Yousef M Al-Saraireh, Fatemah O F O Alshammari, Heba A Hassan, Jaber H Jaradat, Ahmed A Al-Abadleh, Anas O Satari, Sameeh A Al-Sarayreh, Sa'ed M Al-Dalain, Aiman Al-Qtaitat, Jehad M Al Shuneigat, Mohammad Salem Hareedy
{"title":"CYP4B1 Expression in Breast Cancer: An Immunohistochemical Study with Complementary in silico Analyses.","authors":"Yousef M Al-Saraireh, Fatemah O F O Alshammari, Heba A Hassan, Jaber H Jaradat, Ahmed A Al-Abadleh, Anas O Satari, Sameeh A Al-Sarayreh, Sa'ed M Al-Dalain, Aiman Al-Qtaitat, Jehad M Al Shuneigat, Mohammad Salem Hareedy","doi":"10.2147/BCTT.S612743","DOIUrl":"10.2147/BCTT.S612743","url":null,"abstract":"<p><strong>Purpose: </strong>Cytochrome 4B1 (CYP4B1) is a monooxygenase extrahepatic enzyme, recently found expressed in several malignancies. However, the role of CYP4B1 in breast cancer is still undetermined.</p><p><strong>Patients and methods: </strong>The study consisted of two complementary components. First, CYP4B1 protein expression was evaluated by immunohistochemistry using a breast cancer tissue microarray (n = 207 tumors; n = 8 normal breast tissues). Second, in silico analyses were performed using publicly available databases and included transcriptomic expression profiling, survival analysis, protein-protein interaction analysis (PPI), functional enrichment analysis, drug-sensitivity correlations, and AlphaFold-based structural assessment.</p><p><strong>Results: </strong>Immunohistochemical analysis demonstrated focal and heterogeneous CYP4B1 protein expression, which was detected in 18.3% of breast tumors and was significantly associated with lower histological grade. No CYP4B1 immunoreactivity was observed in the sampled normal breast tissues under the experimental conditions. In silico analyses demonstrated reduced CYP4B1 mRNA expression in breast cancer at the population level, compared with normal breast tissue. Survival analysis showed no statistically significant differences between CYP4B1 expression groups. According to PPI analysis, CYP4B1 is part of a closely related redox-regulatory and xenobiotic-metabolizing module enriched in CYPs, GSTs, and SULTs. Structural analysis provided contextual support for the previously reported association of the P427S meander-region substitution with reduced catalytic competence. Weak exploratory correlations were observed between CYP4B1 expression and drug sensitivity metrics; however, these findings were descriptive and did not indicate clinically meaningful resistance.</p><p><strong>Conclusion: </strong>Immunohistochemical analysis demonstrated that CYP4B1 protein expression is focal and heterogeneous, being retained in only a small subset of breast tumors and associated with lower histological grade. Bioinformatics analyses showed reduced CYP4B1 mRNA expression in breast cancer and identified CYP4B1 within xenobiotic metabolism and redox-regulatory networks. Collectively, these findings provide a descriptive multilevel characterization of CYP4B1 in breast cancer; however, its prognostic and therapeutic significance remains exploratory and requires further functional validation.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"612743"},"PeriodicalIF":3.6,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418748","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}
Guangming Yi, Lihua Deng, Liping Su, Huan Jie, Cong Huang, Yujun Wang
{"title":"Radiomics and Deep Learning: Bridging Breast Cancer Imaging Phenotypes and Genomic Heterogeneity.","authors":"Guangming Yi, Lihua Deng, Liping Su, Huan Jie, Cong Huang, Yujun Wang","doi":"10.2147/BCTT.S617698","DOIUrl":"10.2147/BCTT.S617698","url":null,"abstract":"<p><p>Breast cancer is a highly heterogeneous malignancy. Radiomics, combined with deep learning techniques, harnesses the power of advanced medical imaging to extract rich quantitative features that noninvasively capture tumor imaging phenotypes. This approach facilitates the integration of macroscopic imaging data with genomic heterogeneity, thereby bridging the gap between tumor radiographic appearance and underlying molecular profiles. This review systematically outlines the radiomics workflow in breast cancer, encompassing image acquisition, tumor segmentation, feature extraction, feature selection, and modeling strategies. Emphasis is placed on the role of deep learning in automating feature extraction and enabling multimodal data fusion to enhance predictive accuracy. By examining current research progress, we elucidate methods to uncover latent information related to gene mutations, immune microenvironment characteristics, and other genomic alterations from imaging data. This synthesis highlights the potential of radiogenomics to provide novel insights and tools for precision medicine, ultimately fostering personalized diagnosis, prognosis, and treatment planning in breast cancer care.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"617698"},"PeriodicalIF":3.6,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148389836","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":"Advancing Germline Genetic Testing for Breast Cancer in Resource-Restricted Settings: Evidence, Barriers, and a Practical Roadmap for Implementation.","authors":"Hikmat Abdel-Razeq","doi":"10.2147/BCTT.S618067","DOIUrl":"10.2147/BCTT.S618067","url":null,"abstract":"<p><p>Germline genetic testing (GGT) is increasingly integrated in breast cancer management, yet its implementation, particularly in resource-restricted settings, remains a challenge. This narrative review addresses current evidence and international guideline recommendations regarding GGT in breast cancer, with emphasis on clinical utility, evolving testing criteria and implementation challenges, drawing partly on the experience and demographic characteristics of Jordan as an example of a resource-restricted setting. Approximately 10% of patients with breast cancer carry germline pathogenic variants, mostly involving <i>BRCA1</i> and <i>BRCA2</i>. GGT guides systemic therapy including PARP inhibitors, informs surgical decisions and enables cascade testing for at-risk relatives to support prevention and early detection. Recent guideline updates from major international societies have expanded eligibility, with recommendations supporting testing up to age 65 and some advocating universal testing. In low- and middle-income countries, these expanded criteria render a large proportion of patients eligible but raise concerns regarding infrastructure, cost and variant of uncertain significance (VUS) interpretation. While expanded testing increases detection of actionable variants and may improve outcomes, universal GGT remains controversial, and context-adapted strategies are required to balance benefit, feasibility, and sustainability. Overall, integrating GGT into routine breast cancer care represents a key component of precision oncology and hereditary cancer prevention strategies worldwide, especially in early-onset disease populations. Implementation requires multidisciplinary coordination and equitable access to testing services.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"618067"},"PeriodicalIF":3.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343826","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":"Salidroside-Based Nanomedicines for Triple-Negative Breast Cancer: From Molecular Mechanisms to Clinical Translation.","authors":"Xiaoying Ma, Shengyan Dang, Hui Wang, Lei Xia, Ping Ma, Yujuan Qi","doi":"10.2147/BCTT.S605051","DOIUrl":"10.2147/BCTT.S605051","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) presents a substantial therapeutic challenge due to its aggressive biological characteristics and the absence of actionable molecular targets. Salidroside, the principal bioactive compound of <i>Rhodiola rosea</i>, demonstrates significant anticancer potential; however, its clinical application is severely constrained by poor bioavailability (less than 12%) and a short half-life (2.3 hours). This review contributes to the field in three key ways. Firstly, it systematically elucidates the molecular mechanisms of salidroside in TNBC, emphasizing its distinctive dual role in redox homeostasis: inducing ferroptosis in cancer cells while safeguarding normal tissues. Secondly, it critically assesses advanced nanomedicine strategies such as PLGA-PEG nanoparticles, lipid-polymer hybrid nanoparticles, and biomimetic RBC membrane-camouflaged carriers-designed to address pharmacokinetic limitations. Thirdly, and most importantly, it proposes a biomarker-driven framework, centered on BRCA1 methylation and HIF-1α, along with a three-phase translational roadmap to advance salidroside into a precision nanomedicine for TNBC.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"605051"},"PeriodicalIF":3.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13311219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148350626","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":"Efficacy of CDK4/6 Inhibitor Plus Aromatase Inhibitor versus Fulvestrant in Chinese Patients with Hormone Receptor-Positive and Human Epidermal Growth Factor Receptor 2-Negative (HR+/HER2-) Advanced Breast Cancer.","authors":"Yujing Tan, Cheng Zeng, Jiuda Zhao, Weihong Zhao, Hanfang Jiang, Jiani Wang, Fei Ma","doi":"10.2147/BCTT.S574628","DOIUrl":"10.2147/BCTT.S574628","url":null,"abstract":"<p><strong>Purpose: </strong>The multicenter, real-world study aims to explore the clinical efficacy of the cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) plus aromatase inhibitor (AI) versus fulvestrant (FUL) in Chinese patients with hormone receptor-positive and human epidermal growth factor receptor 2-negative (HR+/HER2-) advanced breast cancer (ABC).</p><p><strong>Methods: </strong>We retrospectively collected clinicopathological data of cancer patients receiving CDK4/6i from four cancer centers in China. Clinical benefit rate (CBR), objective response rate (ORR), and progression-free survival (PFS) were compared between AI- and FUL-combined therapy.</p><p><strong>Results: </strong>A total of 315 patients with HR+/HER2- ABC were qualified. 188 (59.7%) patients received AI+CDK4/6i, and 127 (40.3%) patients received FUL+CDK4/6i therapy. In the overall population, the median PFS was 16.8 months versus 14.9 months for AI+CDK4/6i and FUL+CDK4/6i (p=0.34, HR=0.87, 95% CI=0.64-1.17). ORR (19.7% versus 24.4%, p=0.33) and CBR (69.7% versus 77.2%, p=0.16) were comparable between the two treatment regimens. For patients receiving post-first-line (1L) therapy, CBR for FUL+CDK4/6i therapy was 69.1%, which was significantly higher than 52.6% for AI+CDK4/6i therapy (p=0.04). Among ET-resistant subgroups, FUL+CDK4/6i achieved a higher CBR of 70.1% compared with 56.2% for AI+CDK4/6i (p = 0.008). In other subgroups, including patients receiving 1L CDK4/6i, who had a favorable response to ET, with/without liver metastasis at first relapse, the median PFS, ORR, and CBR showed no statistical difference (all p>0.05).</p><p><strong>Conclusion: </strong>In general, both AI and FUL combinations are effective alternatives, irrespective of the CDK4/6i treatment line, liver metastasis at first relapse, or endocrine sensitivity. Further studies are expected.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"574628"},"PeriodicalIF":3.6,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343857","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":"SLC2A9-Mediated Uric Acid Homeostasis Modulates Apoptosis in TNBC.","authors":"Peng Chen, Jiapeng Xu, Yulong Liang, Jinghui Mu, Wenjing Feng, Jiaming Liu, Bolun Li","doi":"10.2147/BCTT.S606599","DOIUrl":"10.2147/BCTT.S606599","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the biological function of SLC2A9 in triple-negative breast cancer (TNBC) and its molecular mechanism of influencing TNBC cells by regulating uric acid (UA) metabolism.</p><p><strong>Methods: </strong>Bioinformatics analysis was performed to screen genes intersecting TNBC and UA metabolism pathways. TNBC cell lines were cultured in vitro, followed by the establishment of SLC2A9 overexpression and knockdown models. Subsequently, the levels of intracellular and extracellular UA were quantified. Cell proliferation, apoptosis, migration, and invasion capabilities were assessed using CCK-8, plate cloning, flow cytometry apoptosis analysis, scratch assay, and Transwell assays. Western blot analysis evaluated the expression of apoptosis-related proteins and UA metabolism proteins.</p><p><strong>Results: </strong>SLC2A9 was significantly downregulated in TNBC tissues and most cell lines. SLC2A9 overexpression inhibited TNBC cell proliferation, migration, and invasion while promoting apoptosis. It also increased extracellular UA secretion and reduced intracellular UA accumulation. Conversely, SLC2A9 knockdown or probenecid treatment reversed these phenotypes. SLC2A9 exerts its effects by upregulating XDH, downregulating ABCG2, and modulating mitochondrial apoptosis pathway protein expression.</p><p><strong>Conclusion: </strong>SLC2A9 regulates the malignant phenotype of TNBC by altering the levels of UA inside and outside the cell. Its anticancer activity depends on UA transport function, making it a promising prognostic biomarker and novel metabolic therapeutic target for TNBC.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"606599"},"PeriodicalIF":3.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13308554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343866","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":"Risk Factors and Prognosis Analysis of Infiltrating Micropapillary Carcinoma of Breast: A Retrospective Study.","authors":"Pengfei He, Yupeng Sha, Yige Lu, Tong Li, Xiaoming Li, Yixin Liu, Hui Pang, Jiguang Han, Quan Yuan","doi":"10.2147/BCTT.S612948","DOIUrl":"10.2147/BCTT.S612948","url":null,"abstract":"<p><strong>Background: </strong>Invasive micropapillary carcinoma (IMPC) is a rare breast cancer subtype with high invasiveness and lymphovascular/lymph node metastasis. While poor prognosis is reported, long-term survival and roles of molecular subtyping/laboratory markers remain unclear.</p><p><strong>Methods: </strong>We retrospectively analyzed 653 IMPC patients from a Chinese center (as of December 2024). Kaplan-Meier estimated progression-free survival (PFS) and overall survival (OS); Cox regression assessed prognostic factors.</p><p><strong>Results: </strong>Among 653 patients with IMPC, the molecular subtype distribution was as follows: HR+/HER2-, 48.2%; HR+/HER2+, 35.4%; HR-/HER2-, 11.0%; and HR-/HER2+, 5.4%. Most patients had T1-2 disease and were postmenopausal. The 3-year and 5-year OS rates were 97.42% and 93.73%, respectively, while the 3-year and 5-year PFS rates were 90.66% and 81.20%, respectively. Kaplan-Meier analysis showed significant differences in PFS among molecular subtypes, but not in OS. In multivariable analysis, the HR+/HER2+ subtype and higher total bilirubin were independently associated with better PFS, whereas higher systemic immune-inflammation index and stage IIIB were associated with worse PFS. Poorer OS was independently associated with advanced stage, no surgery, alcohol consumption history, higher systemic immune-inflammation index, menopausal status, and elevated blood glucose, while mastectomy and endocrine therapy were associated with better OS.</p><p><strong>Conclusion: </strong>IMPC shows favorable OS but requires progression risk monitoring. PFS varied by molecular subtype, while OS did not. Molecular typing, clinical stage, and inflammatory/biochemical markers aid prognosis and personalized treatment.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"612948"},"PeriodicalIF":3.6,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13291655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148326953","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}
Manish Charan, Travis H Jones, Dinesh K Ahirwar, Nandini Acharya, Vish V Subramaniam, Konstantin Shilo, Ramesh K Ganju, Jonathan W Song
{"title":"Induced Electric Fields Inhibit Breast Cancer Growth and Metastasis and Modulate the Immune Tumor Microenvironment.","authors":"Manish Charan, Travis H Jones, Dinesh K Ahirwar, Nandini Acharya, Vish V Subramaniam, Konstantin Shilo, Ramesh K Ganju, Jonathan W Song","doi":"10.2147/BCTT.S604098","DOIUrl":"10.2147/BCTT.S604098","url":null,"abstract":"<p><strong>Introduction: </strong>Metastatic triple-negative breast cancer (TNBC) remains highly challenging to treat despite advances in oncology. This study investigated whether non-invasive alternating, low-intensity induced electric fields (iEFs) could suppress tumor growth and metastasis while modulating anti-tumor immunity in TNBC.</p><p><strong>Methods: </strong>Orthotopic TNBC mouse models were treated with alternating (100 kHz) and low-intensity (2.7 mV/cm peak), induced electric fields (iEFs), which were delivered non-invasively via a solenoid coil system. Tumor growth and lung metastasis were assessed following treatment. Immune profiling was performed to evaluate changes in T cell states and myeloid cell populations within both primary tumors and metastatic lung tissue.</p><p><strong>Results: </strong>iEF treatment significantly reduced primary tumor growth (n=9) and lung metastases (n=5). Within the tumor microenvironment, iEFs decreased infiltration of immunosuppressive myeloid cells (n=8). In the lung metastatic niche, iEF therapy increased CD8+ T cell abundance while reducing immunosuppressive myeloid populations (n=8). We also observed that iEFs reduced the metastatic potential of cancer cells by inhibiting epithelial-to-mesenchymal transition (n=3).</p><p><strong>Conclusion: </strong>Induced electric field therapy enhances anti-tumor immunity and suppresses metastatic progression in TNBC by enhancing T cell activity and remodeling immunosuppressive myeloid environments. These findings support iEFs as a promising non-invasive immunomodulatory strategy for metastatic TNBC.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"604098"},"PeriodicalIF":3.6,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13282987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293211","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}
Guanling Chen, Baoliang Yin, Muhammad Khan, Yipeng Yang, Qian Sun, Tingfeng Zhang, Hong Hu, Jie Lin
{"title":"Pan-Cancer Analysis of a Depression-Related Gene Signature Identifies an Immunosuppressive Tumor Microenvironment and Links to Immunotherapy Response in Breast Cancer.","authors":"Guanling Chen, Baoliang Yin, Muhammad Khan, Yipeng Yang, Qian Sun, Tingfeng Zhang, Hong Hu, Jie Lin","doi":"10.2147/BCTT.S578930","DOIUrl":"10.2147/BCTT.S578930","url":null,"abstract":"<p><strong>Background: </strong>Depression has been increasingly associated with cancer progression and patient outcomes, yet its molecular and immunological correlates within tumors remain incompletely understood. This study aimed to investigate depression-associated gene signature across cancers and evaluate their relationship with tumor biology, immune microenvironment, and clinical outcomes, with a focus on breast cancer.</p><p><strong>Methods: </strong>A depression-related gene signature comprising 382 genes was obtained from the Molecular Signatures Database and used to compute a DScore via single-sample gene set enrichment analysis (ssGSEA) across over 10,000 tumor samples from 33 cancer types in The Cancer Genome Atlas (TCGA). Tumor microenvironment features were assessed using ESTIMATE and CIBERSORT, and cell-type-specific patterns were evaluated using single-cell RNA sequencing. CACNA1H was validated using qPCR and IHC in breast cancer samples.</p><p><strong>Results: </strong>DScore exhibited tissue-specific patterns across cancers and was elevated in several tumor types, including gastrointestinal, brain, renal, and endocrine malignancies. Higher DScore was associated with older age, advanced stage, and poorer survival across multiple malignancies, including breast, ovarian, uterine, and lung cancers, whereas inverse associations with survival were observed in selected brain, kidney, and endocrine cancers. Higher DScore was further associated with genomic instability, an immunosuppressive tumor microenvironment (TME), and poorer survival across multiple cancers, particularly in breast and ovarian cancers. In breast cancer, this phenotype was characterized by monocytic-lineage enrichment, increased M2 macrophages, and reduced CD8⁺ T-cell infiltration. Consistent with these findings, higher DScore was associated with reduced benefit from immune checkpoint therapy in breast and bladder cancers, with non-responders exhibiting higher DScore predominantly enriched in monocytic-lineage cells. CACNA1H was identified as a depression-related gene correlated with poor prognosis in breast cancer and was validated in independent cohorts.</p><p><strong>Conclusion: </strong>Depression-associated gene expression patterns are linked to tumor biology and immune features across cancers, with particularly strong relevance in breast cancer. These findings highlight the need for further research into how psychological, molecular, and immune factors interact in cancer progression and treatment response.</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"578930"},"PeriodicalIF":3.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148270212","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":"Rab1A-Mediated Exosomal Sorting of miR-200c Enhances Breast Cancer Lung Metastasis [Retraction].","authors":"","doi":"10.2147/BCTT.S631806","DOIUrl":"https://doi.org/10.2147/BCTT.S631806","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/BCTT.S400974.].</p>","PeriodicalId":9106,"journal":{"name":"Breast Cancer : Targets and Therapy","volume":"18 ","pages":"631806"},"PeriodicalIF":3.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148275966","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}