Granulomatous lobular mastitis (GLM) presents significant challenges, including high rates of morbidity, recurrence, and disability, ultimately impacting women’s health and quality of life. Local autoimmune imbalance involving dysregulated cytokines and immune cells has been recognized to play a key role in the pathology of GLM. Traditional Chinese medicine (TCM), with its multi-component, multi-pathway and multi-target characteristics, offers unique advantages and broad prospects in the treatment of GLM. Here, we review the relationship between immune dysregulation and GLM, as well as the regulatory mechanisms of TCM-based interventions, with the aim of providing new insights and foundational knowledge for the clinical treatment of GLM, while promoting the further application and development of TCM-based strategies for the treatment of GLM.

Breast cancer (BC) is one of the most prevalent malignant tumors among women globally, with the number of cases accounting for even more than 1/3 of all tumor patients in women. Recent studies have found that the incidence of BC is increasing every year. Despite the great progress made in BC treatment, the characteristics of BC cells, such as strong immune evasion, easy recurrence and drug resistance, are still the main reasons limiting the survival of BC patients. Epigenetics is becoming an important method to reveal the development of cancer, mainly through the study of DNA methylation, histone modification, chromatin structure changes and non-coding RNA. In addition, researchers have found that epigenetic markers have great potential for early detection and personalized treatment of BC. Inhibitors targeting epigenetically modified enzymes are effective in treating a wide range of tumors and provide significant patient survival and quality of life. Therefore, this review will comprehensively summarize the role of epigenetic modifications in BC development. Second, this paper will focus on summarizing how epigenetic modifications induce the formation of tumor immune microenvironment (TIME) in BC. Targeting the mechanism of action of epigenetic modifications provides new perspectives to unravel the complex process of BC development, while paving the way for the development of novel diagnostic and therapeutic targets. In the future, by integrating multi-omics data to enable a deeper understanding of the pathogenesis of BC, we will be able to promote the overall development of precision medicine.

Breast cancer is one of the most prevalent cancers in women globally. Its treatment and prognosis are significantly influenced by the tumor microenvironment and tumor heterogeneity. Precision therapy enhances treatment efficacy, reduces unwanted side effects, and maximizes patients’ survival duration while improving their quality of life. Spatial transcriptomics is of significant importance for the precise treatment of breast cancer, playing a critical role in revealing the internal structural differences of tumors and the composition of the tumor microenvironment. It offers a novel perspective in studying the spatial structure and cell interactions within tumors, facilitating more effective personalized treatments for breast cancer. This article will summarize the latest findings in the diagnosis and treatment of breast cancer from the perspective of spatial transcriptomics, focusing on the revelation of the tumor microenvironment, identification of new therapeutic targets, enhancement of disease diagnostic accuracy, comprehension of tumor progression and metastasis, assessment of drug responses, creation of high-resolution maps of tumor cells, representation of tumor heterogeneity, and support for clinical decision-making, particularly in elucidating the tumor microenvironment, tumor heterogeneity, immunotherapy and their correlation with clinical outcomes.

Development of safe and effective chemopreventive agents is a winning strategy in reducing the morbidity and mortality of breast cancer. The current study was to investigate the mechanism-based chemopreventive potential of a Chinese herb formula Yanghe Huayan (YHHY) Decoction on the classical 7,12-dimethylbenz(a)anthracene (DMBA) induced rat mammary carcinogenesis model. Female Sprague-Dawley rats at 42 days of age were orally administered with a human equivalent dose of YHHY Decoction at 0.02 ml/g (10 mg/ml) once daily, starting 1 wk. before and 4 wks following DMBA treatment. Mammary tumor occurrence was monitored every day. The length of time before palpable tumor is examined is defined as tumor-free survival time. High performance liquid chromatography (HPLC) analyses were adopted to identify major chemical compositions of the decoction. Following bioinformatics data mining and experimental analyses were performed to demonstrate the underlying mechanism of action. DMBA animals receiving YHHY Decoction exhibited a significant delay (P = 0.014) and in some animals prevention (P = 0.046) of tumor occurrence without obvious toxicity. Oncogenic myc activation was significantly suppressed in the DMBA-induced rats by the YHHY treatment. Eight major chemical compositions of the decoction were identified and were shown to interfere with multiple tumorigenic pathways simultaneously in the mammary tumors, including inducing tumor apoptosis and up-regulating pro-apoptotic protein Bax and down-regulating anti-apoptotic protein Bcl-2; suppressing abnormal cell proliferation and the MAPK/ERK, PI3K/AKT signalings; blocking neo-angiogenesis and the VEGF/KDR signaling, and inhibiting oxidative stress in the mammary tumors. The multi-components and multi-targeting properties of the YHHY Decoction support its use as a potent chemopreventive drug in breast cancer.

Wogonin is a compound extracted from the medicinal plant Scutellaria baicalensis Geogi and has been found to exert antitumor activities in a variety of malignancies. However, the molecular mechanisms involved in the anti-gastric cancer (GC) effects of wogonin remain poorly understood. In the present study, we found that wogonin treatment inhibited the proliferation of GC cells, induced apoptosis and G0/G1 cell arrest, and suppressed the migration and invasion of SGC-7901 and BGC-823 cells in vitro. In addition, wogonin inhibited in vivo tumor growth in SGC-7901 xenograft mice. Transcriptomic analysis suggested that wogonin affected several signaling pathways closely related to tumor proliferation and metastasis, including the STAT3 signaling pathway. Further research indicated that wogonin may exert antitumor effects in GC cells by downregulating the JAK-STAT3 pathway. Altogether, our results demonstrate that wogonin exerts antitumor effects by perturbing JAK-STAT3 signaling in GC cells and that wogonin may be a potential therapeutic option for GC.