accel highly correlates with risk for developing subtype-specific BC and to what degree the risk is modified by hormones and lifestyle factors. DNAm age in PBLs was tightly correlated with age in this age range, and older DNAm age and epigenetic age accel were significantly associated with risk for developing overall BC and luminal subtypes. Of note, in women with bilateral oophorectomy before natural menopause experiencing shorter lifetime estrogen exposure than those with natural menopause, epigenetic age accel substantially influenced BC development, independent of obesity status and exogeneous estrogen use. Our findings contribute to better understanding of biologic aging processes that mediate BC carcinogenesis, detecting a non-invasive epigenetic aging marker that better reflects BC development, and ultimately identifying the elderly with high risk who can benefit from epigenetically targeted preventive interventions.

Selecting the Right Dose to Move Breast Cancer Prevention Forward.

The uptake and adherence of preventive therapy of breast cancer in clinical practice are low because of fear of serious adverse events and menopausal symptoms. Low-dose tamoxifen has been shown to retain efficacy while reducing toxicity in high-risk women. In this issue of the journal, Cornell and colleagues evaluated uptake, adherence, and tolerability of low-dose tamoxifen in high-risk women. More than 70% of patients reported that they took low-dose tamoxifen after counseling and were still taking the medication at 1 year. This paradigm shift may move the field of breast cancer prevention forward and reduce breast cancer incidence and mortality. See related article by Cornell et al., p. 565.

Relationship Between Perceived COVID-19 Risk and Change in Perceived Breast Cancer Risk: Prospective Observational Study.

Whether COVID-19 is associated with a change in risk perception about other health conditions is unknown. Because COVID-19 occurred during a breast cancer study, we evaluated the effect of COVID-19 risk perception on women's breast cancer risk perception. This study aims to evaluate the relationship between perceived risk of COVID-19 and change in perceived breast cancer risk. We hypothesized that women who perceived greater COVID-19 risk would evidence increased perceived breast cancer risk and this risk would relate to increased anxiety and missed cancer screening. Women aged 40-74 years with no breast cancer history were enrolled in a US breast cancer prevention trial in outpatient settings. They had provided breast cancer risk perception and general anxiety before COVID-19. We performed a prospective observational study of the relationship between the perceived risk of COVID-19 and the change in perceived breast cancer risk compared to before the pandemic. Each woman was surveyed up to 4 times about COVID-19 and breast cancer risk perception, general anxiety, and missed medical care early in COVID-19 (May to December 2020). Among 13,002 women who completed a survey, compared to before COVID-19, anxiety was higher during COVID-19 (mean T score 53.5 vs 49.7 before COVID-19; difference 3.8, 95% CI 3.6-4.0; P<.001) and directly related to perceived COVID-19 risk. In survey wave 1, anxiety increased by 2.3 T score points for women with very low perceived COVID-19 risk and 5.2 points for those with moderately or very high perceived COVID-19 risk. Despite no overall difference in breast cancer risk perception (mean 32.5% vs 32.5% before COVID-19; difference 0.24, 95% CI -0.47 to 0.52; P=.93), there was a direct relationship between change in perceived breast cancer risk with COVID-19 risk perception, ranging in survey wave 4 from a 2.4% decrease in breast cancer risk perception for those with very low COVID-19 risk perception to a 3.4% increase for women with moderately to very high COVID-19 risk perception. This was not explained by the change in anxiety or missed cancer screening. After adjustment for age, race, education, and survey wave, compared to women with very low perceived COVID-19 risk, perceived breast cancer risk increased by 1.54% (95% CI 0.75%-2.33%; P<.001), 4.28% (95% CI 3.30%-5.25%; P<.001), and 3.67% (95% CI 1.94%-5.40%; P<.001) for women with moderately low, neither high nor low, and moderately or very high perceived COVID-19 risk, respectively. Low perceived COVID-19 risk was associated with reduced perceived breast cancer risk, and higher levels of perceived COVID-19 risk were associated with increased perceived breast cancer risk. This natural experiment suggests that a threat such as COVID-19 may have implications beyond the pandemic. Preventive health behaviors related to perceived risk may need attention as COVID-19 becomes endemic.

Improving communication to increase uptake of high-risk breast cancer prevention appointments: Building a better letter

ObjectiveMailed letters to women identified as being at high-risk for developing breast cancer were not having the desired effect for encouraging appointments with prevention-focused providers at a large Midwest healthcare system. A partnership with communication scholars sought to revise the letter to increase awareness, intentions, and appointments. MethodsGuided by the Extended Parallel Process Model, survey responses were collected from letter recipients over the course of two years, both pre and post letter revision. Appointments attributed to letters were also tracked. ResultsRecipients of the revised letter had increased knowledge regarding the length of prevention appointments and indicated greater self-efficacy and intentions to make and attend appointments compared to those who received the non-revised letter. A greater percentage who received the revised letter also made appointments. ConclusionPartnering with communication scholars helped with improving a letter mailed to thousands of patients each year. Finding ways to increase response-efficacy of breast cancer prevention activities within communications may assist in increasing appointments. InnovationCross-disciplinary partnerships across the medical and social sciences – while not quick or simple - are essential for finding ways to improve patient wellbeing and hopefully reducing the prevalence of preventable diseases in the future.

Unveiling Inequities: Racial Disparities in Risk-Reducing Mastectomy for Breast Cancer Prevention

Unveiling Inequities: Racial Disparities in Risk-Reducing Mastectomy for Breast Cancer Prevention

Reprogramming SREBP1-dependent lipogenesis and inflammation in high-risk breast with licochalcone A: a novel path to cancer prevention.

Anti-estrogens have had limited impact on breast cancer (BC) prevention. Novel agents with better tolerability, and efficacy beyond estrogen receptor (ER) positive BC are needed. We studied licochalcone A (LicA) for ER-agnostic BC prevention. We evaluated antiproliferative effects of LicA in seven breast cell lines and its suppression of ER+ and ER- xenograft tumors in mice. High-risk human breast tissue was treated with LicA ex vivo , followed by RNA sequencing and metabolism flux modeling. Confirmatory testing was performed in an independent specimen set and ER+/- BC cell lines using NanoString metabolic panel, proteomics, western blots, and spatiotemporally resolved cholesterol quantification in single cells. LicA suppressed proliferation in vitro and xenograft tumor growth in vivo . It downregulated pivotal steps in PI3K-AKT-SREBP1-dependent lipogenesis, suppressed PI3K and AKT phosphorylation, SREBP1 protein expression, and cholesterol levels in the plasma membrane inner leaflet, to the levels in normal breast cells. LicA also suppressed prostaglandin E2 synthesis and PRPS1-catalyzed de novo nucleotide biosynthesis, stalling proliferation; further evident by reduced MKI67 and BCL2 proteins. LicA targets SREBP1, a central regulator of lipogenesis and immune response, reducing pro-tumorigenic aberrations in lipid homeostasis and inflammation. It is a promising non-endocrine candidate for BC prevention.

Variation in human gut microbiota impacts tamoxifen pharmacokinetics.

Tamoxifen is the most prescribed drug used to prevent breast cancer recurrence, but patients show variable responses to tamoxifen. Such differential inter-individual response has a significant socioeconomic impact as one in eight women will develop breast cancer and nearly half a million people in the United States are treated with tamoxifen annually. Tamoxifen is orally delivered and must be activated by metabolizing enzymes in the liver; however, clinical studies show that neither genotype nor hepatic metabolic enzymes are sufficient to predict why some patients have sub-therapeutic levels of the drug. Here, using gnotobiotic- and antibiotics-treated mice, we show that tamoxifen pharmacokinetics are heavily influenced by gut bacteria and prolonged exposure to tamoxifen. Interestingly, 16S rRNA gene sequencing shows tamoxifen does not affect overall microbiota composition and abundance. Metabolomics, however, reveals differential metabolic profiles across the microbiomes of different donors cultured with tamoxifen, suggesting an enzymatic diversity within the gut microbiome that influences response to tamoxifen. Consistent with this notion, we found that β-glucuronidase (GUS) enzymes vary in their hydrolysis activity of glucuronidated tamoxifen metabolites across the gut microbiomes of people. Together, these findings highlight the importance of the gut microbiome in tamoxifen's pharmacokinetics.IMPORTANCEOne in eight women will develop breast cancer in their lifetime, and tamoxifen is used to suppress breast cancer recurrence, but nearly 50% of patients are not effectively treated with this drug. Given that tamoxifen is orally administered and, thus, reaches the intestine, this variable patient response to the drug is likely related to the gut microbiota composed of trillions of bacteria, which are remarkably different among individuals. This study aims to understand the impact of the gut microbiome on tamoxifen absorption, metabolism, and recycling. The significance of our research is in defining the role that gut microbes play in tamoxifen pharmacokinetics, thus paving the way for more tailored and effective therapeutic interventions in the prevention of breast cancer recurrence.

Inequality in breast cancer: Global statistics from 2022 to 2050

This study evaluates the global inequalities of breast cancer incidence and mortality from 2022 to 2050 with the latest GLOBOCAN estimates. It focuses on disparities across continents, age groups and Human Development Index (HDI) levels. In 2022, Africa shows the highest positive slope values of age-standardized rates (world) of mortality vs. incidence, both for those under 40 (0.346) and those 40 and older (0.335). These values contrast with those for Asia (0.085, 0.208), Europe (0.002, −0.014), Latin America and the Caribbean (0.17, 0.303), Northern America (−0.078, −0.188), and Oceania (0.166, −0.001). In both age groups, lower HDI levels are correlated with higher slope values and vice versa. Projections to 2050 indicate significant increases in the burden of breast cancer, with persistent yet varied disparities and differences. This highlights the need for differentiated strategies in breast cancer prevention, early-stage diagnosis, and treatment.

Treatment and Prevention Strategies of Breast Cancer

Abstract. With the increasing trend of late childbearing and low childbearing, the incidence of breast cancer is increasing rapidly worldwide. At present, breast cancer has become one of the more frequent malignant tumor diseases in women and has aroused widespread concern in society. The cause of the disease is not completely clear, with the deepening of research, the relevant detection methods are constantly updated, as far as possible early diagnosis. At present, the main methods of breast cancer prevention are lifestyle adjustment, including reducing alcohol intake, maintaining a healthy weight and chemical prevention, but the methods are limited, so the research on breast cancer prevention is particularly important. At the same time, medical workers should educate the majority of women about disease prevention, so that women can establish a correct concept of prevention and treatment, so as in order to lower the prevalence of breast cancer and improve the women health.

Chemoprevention strategies in hereditary breast and ovarian cancer syndromes.

Hereditary breast and/or ovarian cancer syndromes are inherited disorders in which there is an increased risk of developing breast and/or ovarian cancer in the lifetime, usually at a younger age compared to the general population. Cancer prevention in these syndromes includes prophylactic surgeries, personalized surveillance programs and chemopreventive strategies. Chemoprevention exploits the use of certain drugs or other substances to help lower the risk of developing cancer. In this context, tamoxifen was the first agent considered for breast cancer prevention, followed by raloxifene and the third-generation aromatase inhibitors. On the other hand, the first and most widespread type of chemoprevention for ovarian cancer was combined hormonal contraceptive use. Although several strategies have been studied and showed promising results, only a few of these are currently applied in daily clinical practice. Side effects along with several psychological variables such as cancer perceived risk, worries and related distress, strongly influence women's decision on chemoprevention. The present review explores and summarizes the available evidence on breast and ovarian cancer chemoprevention approaches.

Self-screening practice of breast cancer and associated factors among female students in Ethiopian universities using the theory of planned behavior: a cross sectional study

BackgroundBreast cancer is the most common cancer among females. Assessing self-screening practices for breast cancer patients is vital for developing targeted interventions. The current study aimed to assess self-screening practices for breast cancer and associated factors via the theory of planned behavior constructs among female students in Ethiopian universities.MethodsA cross-sectional study design was conducted using the theory of planned behavior constructs. The data were collected from January 30, 2022, to February 30, 2022, in Ethiopia. A structured, self-administered questionnaire was used. The validity and reliability tests were checked to use the questionnaire in the main study through a pilot test. The data were collected through online Google Forms by distributing them to university students via Telegram groups, Imo, emails, and Facebook. The collected data were exported to SPSS version 26 for analysis. Bivariate analysis was used to identify the candidate variables for multiple logistic regression (P value < 0.02). Those variables with a P value less than 0.05 were considered significant predictors of breast cancer screening practices.ResultsA total of 418 female students participated in the study. The respondents were aged between 18 and 37 years. In the current study, 318 (76.1%; 95% CI: 72.0, 80.4) university students had good screening practices for breast cancer. Nonhealth-related departments (AOR = 1.95; 95% CI: 1.11, 3.44), having training in breast cancer self-examination (AOR = 1.87; 95% CI: 1.04, 3.35), having a good attitude (AOR = 1.96; 95% CI: 1.11, 3.47), having good behavioral control (AOR = 4.1; 95% CI: 2.18, 7.71), and having good behavioral intentions (AOR = 1.88; 95% CI: 1.09, 3.24) were associated with self-screening practices for breast cancer patients.ConclusionDesigning a theory of planned behavior-based educational interventions improve self-screening practices for breast cancer among university female students. These insights could guide the development of future breast cancer awareness and prevention programs in university settings, with the goal of increasing early detection rates and lowering the risk of breast cancer. The study also serves as foundational information for designing future research using more advanced study design methods.

Can resistance exercise prevent breast cancer–related lymphoedema? A systematic review and metanalysis protocol

IntroductionEvidence shows that resistance training (RT) reduces lymphoedema in patients with breast cancer–related lymphoedema (BRCL), making it a safe and efficient intervention. However, it is uncertain if RT is safe...

Unleashing the potential of Genistein and its derivatives as effective therapeutic agents for breast cancer treatment.

Breast cancer remains one of the leading causes of cancer-related deaths among women worldwide. Genistein (Gen), a phytoestrogen soy isoflavone, has emerged as a promising agent in the prevention and treatment of breast cancer due to its ability to function as a natural selective estrogen receptor modulator (SERM). This review explores the multifaceted mechanisms through which Gen and its derivatives exert their anticancer effects, including modulation of the PI3K/Akt signaling pathway, regulation of apoptosis, inhibition of angiogenesis, and impacts on DNA methylation and enzyme functions. We discuss the dual roles of Gen in both enhancing and inhibiting estrogen receptor (ER)-dependent pathways., highlighting its complex interactions with ERα and ERβ. Furthermore, the review examines the synergistic effect of combining Gen with conventional chemotherapeutic agents such as doxorubicin, cisplatin, and selenium, as well as other natural compounds like lycopene. Clinical studies suggest that while isoflavones may not significantly influence breast cancer progression in general, the high consumption of soy isoflavones is associated with reduced recurrence rates in breast cancer survivors. Importantly, Gen's ability to modulate key signaling pathways and enhance the efficacy of existing treatments improves its potential as a valuable adjunct in breast cancer therapy. In conclusion, Gen and its derivatives offer a novel and promising approach for treatment of breast cancer. Continued research into their mechanisms of action and clinical applications will be essential in optimizing their therapeutic potential and translating these findings into effective clinical interventions.

Biomaterials' enhancement of immunotherapy for breast cancer by targeting functional cells in the tumor micro-environment.

Immunotherapy for breast cancer is now being considered clinically, and more recently, the number of investigations aimed specifically at nano-biomaterials-assisted immunotherapy for breast cancer treatment is growing. Alterations of the breast cancer micro-environment can play a critical role in anti-tumor immunity and cancer development, progression and metastasis. The improvement and rearrangement of tumor micro-environment (TME) may enhance the permeability of anti-tumor drugs. Therefore, targeting the TME is also an ideal and promising option during the selection of effective nano-biomaterial-based immuno-therapeutic strategies excepted for targeting intrinsic resistant mechanisms of the breast tumor. Although nano-biomaterials designed to specifically release loaded anti-tumor drugs in response to tumor hypoxia and low pH conditions have shown promises and the diversity of the TME components also supports a broad targeting potential for anti-tumor drug designs, yet the applications of nano-biomaterials for targeting immunosuppressive cells/immune cells in the TME for improving the breast cancer treating outcomes, have scarcely been addressed in a scientific review. This review provides a thorough discussion for the application of the different forms of nano-biomaterials, as carrier vehicles for breast cancer immunotherapy, targeting specific types of immune cells in the breast tumor microenvironment. In parallel, the paper provides a critical analysis of current advances/challenges with leading nano-biomaterial-mediated breast cancer immunotherapeutic strategies. The current review is timely and important to the cancer research field and will provide a critical tool for nano-biomaterial design and research groups pushing the clinical translation of new nano-biomaterial-based immuno-strategies targeting breast cancer TME, to further open new avenues for the understanding, prevention, diagnosis and treatment of breast cancer, as well as other cancer types.

NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid

BackgroundNAD(P)-dependent steroid dehydrogenase-like protein (NSDHL), which is involved in breast tumor growth and metastasis, has been implicated in the maintenance of cancer stem cells. However, its role in regulating breast cancer stem-like cells (BCSCs) remains unclear. We have previously reported the clinical significance of NSDHL in patients with estrogen receptor-positive (ER +) breast cancer. This study aimed to elucidate the molecular mechanisms by which NSDHL regulates the capacity of BCSCs in the ER + human breast cancer cell line, MCF-7.MethodsNSDHL knockdown suppressed tumor spheroid formation in MCF-7 human breast cancer cells grown on ultralow-attachment plates. RNA sequencing revealed that NSDHL knockdown induced widespread transcriptional changes in the MCF-7 spheroids. TGF-β signaling pathway was the most significantly enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway (fold change ≥ 2, P ≤ 0.05) identified in NSDHL-knockdown MCF-7 spheroids compared with the control. In orthotopic tumor models injected with NSDHL-knockdown MCF-7 spheroids, tumor initiation and growth were strongly suppressed compared with those in the control.ResultsBCSC populations with CD44+/CD24- and CD49f+/EpCAM + phenotypes and high ALDH activity were decreased in NSDHL-knockdown MCF-7 spheroids and xenograft tumors relative to controls, along with decreased secretion of TGF-β1 and 3, phosphorylation of Smad2/3, and expression of SOX2. In RNA-sequencing data from The (TCGA) database, a positive correlation between the expression of NSDHL and SOX2 was found in luminal-type breast cancer specimens (n = 998). Our findings revealed that NSDHL plays an important role in maintaining the BCSC population and tumor-initiating capacity of ER-positive MCF-7 spheroids, suggesting that NSDHL is an attractive therapeutic target for eliminating BCSCs, thus preventing breast cancer initiation and progression.ConclusionsOur findings suggest that NSDHL regulates the BCSC/tumor-initiating cell population in MCF-7 spheroids and xenograft tumors.

Long-term trends in the burden of breast cancer in China over three decades: a joinpoint regression and age-period-cohort analysis based on Global Burden of Disease 2021.

We analyzed the trends in breast cancer (BC) morbidity, prevalence, and mortality among Chinese residents from 1990 to 2021. We then used joinpoint regression to further assess BC morbidity and mortality. We screened the morbidity, mortality, and prevalence of BC in Chinese residents (1990-2021) from the Global Burden of Disease. We used age-period-cohort (APC) modeling to assess the effects of age, period, and cohort on BC morbidity and mortality separately. We also used the joinpoint model to characterize trends in BC morbidity and mortality in China. From 1990 to 2021, age-standardized rates of morbidity have risen significantly, whereas mortality has declined. We discovered that the risk of morbidity and death rose with age by using the APC model. We also found that mortality and morbidity roughly continued to increase over time, and finally, we found that the later the birth cohort, the lower the mortality and the higher the morbidity. From 1990 to 2021, the burden of BC disease in China will continue to rise, and the situation of BC prevention and control will remain severe. Therefore, regular imaging and palpation examinations should be performed in the regular population over 40 years of age. When treating patients with BC, healthcare workers should develop individualized treatment plans to further reduce mortality.

Statin prescription disparities in patients with breast cancer and diabetes for primary cardiovascular disease prevention.

This brief report examines statin prescription trends for primary cardiovascular disease (CVD) prevention in breast cancer (BC) survivors with diabetes, a large population at particularly high CVD risk. A population-based, retrospective cohort study was conducted using Surveillance, Epidemiology, and End Results (SEER) cancer registry data linked to Medicare claims. We identified women with preexisting diabetes who were diagnosed with stage 0-III primary BC between 2008 and 2017 without preexisting CVD. We assessed statin prescription rates over time and also examined differences in statin prescription rates according to patient sociodemographic characteristics. Using a multivariate logistic regression adjusted for sociodemographic and clinical variables, independent predictors of statin prescription were identified. Of 8,423 BC patients with diabetes without preexisting CVD, 5,698 (68%) had a statin prescription. Statin prescriptions increased over time (BC diagnosis year 2008-2009: 65%, 2010-2011: 67%, 2012-2013: 66%, 2014-2015: 69%, 2016-2017: 70%; p = 0.01) and differed by age (66-69: 66%, 70-74: 70%, 75-79: 69%, ≥80: 65%; p < 0.01) and race (White: 68%, Black: 62%, Latina: 66%, Other: 72%; p < 0.01). In a multivariate analysis, race (Black vs. White: OR 0.80, 95% CI: 0.68-0.95) remained a predictor of statin prescription. In older early-stage BC survivors, statin prescriptions increased over time and varied by age, race, and BC stage. These findings can potentially inform strategies to improve guideline-concordant statin prescriptions in a group at high risk for CVD and reduce disparities.