BackgroundBreast cancer is the most common cancer among women. Chinese herbal medicine, which is based on accurate Chinese medicine (CM) syndrome diagnosis, plays a vital role during cancer treatment. This study aimed to validate the established CM syndrome diagnostic criteria for early breast cancer, enhancing their application in clinical settings.MethodsA multicenter prospective clinical study was conducted to collect epidemiological data on CM syndromes. Two attending doctors from the CM breast department performed syndrome differentiation using established diagnostic criteria and compared it to two clinical experts with associate senior professional titles. Metrics such as sensitivity, specificity, and accuracy were utilized to assess the validity of the diagnostic test.ResultsA total of 641 eligible cases were enrolled from June 2022 to October 2023 from seven hospitals in China. The sensitivity rates for all syndromes ranged from 70.37% to 92.00%, with the highest rate for Spleen and Stomach disharmony in the postoperative stage. Specificity varied from 86.84% to 98.89%, with most criteria exceeding 90%. Overall accuracy of the diagnostic criteria was between 84.25% and 94.45%. Positive predictive values ranged from 72.22% to 98.21%, while negative predictive values spanned from 79.25% to 98.82%, with most syndromes above 80%. The concordance rate for diagnostic criteria ranged from 90.91% to 96.45%, with Kappa values between 0.747 and 0.926.ConclusionsThis study demonstrated that the diagnostic criteria exhibit high reliability, confirming the validity of CM syndrome diagnostic criteria among different treatment stages for early breast cancer and contributing to standardizing clinical practice.

BACKGROUND:Lapatinib, an FDA-approved tyrosine kinase inhibitor, treats HER2+ advanced/metastatic breast cancer. This study comprehensively analyzed its adverse reaction profile using FDA Adverse Event Reporting System (FAERS) to guide clinical use. RESEARCH DESIGN AND METHODS:Adverse event (AE) reports for lapatinib from the second quarter of 2007 to the second quarter of 2024 in FAERS were analyzed using Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Multi-item Gamma Poisson Shrinkage (MGPS) and Bayesian Confidence Propagation Neural Network (BCPNN) to identify AE signals. RESULTS:Among 8300 AE reports, females (91.47%) and ages 40-59.9 (33.71%) were predominant. 20 system organ classifications (SOCs) were affected, with gastrointestinal disorders (ROR = 3.46) and skin disorders (ROR = 2.47) most significant. Based on the PT level, a total of 111 PTs were analyzed that met the four algorithms, including typical AEs such as diarrhea (n = 3410), vomiting (n = 856), and rash (n = 856), as well as some rare AEs that were not prompted by the drug inserts, such as neutropenia (n = 252), pericardial effusion (n = 43), lymphedema (n = 20). The majority of lapatinib-associated AEs had onset within 30 days (51%). CONCLUSIONS:Lapatinib has a generally favorable safety profile, but gastrointestinal toxicity and dermatotoxicity require close monitoring to prevent serious AEs.

Background: Irritable Bowel Syndrome (IBS) is a chronic disease with recurrent functional gastrointestinal. The pathogenesis and pathophysiology of this disease are highly complex, and the existing pharmaceutical treatment methods do not address all IBS symptoms. It is very important to develop a drug that can treat the disease and clarify its mechanism of action. This study aimed to address the effects of Changkang granules on IBS rats and then exploring the possible underlying mechanism using the gut microbiota -metabolomics method. Methods: The IBS rats was established by administering senna leaf water and applying restraint stress to investigate the efficacy of Changkang granules. With the methods of 16S rRNA sequencing technology and non-targeted metabolomics to explore the role of Changkang granules in IBS and identify the potential mechanisms involved. Results: Changkang granules can improve the visceral hypersensitivity of IBS by inhibiting the serum SP level of model rats, increasing the expression of serum CGRP and VIP in colon tissue. The underlying mechanism of action could involve increase the beneficial bacteria such as Bifidobacteria, Clostridium and Coprococcus, thereby up-regulating the levels of metabolites such as arachidonic acid (DHA) and γ-aminobutyric acid (GABA), down-regulating the expression of 2-hydroxybutyric acid (HA), inhibiting intestinal microecological disorders, improving the protective effect on the intestine, interfering with the MAPK metabolic pathway by reducing HA content, reducing inflammatory factors such as NF-κB, preventing inflammation, improving disease resistance, and relieving IBS symptoms. Conclusion: Changkang granule has a therapeutic effect on IBS rats, and its mechanism may be achieved by regulating gut microbiota and regulating metabolites such as GABA and 2-hydroxybutyric acid HA, which highlights a novel method for the treatment of IBS.

Granulomatous mastitis (GM) is a form of non-lactational breast inflammation that is closely associated with autoimmune processes, however its underlying pathogenesis remains elusive. In this study, we employed single-cell RNA sequencing (scRNA-seq) to conduct a comparative analysis of GM lesion tissues versus normal breast tissues, thereby unveiling the immune profile of GM tissues. Our investigation centered on T and NK cells, macrophages, epithelial cells, and endothelial cells. Notably, we observed a substantial infiltration of immune cells in GM tissues, accompanied by immune disorders, an elevation in Th1 cell counts, enrichment of the toll-like receptor (TLR) pathway, and upregulation of various factors including interferon-γ (IFN-γ), C–C motif chemokine ligand 3 (CCL3), CCL4, chemokine (C-X-C motif) ligand (CXCL) 13, CD69, signal transducer and activator of transcription 1 (STAT1), and heat shock protein family A member 1A (HSPA1A). Furthermore, the macrophage subpopulations in GM tissues exhibited a transition to a pro-inflammatory phenotype, enriched for pathways such as interferon-γ (IFN-γ), IFN-α, interleukin-6/janus kinase/signal transducer and activator of transcription 3 (IL-6/JAK/STAT3), and tumor necrosis factor-α/nuclear factor-κB (TNF-α/NF-κB). Mammary luminal cells demonstrated an impaired estrogenic profile yet displayed upregulation of prolactin downstream signaling pathways, namely the JAK/STAT and mitogen-activated protein kinase (MAPK) pathways. Additionally, vascular endothelial cells were found to recruit immune cells and exhibited a prominent angiogenic profile in GM tissues. Cellular interaction analysis unveiled an intricate network of interactions between mesenchymal and immune cells. This study provides a comprehensive immune landscape of granulomatous mastitis and offers some potential therapeutic targets for the disease.

Hypertrophic Scar (HS) is a common fibrotic disease of the skin, usually caused by injury to the deep dermis due to trauma, burns, or surgical injury. The main feature of HS is the thickening and hardening of the skin, often accompanied by itching and pain, which seriously affects the patient’s quality of life. Macrophages are involved in all stages of HS genesis through phenotypic changes. M1-type macrophages primarily function in the early inflammatory phase by secreting pro-inflammatory factors, while M2-type macrophages actively contribute to tissue repair and fibrosis. Despite advances in understanding HS pathogenesis, the precise mechanisms linking macrophage phenotypic changes to fibrosis remain incompletely elucidated. This review addresses these gaps by discussing the pathological mechanisms of HS formation, the phenotypic changes of macrophages at different stages of HS formation, and the pathways through which macrophages influence HS progression. Furthermore, emerging technologies for HS treatment and novel therapeutic strategies targeting macrophages are highlighted, offering potential avenues for improved prevention and treatment of HS.

Background:Granulomatous mastitis (GM) is an immune-related, clinically refractory disease, the translational research of which has been hindered by the lack of animal models. Establishing a stable rat model of GM is critical for elucidating its mechanisms and developing therapeutic approaches. Methods:The first batch of rats was randomly divided into a normal group, a low-dose group (0.2 mL), a middle-dose group (0.4 mL), and a high-dose group (0.8 mL). Except for the normal group, the remaining groups were subjected to model establishment using a tissue homogenate-complete Freund's adjuvant (CFA) suspension. The optimal dose was determined based on gross morphology, mammary inflammation index, and histopathological evaluation. The second batch of rats was modeled using the optimal dose, with a comparable number of normal rats as controls. At 7, 14, 21, and 28 days post-modeling, mammary gland appearance, histomorphology, and serum/tissue mRNA expression levels of key inflammatory factors (TNF-α, IL-1β, IFN-γ, IL-2) were observed. Results:Rats in the middle-dose group exhibited characteristic features of human GM, including gross morphological changes such as breast swelling, ulceration, and fistula formation. Histologically, granulomas characterized by epithelioid cells and Langhans multinucleated giant cells, along with persistent inflammatory cell infiltration, were observed. Compared with the parallel normal group, the expression levels of IL-2, IL-1β, TNF-α, and IFN-γ were significantly elevated in the model group, with their expression fluctuating over time. Conclusion:The 0.4 mL tissue homogenate-CFA injection method successfully induced a stable, reproducible, and long-lasting rat model that closely mimics human GM. This model provides a robust foundational platform for future research.

Triple-negative breast carcinoma (TNBC) remains a formidable clinical hurdle owing to its high aggressiveness and scant therapeutic options. Nonetheless, the evolving landscape of immunotherapeutic strategies opens up promising avenues for tackling this hurdle. This review discusses the advancing immunotherapy for TNBC, accentuating personalized interventions due to tumor microenvironment (TME) diversity. Immune checkpoint inhibitors (ICIs) hold pivotal significance, both as single-agent therapies and when administered alongside cytotoxic agents. Moreover, the concurrent inhibition of multiple immune checkpoints represents a potent approach to augment the efficacy of cancer immunotherapy. Synergistic effects have been observed when ICIs are combined with targeted treatments like PARP inhibitors, anti-angiogenics, and ADCs (antibody-drug conjugates). Emerging tactics include tumor vaccines, cellular immunotherapy, and oncolytic viruses, leveraging the immune system’s ability for selective malignant cell destruction. This review offers an in-depth examination of the diverse landscape of immunotherapy development for TNBC, furnishing meticulous insights into various advancements within this field. In addition, immunotherapeutic interventions offer hope for TNBC, needing further research for optimization.

The two primary types of non-puerperal mastitis (NPM) are granulomatous lobular mastitis (GLM) and plasma cell mastitis (PCM). Existing research indicates that immune inflammatory response is considered to be the core of the pathogenesis of GLM and PCM, and both innate and adaptive immune responses play an important role in the pathophysiology of PCM and GLM. However, the regulatory balance between various immune cells in these diseases is still unclear. Consequently, we present a comprehensive summary of the immune-related variables and recent advances in GLM and PCM.

BackgroundBreast cancer is the most prevalent cancer globally and is associated with significant mortality. Recent research has provided crucial insights into the role of gut microbiota in the onset and progression of breast cancer, confirming its impact on the disease’s management. Despite numerous studies exploring this relationship, there is a lack of comprehensive bibliometric analyses to outline the field’s current state and emerging trends. This study aims to fill that gap by analyzing key research directions and identifying emerging hotspots.MethodPublications from 2013 to 2023 were retrieved from the Web of Science Core Collection database. The VOSviewer, R language and SCImago Graphica software were utilized to analyze and visualize the volume of publications, countries/regions, institutions, authors, and keywords in this field.ResultsA total of 515 publications were included in this study. The journal Cancers was identified as the most prolific, contributing 21 papers. The United States and China were the leading contributors to this field. The University of Alabama at Birmingham was the most productive institution. Peter Bai published the most papers, while James J. Goedert was the most cited author. Analysis of highly cited literature and keyword clustering confirmed a close relationship between gut microbiota and breast cancer. Keywords such as “metabolomics” and “probiotics” have been prominently highlighted in the keyword analysis, indicating future research hotspots in exploring the interaction between metabolites in the breast cancer microenvironment and gut microbiota. Additionally, these keywords suggest significant interest in the therapeutic potential of probiotics for breast cancer treatment.ConclusionResearch on the relationship between gut microbiota and breast cancer is expanding. Attention should be focused on understanding the mechanisms of their interaction, particularly the metabolite-microbiota-breast cancer crosstalk. These insights have the potential to advance prevention, diagnosis, and treatment strategies for breast cancer. This bibliometric study provides a comprehensive assessment of the current state and future trends of research in this field, offering valuable perspectives for future studies on gut microbiota and breast cancer.

As the global incidence of breast cancer continues to surge, the pursuit of novel, low-toxicity, and highly efficacious therapeutic strategies has emerged as a pivotal research focus. Curcumin (CUR), an active constituent of traditional Chinese medicine (TCM) renowned for its antimicrobial, anti-inflammatory, antioxidant, and antitumor properties, exhibits immense potential in breast cancer therapy. Nevertheless, CUR's poor water solubility, chemical instability, and unfavorable pharmacokinetics have impeded its clinical utilization. To address these challenges, nano-delivery systems have been extensively exploited for CUR administration, enhancing its in vivo stability and bioavailability, and facilitating precise targeting of breast cancer lesions. Therefore, we elaborate on CUR's chemical foundations, drug metabolism, and safety profile, and elucidate its potential mechanisms in breast cancer therapy, encompassing inducing apoptosis and autophagy, blocking cell cycle, inhibiting breast cancer metastasis, regulating tumor microenvironment and reversing chemotherapy resistance. The review primarily emphasizes recent advancements in CUR-based nano-delivery systems for the treatment and diagnosis of breast cancer. Liposomes, nanoparticles (encompassing polymer nanoparticles, solid lipid nanoparticles, mesoporous silica particles, metal/metal oxide nanoparticles, graphene nanomaterials, albumin nanoparticles, etc.), nanogels, and nanomicelles can serve as delivery carriers for CUR, exhibiting promising anti-breast cancer effects in both in vivo and in vitro experiments. Furthermore, nano-CUR can be integrated with fluorescence imaging, magnetic resonance imaging, computed tomography imaging, ultrasound, and other techniques to achieve precise localization and diagnosis of breast cancer masses. While this article has summarized the clinical studies of nano-curcumin, it is noteworthy that the research literature on nano-CUR applied to breast cancer diagnosis and the translation of nano-CUR clinical studies in BC patients remain limited. Therefore, future research should intensify exploration in this direction.

The molecular categorization of colon cancer patients remains elusive. Gene set enrichment analysis (GSEA), which investigates the dysregulated genes among tumor and normal samples, has revealed the pivotal role of epithelial-to-mesenchymal transition (EMT) in colon cancer pathogenesis. In this study, we employed multi-clustering method for grouping data, resulting in the identification of two clusters characterized by varying prognostic outcomes. These two subgroups not only displayed disparities in overall survival (OS) but also manifested variations in clinical variables, genetic mutation, and gene expression profiles. Using the nearest template prediction (NTP) method, we were able to replicate the molecular classification effectively within the original dataset and validated it across multiple independent datasets, underscoring its robust repeatability. Furthermore, we constructed two prognostic signatures tailored to each of these subgroups. Our molecular classification, centered on EMT, hold promise in offering fresh insights into the therapy strategies and prognosis assessment for colon cancer.

肉芽肿性乳腺炎属中医学"粉刺性乳痈"范畴,其发病主要责之于肝,病机为木失条达,乳络郁阻,致使气血瘀滞,津停痰生,聚结成块,最终郁蒸腐肉酿脓,溃后不愈成瘘而成.中医依据"木郁达之",分期辨治:初期以肝气郁结为主,治以疏肝理气、化痰散结以达之;中期郁火酿脓,治以清泻肝火、消痈托脓以达之;末期木气失和,脾土受累,治以养肝解郁、培土和中以达之.附验案1则以佐证.

目的 观察西黄胶囊对非哺乳期乳腺炎大鼠模型创面愈合及白细胞介素-6(interleukin-6,IL-6)/非受体型酪氨酸蛋白激酶 2(Janus kinase 2,JAK2)/信号转导及转录激活蛋白 3(signal transducer and activator of transcription 3,STAT3)信号通路的影响.方法 复制非哺乳期乳腺炎大鼠模型,随机分为模型对照组、阳性药物组、中药治疗组、联合用药组,每组 10 只,另选取 10 只同批次SPF级健康SD大鼠作为假手术组.干预后观察并评估各组大鼠的创面愈合情况及乳腺炎症指数,HE染色法观察各组大鼠乳腺组织的病理改变;免疫组织化学法检测各组大鼠乳腺组织B淋巴细胞瘤-2基因关联X蛋白(B-cell lymphoma-2-associated X,BAX)、B淋巴细胞瘤-2基因(B-cell lymphoma-2,Bcl-2)的平均光密度值;Western blot法及RT-PCR法检测各组大鼠乳腺组织IL-6、JAK2、STAT3、人胱天蛋白酶 9(Caspase-9)蛋白及mRNA的表达水平.结果 与假手术组大鼠比较,模型对照组大鼠的创面愈合率明显降低(P＜0.05),而乳腺炎症指数,乳腺组织BAX、Bcl-2平均光密度值,IL-6、JAK2、STAT3、Caspase-9 蛋白及mRNA的表达水平显著升高(P＜0.05).HE染色可见模型对照组大鼠乳腺腺叶存在明显的肉芽肿变性,周围充斥大量炎症细胞,阳性药物组、中药治疗组、联合用药组大鼠的病理情况存在不同程度的缓解,炎性细胞浸润及肉芽肿组织明显减少,"空泡样"坏死存在不同程度的愈合.与模型对照组比较,阳性药物组、中药治疗组、联合用药组的创面愈合率、Bcl-2 光密度值均明显升高(P＜0.05);其中联合用药组的创面愈合率、Bcl-2 光密度值明显高于阳性药物组及中药治疗组(P＜0.05);阳性药物组的创面愈合率高于中药治疗组(P＜0.05),Bcl-2光密度值与中药治疗组比较差异无统计学意义(P＞0.05).与模型对照组比较,阳性药物组、中药治疗组、联合用药组的BAX光密度值、乳腺炎症指数均明显下降(P＜0.05);其中联合用药组的BAX光密度值、乳腺炎症指数明显低于阳性药物组及中药治疗组(P＜0.05);阳性药物组的乳腺炎症指数低于中药治疗组(P＜0.05),BAX光密度值与中药治疗组比较差异无统计学意义(P＞0.05).与模型对照组比较,阳性药物组、中药治疗组、联合用药组的IL-6、JAK2、STAT3、Caspase-9 蛋白及mRNA的表达水平均明显降低(P＜0.05);其中联合用药组上述蛋白及mRNA表达水平明显低于阳性药物组及中药治疗组(P＜0.05),而阳性药物组的上述蛋白及mR-NA表达水平均明显高于中药治疗组(P＜0.05).结论 西黄胶囊能有效促进非哺乳期乳腺炎大鼠模型的乳腺组织创面愈合,抑制乳腺组织细胞凋亡及炎症反应,其作用机制可能与西黄胶囊抑制IL-6/JAK2/STAT3信号通路相关.

目的:使用不同机器学习算法开发乳腺癌发病风险预测模型.方法:采用湖南中医药大学第一附属医院乳腺科患者数据库作为数据来源;根据乳腺癌相关风险因素,选取数据库中的初潮时间、流产次数、生育情况、月经及母乳喂养情况、乳腺癌家族史、作息时间、饮食习惯及中医证候特征等作为建模候选变量,提取其人口学特征、生命体征、病理检查等数据;使用6种机器算法开发模型,并对不同机器学习算法在预测模型中使用的效果进行评估.结果:综合两种计算方法对两种建模算法的特征重要度预测结果,可以得出年龄、燥热、流产次数、是否曾患乳腺炎、生活中是否经常锻炼、第一次月经时间等变量对乳腺癌的预测可能有重要作用.随机森林算法的预测结果最好,准确率为0.86,AUC值达0.89,XGboost和GBDT算法的准确率都为0.85,AUC值也同为0.85,其次是逻辑回归算法的准确率和AUC值都为0.84,SVC和DT算法的预测准确率分别为0.83、0.79,AUC值分别为0.82、0.71.从各算法的建模结果可以看出,随机森林算法由于集成学习的特性,本身的精度比一般单个算法的要好,预测结果的准确性也高.结论:基于森林算法的乳腺癌患者发病风险预测模型对辅助临床医生指导患者乳腺癌发病风险预防有重要意义.

乳腺癌相关淋巴水肿是乳腺癌术后最常见的并发症,其成因与手术破坏局部淋巴管导致局部微循环障碍、微血管失调、神经损伤等导致淋巴回流受阻有关.刘丽芳教授基于现代研究对乳腺癌相关淋巴水肿的认识,结合其临床表现,认为乳腺癌相关淋巴水肿可从中医学的"络病"视角进行论治.认为乳腺癌相关淋巴水肿的病因病机为金刃损伤络脉,耗伤气血以致络脉虚损,日久成积.络脉不通是乳腺癌相关淋巴水肿形成的核心病理环节.治疗上遵"络脉以通为用"之旨,将通络之法贯穿治疗全程,并灵活运用养络充络、祛瘀通络、剔邪搜络之法治疗乳腺癌相关淋巴水肿,常使用圣愈汤合三甲复脉汤、补阳还五汤、国医大师熊继柏经验方黄芪虫藤饮加减治疗,以收行气通络、开闭消肿之效,在临床上取得了良好的疗效.附临床验案,以期为临床治疗该病提供新思路和参考.

黑布药膏系常用的院内制剂,由五倍子、蜈蚣等制成,临床疗效确切,但其药效物质基础尚未全面阐明.本研究采用超高效液相色谱-高分辨飞行时间质谱联用技术(UPLC-Q-TOF-MS/MS)对黑布药膏及其生药混合物的化学成分进行定性分析,并探讨了制剂前后成分的差异.在电喷雾(ESI)正、负离子模式下,根据精确相对分子质量、特征碎片离子、色谱保留时间等初步鉴定出73个化合物,其中生药混合物、黑布药膏分别鉴定了57、65个化合物,包括鞣质类、酚酸类、核苷类、氨基酸类等,在制备过程中,化学结构发生变化的成分主要集中在鞣质类.结果表明,UPLC-Q-TOF-MS/MS技术可以灵敏、高效地表征黑布药膏制剂中所含的化学成分及其在制剂过程中的结构变化,为充分阐明黑布药膏药效物质基础和制剂工艺的合理性及后续制剂质量标准提升研究提供重要依据.

垫棉法临床运用十分广泛,"助疮回阳"是其重要作用之一,通过垫衬、绷缚使得创面保暖回阳、气血得以通畅,从而助痈疮发溃、促进愈合.阳虚为肉芽肿性乳腺炎的基本病机,依据"外治之理,即内治之理",垫棉法"助疮回阳"作用是温阳法在该病外治中的体现,也为垫棉法在临床中的应用开辟了新视野.

总结刘丽芳教授治疗乳腺癌巩固期的临证经验.刘教授认为乳腺癌巩固期患者虽已经历手术、化疗、靶向治疗等,但相当部分患者仍处于脾肾亏虚、瘀毒蕴结的病理生理状态,影响其生存质量,故提出补益脾肾、活血解毒作为这一时期核心治法,以期提高中医药干预乳腺癌巩固期临床疗效.

Breast cancer is the most prevalent cancer worldwide and its incidence increases with age, posing a significant threat to women's health globally. Due to the clinical heterogeneity of breast cancer, the majority of patients develop drug resistance and metastasis following treatment. Ferroptosis, a form of programmed cell death dependent on iron, is characterized by the accumulation of lipid peroxides, elevated levels of iron ions and lipid peroxidation. The underlying mechanisms and signalling pathways associated with ferroptosis are intricate and interconnected, involving various proteins and enzymes such as the cystine/glutamate antiporter, glutathione peroxidase 4, ferroptosis inhibitor 1 and dihydroorotate dehydrogenase. Consequently, emerging research suggests that ferroptosis may offer a novel target for breast cancer treatment; however, the mechanisms of ferroptosis in breast cancer urgently require resolution. Additionally, certain natural compounds have been reported to induce ferroptosis, thereby interfering with breast cancer. Therefore, this review not only discusses the molecular mechanisms of multiple signalling pathways that mediate ferroptosis in breast cancer (including metastasis, invasion and proliferation) but also elaborates on the mechanisms by which natural compounds induce ferroptosis in breast cancer. Furthermore, this review summarizes potential compound types that may serve as ferroptosis inducers in future tumour cells, providing lead compounds for the development of ferroptosis-inducing agents. Last, this review proposes the potential synergy of combining natural compounds with traditional breast cancer drugs in the treatment of breast cancer, thereby suggesting future directions and offering new insights.

Abstract Background Although preceding observational research mentioned a potential connection between meningioma and breast cancer, verifying an unambiguous causal relationship has turned out problematic. Aiming to determine if breast cancer and the risk of meningioma intersect, we utilized a bidirectional two-sample Mendelian randomization (MR) analysis in this study. Besides, we investigated the influence of various estrogen receptor (ER) phenotypes on that association. Methods Breast cancer data from the Breast Cancer Association Consortium (BCAC) coupled with meningioma data from the FinnGen cohort were adopted in our investigation. Total participants of European descent were divided into four groups: 228,951 individuals (122,977 cases of breast cancer and 105,974 controls), 175,475 individuals (69,501 cases of ER-positive breast cancer and 105,974 controls), 127,442 individuals (21,468 cases of ER-negative breast cancer and 105,974 controls), and 287,614 individuals (1.237 cases of meningioma and 286,377 controls). The MR research, which utilized the power of the inverse variance weighting (IVW), weighted median (WM), and MR-Egger means, used tightly opted instrumental SNPs that were profoundly connected with exposure. Results According to the results of our forward MR study, there was a significant causal correlation between total breast cancer on meningioma (MR-Egger: OR = 1.4, 95% CI = 1.05–1.90, P = 0.022; WM: OR = 1.3, 95% CI = 1.02–1.50, P = 0.0248; IVW: OR = 1.2, 95% CI = 1.05–1.4, P = 0.0075). Furthermore, there was a probable causative relationship among ER-positive (ER+) breast cancer on meningioma (IVW: OR = 1.20, 95% CI: 1.03–1.30, P = 0.014), whereas no apparent connection between ER-negative breast cancer on meningioma emerged. Meningioma had little impact on the risk of breast cancer and breast cancer with different ER states, as shown to the inverse MR analysis drawing on the IVW, MR-Egger, and WM tests. Conclusion Following what comes of our forward MR investigation, there existed an unambiguous connection between the breast cancer in the population of European descent on meningioma. Likewise, we uncovered a potential combination referring to a causative relationship among ER + breast cancer on meningioma. However, there was no confirmation that suffering ER-breast cancer increases the possibility to grow meningioma. Furthermore, there was no causal relationship between overall breast cancer and breast cancer with different ER status on meningioma by our reverse MR examination.