Journal of Mammary Gland Biology and Neoplasia最新文献

{"title":"Branching out: the diverse roles of stem and progenitor cells in mammary gland development.","authors":"Andrew Olander, Shaheen S Sikandar","doi":"10.1007/s10911-026-09595-x","DOIUrl":"10.1007/s10911-026-09595-x","url":null,"abstract":"<p><p>Tissue specific stem cells are critical in maintaining organ function throughout life. Understanding the dynamics and heterogeneity of stem cells and progenitors is essential to understanding how diseased cell states such as cancer evolve. Studies in the mammary gland have revealed significant heterogeneity in stem cell identity during embryonic development, puberty, adulthood and aging. In this review, we discuss the dynamics of lineage commitment in the mammary gland and the current understanding of mammary stem cells versus lineage committed progenitors at different stages. As breast cancer risk increases with age, we also review recent studies on the aged mammary gland in relation to lineage identity and provide perspectives for future research in understanding the niche of mammary epithelial cells.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13086781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of DCAF8 in Mammary Ductal Elongation and Branching Morphogenesis.","authors":"Qianying Han, Miaomiao Ban, Ting Zhang, Tianyun Yu, Xingyue Yan, Yumeng Hu, Pengfei Wu, Yanfang Ma, Luzheng Xu, Yanrong Su, Li Li, Mo Li, Genze Shao","doi":"10.1007/s10911-026-09604-z","DOIUrl":"10.1007/s10911-026-09604-z","url":null,"abstract":"<p><p>Postnatal mammary gland development involves the formation of a highly branched epithelial ductal tree, primarily through the elongation and branching morphogenesis of mammary epithelial ducts. Multiple factors are involved in this process, in which both estrogen and progesterone receptors (ER/PR) play a crucial role. In this study, we identified a role of DCAF8 in promoting mammary ductal elongation and branching through its impacts on ER/PR signaling. Homozygous Dcaf8 knockout mice exhibited significant delay in mammary ductal elongation during puberty, which was characterized by a reduction in mammary ductal elongation area and distance, and terminal end buds (TEBs); abnormal branching morphogenesis of mammary ducts was also observed in adult Dcaf8 null mice, which was characterized by a reduction of lateral branches and an increase of ductal bifurcation. To further elucidate the mechanism underlying DCAF8’s role in mouse mammary development, we performed transcriptomic sequencing and biochemical experiments. The results revealed that downstream key effectors of the PR signaling pathway were significantly downregulated, while the expression of ERβ, a potential inhibitor of ERα/PR signaling, was significantly elevated in the mammary gland of Dcaf8 null mice. Collectively, this study suggests that DCAF8 may play an important role in mammary development by promoting ductal elongation and branching morphogenesis, through ERβ-mediated inhibition of ERα/PR signaling pathway.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Clonal Hematopoiesis of Indeterminate Potential on Treatment Response and Tumor Microenvironment in Breast Cancer Patients Undergoing Neoadjuvant Chemotherapy.","authors":"Muyuan Yang, Gengshen Yin, Yifan Yu, Dihui Zhang, Xiaoying Wang, Xingchen Zhou, Xinyu Liu, Shuya Huang, Ying Shan, Xianfang Liu, Fei Wang, Juandong Wang, Yang Song, Yang Wu, Dong-Xu Liu, Zhigang Yu, Yujuan Xiang","doi":"10.1007/s10911-026-09603-0","DOIUrl":"10.1007/s10911-026-09603-0","url":null,"abstract":"<p><p>Clonal hematopoiesis of indeterminate potential (CHIP) is associated with systemic inflammation and solid tumor progression, but its impact on breast cancer therapy remains unclear. This study investigated whether CHIP influences neoadjuvant chemotherapy (NAC) response and shapes the tumor microenvironment (TME) in breast cancer. We analyzed tumor sequencing data from The Cancer Genome Atlas (TCGA), focusing on mutations in CHIP-driver genes within a variant allele frequency range of 2–33.3%, a signature indicative of tumor-infiltrating clonal hematopoiesis (TI-CH). Patients harboring these TI-CH-associated mutations exhibited significantly worse overall and disease-free survival. In a retrospective cohort of 44 NAC-treated patients, CHIP mutations were detected in 15.9% of patients, most frequently in DNMT3A and NOTCH3. CHIP positivity was significantly associated with extensive residual disease (residual cancer burden, RCB III; P = 0.027) and chemotherapy resistance. CHIP-positive patients also showed elevated post-treatment markers of renal stress (creatinine) and hypercoagulability (D-dimer). Transcriptomic analysis revealed an immunosuppressive TME in CHIP-positive tumors after NAC, characterized by reduced CD8 + T cell infiltration and dysregulation of immune pathways including antigen processing and presentation, T cell receptor signaling, and primary immunodeficiency. Notably, CHIP-positive tumors also carried a higher tumor mutational burden, suggesting a state of “immune ignorance” where defective myeloid-driven immunity overrides neoantigen abundance. Collectively, these findings demonstrate that CHIP promotes an immunosuppressive TME and systemic inflammation, both linked to chemotherapy resistance and poor outcomes in breast cancer. Our results identify CHIP as a potential biomarker for risk stratification and a therapeutic target to overcome therapy resistance.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13068755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methods for Preserving Human Milk Cellular and Milk Fat Globule RNA.","authors":"Zhengfei Li, Nicole Fischbein, Flora Jin, Wesley Mui, Raimundo Co, Amy Sarah Ginsburg, Victoria Laleau, Sarah Nyquist, Kimberly O O'Brien, Nadav Ahituv, Valerie Flaherman, Yarden Golan","doi":"10.1007/s10911-026-09601-2","DOIUrl":"10.1007/s10911-026-09601-2","url":null,"abstract":"<p><p>Human breast milk contains RNA in various fractions, including milk cells and milk fat globules (MFG), making it a valuable resource for studying lactation physiology. However, preserving RNA integrity, especially in low-resource or at-home collection settings, is challenging due to rapid RNA degradation.This study aimed to evaluate RNA preservation methods for milk cells and MFG, using RNAlater for stabilization before freezing. Human milk samples (n = 26) were collected from lactating participants and either frozen (standard practice) or mixed with RNAlater (1:1, v/v) before freezing. RNA was extracted from separated cellular and MFG fractions and assessed for concentration, quality (RNA quality number-RQN and 28 S/18S ratio), and gene expression (ACTB, LALBA, PRLR, PTPRC) using RT-qPCR.Samples preserved with RNAlater showed significantly improved RNA integrity, particularly in the MFG fraction, compared to those frozen without RNAlater. Gene expression was largely stable across preservation methods. Delays in mixing with RNAlater led to declining RQN values in milk cell fractions, underscoring the need for prompt stabilization. Lastly, we show that this method can be used in low-resource countries by extracting RNA from samples collected in a randomized clinical trial in Guinea-Bissau and shipped to the US for analysis. This procedure led to improved yield and integrity of these samples.These findings demonstrate that RNAlater pre-freezing stabilization enhances RNA quality and yield, and supports its use for milk gene expression analysis. This approach provides a practical, scalable solution for RNA preservation in clinical and field research, including remote and low-resource settings, as it requires minimal experience and equipment.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147284345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LMO2 Regulates Epithelial-Mesenchymal Plasticity of Mammary Epithelial Cells.","authors":"Veronica Haro Acosta, Andrew Olander, Isobel J Fetter, Maria A Juarez, Shaheen S Sikandar","doi":"10.1007/s10911-026-09598-8","DOIUrl":"10.1007/s10911-026-09598-8","url":null,"abstract":"<p><p>Cellular plasticity in mammary epithelial cells enables dynamic cell state changes essential for normal development but can be hijacked by breast cancer cells to drive tumor progression and metastasis. However, the molecular factors that maintain cellular plasticity through the regulation of a hybrid cell state (epithelial/mesenchymal) are not fully defined. As LMO2 has been previously shown to regulate metastasis in breast cancer, here we determine the role of LMO2 in normal mammary epithelial cells. Using lineage tracing and knockout mouse models, we find that Lmo2 lineage-traced cells are present in the luminal and basal layer of the mammary gland but have limited proliferative potential. Lmo2 loss does not impact mammary gland development, but acute deletion decreases in vivo reconstitution. Moreover, LMO2 knockdown in mouse and human mammary epithelial cells (MECs) reduces organoid formation. We find that LMO2 regulates the epithelial cell state in MECs and LMO2 knockdown promotes mesenchymal differentiation. Transcriptional profiling of LMO2 knockdown cells reveals significant enrichment in the epithelial-mesenchymal transition (EMT) pathway and upregulation of MCAM, a mesenchymal marker and negative regulator of regenerative capacity in the mammary gland. Altogether, we show that LMO2 plays a role in maintaining cellular plasticity in MECs, adding insight into the normal differentiation programs hijacked by cancer cells to drive tumor progression.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13004756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient-Derived Procoagulant Breast Fibroblasts Expressing Tissue Factor Promote Breast Cancer Cell Migration.","authors":"Hadiyat A Ogunlayi, John Castle, Emma L Blower, Anne Armstrong, Robert B Clarke, Cliona C Kirwan","doi":"10.1007/s10911-026-09596-w","DOIUrl":"10.1007/s10911-026-09596-w","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) play a key role in breast cancer progression and exhibit a procoagulant phenotype within the tumour microenvironment (TME). We hypothesised that this procoagulant phenotype correlates with a CAF-like phenotype and that fibroblasts distant from the immediate TME are less procoagulant. We also proposed that the procoagulant phenotype contributes functionally to breast cancer progression.Primary fibroblasts were cultured from human breast tumour tissue and matched normal breast tissue from regions distant to the tumour. Conditioned media (CM) from these cells were collected for analysis. We conducted immunocytochemistry, western blotting, transforming growth factor beta 1 (TGFβ1) ELISA, tissue factor (TF) activity and procoagulant activity assays. A positive correlation was found between the expression of TF and alpha-smooth muscle actin (α-SMA), a CAF marker, and between fibroblast procoagulant activity and secretion of the CAF inducer, TGFβ1.Interestingly, fibroblasts from distant breast tissue exhibited CAF-like and procoagulant phenotypes similar to tumour-associated fibroblasts. To assess functional relevance, scratch wound migration assays were performed using MCF-7 breast cancer cells. Inhibition of TF derived from both tumour and distant fibroblasts significantly reduced MCF-7 cell migration. Combined inhibition of TF and TGFβ1 in distant fibroblast CM further suppressed migration.These findings suggest that tumour-derived influences may extend beyond the immediate TME, inducing a CAF-like, procoagulant phenotype in fibroblasts from histologically normal breast tissue. Furthermore, fibroblast-derived TF promotes breast cancer cell migration which is important for the processes of invasion and metastasis. This further highlights TF as a promising therapeutic target in breast cancer.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12996003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights from Genomic Sequencing of Preclinical Breast Cancer Models Establish Human Parallels to Increase Therapeutic Applicability.","authors":"Anthony J Schulte, Eran R Andrechek","doi":"10.1007/s10911-026-09599-7","DOIUrl":"10.1007/s10911-026-09599-7","url":null,"abstract":"<p><p>The study of breast cancer is complicated by the heterogeneity inherent within the disease. Numerous models have been developed to study the initiation, progression, and treatment of breast cancer. These include carcinogen induced mouse models, genetically engineered mouse models, and patient derived xenografts. The relevance of these mouse models to humans must be precisely defined for appropriate understanding of disease mechanisms to derive intervening treatments. Sequencing projects such as The Cancer Genome Atlas Project (TCGA) and Catalogue Of Somatic Mutations In Cancer (COSMIC) were pivotal developments in understanding driving events in human cancers. These studies have revealed that in addition to activation of strong oncogenes, or loss of tumor suppressors, that secondary events are necessary for tumor development and progression. These techniques should also be applied to mouse models of human breast cancer. For all the available models studied and reviewed here, whole genome sequencing (WGS) in conjunction with gene expression analysis has revealed conserved events between human and mouse model systems. This identification of conserved, critical events driving breast cancer has led to novel targets based on breast cancer subtype, ultimately resulting in new therapeutic opportunities. The combination of sequencing and choice of the appropriate mouse model can provide a powerful tool in developing appropriate pre-clinical models of breast cancer.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Anticancer Effects of Apatinib and PD-L1 Inhibition in Breast Cancer.","authors":"Danyang Han, Juanjuan Xu, Cairu Guo","doi":"10.1007/s10911-026-09600-3","DOIUrl":"10.1007/s10911-026-09600-3","url":null,"abstract":"<p><p>Studies in breast cancer have demonstrated that apatinib exhibits both antiangiogenic and antitumor effects, while PD-L1 inhibitors have similarly shown meaningful clinical benefit. Building upon these observations, this study evaluated the potential synergistic antitumor effects of combining apatinib with a PD-L1 inhibitor and examined the mechanistic basis for their interaction in breast cancer. Notably, we found that this regimen could significantly suppress the proliferation, migration, and invasion of MCF-7 and MDA-MB-231 cells, and promote cell apoptosis. In addition, the levels of p-ERK, NF-κB, and Slug were markedly reduced in vitro. Collectively, these findings support the potential clinical utility of combining apatinib and PD-L1 inhibition, as evidenced by consistent in vitro and in vivo synergy.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12948880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing Human Milk RNA Degradation Over Time to Optimize Storage of Human Milk for RNA Quality.","authors":"Meghan R Crimmins, Brittany Reed, Larissa L da Cruz, Clark R Sims, Sarah Sobik, Elisabet Børsheim, Craig Porter, Rosalia C M Simmen, Aline Andres","doi":"10.1007/s10911-026-09597-9","DOIUrl":"10.1007/s10911-026-09597-9","url":null,"abstract":"<p><p>Human milk is rich in bioactive components beyond nutrition, including RNAs-especially miRNAs. It is the most RNA-rich biofluid. While storage effects on other milk components are well studied, RNA preservation has been minimally explored, primarily focusing on miRNAs in exosomes under refrigeration. The goal of this clinical study was to determine optimal collection and storage methods to preserve RNA quantity and quality in human milk, predominantly focusing on RNA stability in research laboratory settings when isolation of milk fat globules is not feasible. The study recruited 30 lactating women in central Arkansas. Milk samples were collected in-clinic and processed immediately for baseline RNA data. Remaining aliquots were stored at 4 °C, -20 °C, or -80 °C with or without RNAlater. RNA was extracted at 4 h, 24 h, 1 week, 4 weeks, 12 weeks, and 24 weeks using Qiagen miRNeasy and MinElute kits. RNA quality (RINe) and concentration (ng/µL) were assessed with Agilent TapeStation with additional quality analysis through qPCR. RNA quality declined over time at all storage temperatures in samples without RNAlater. Addition of RNAlater prevented decreases in RINe scores at most time points, maintaining RINe > 7 for up to 6 months, though it reduced total RNA concentration. qPCR also showed improved mRNA stability with RNAlater. miRNAs were analyzed using Agilent Bioanalyzer Small RNA kits with qPCR for quality analysis. RNAlater was not beneficial for miRNA preservation, and miRNAs remained stable when stored frozen without RNAlater. qPCR verified miRNA stability when frozen. In conclusion, RNA in human milk degrades over time. For mRNA analysis, storage with RNAlater at -80 °C is recommended. For miRNA analysis, storage at -20 °C or -80 °C without preservatives is optimal. These findings offer preliminary guidance for HM RNA storage, and researchers are advised to conduct method testing before full study implementation.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":"31 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12923474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146227173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased Toll-Like Receptor-4 Signalling in Breast Tissue of High Fibroglandular Density.","authors":"Hanieh Heydarlou, Leigh J Hodson, Pallave Dasari, Eric Smith, Wendy V Ingman","doi":"10.1007/s10911-025-09593-5","DOIUrl":"10.1007/s10911-025-09593-5","url":null,"abstract":"<p><p>High mammographic breast density relates to the abundance of fibroglandular tissue in comparison to fatty tissue in the breast and is associated with increased breast cancer risk. Chronic low-level inflammation has been implicated as a driver of high density and cancer risk, however little is understood of the underlying cause of inflammation. This research aimed to investigate the role of the innate immune recognition receptor toll-like receptor-4 (TLR4) in inflammation associated with high fibroglandular density. Immunohistochemical analysis was performed on paired breast tissue samples of high and low fibroglandular density tissue (n = 22 pairs) to investigate the expression of TLR4, TLR4 agonists lipopolysaccharide (LPS) and damage response protein high-mobility group protein 1 (HMGB1), as well as activation of downstream mediators myeloid differentiation primary response 88 (MYD88) and nuclear factor kappa B (NFKB). Mammary epithelial cell organoids (n = 5) were cultured in vitro with LPS to investigate the expression of genes associated with inflammation. TLR4 was primarily expressed in basal epithelial cells, stromal macrophages, and some expression was detected in luminal epithelial cells. Increased expression of TLR4, MYD88, NFKB, and HMGB1 was observed in epithelial cells in high fibroglandular density tissue. There was increased expression of the genes encoding inflammatory cytokines tumour necrosis factor alpha (TNFA) and C-C motif ligand 2 (CCL2) in mammary epithelial cell organoids treated with LPS. The TLR4 signalling pathway may be a mediator of local breast inflammation associated with regions of high breast density and the damage response protein HMGB1 may be a trigger for TLR4 activation.</p>","PeriodicalId":16413,"journal":{"name":"Journal of Mammary Gland Biology and Neoplasia","volume":" ","pages":"4"},"PeriodicalIF":3.1,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}