NPJ Breast CancerPub Date : 2026-06-25DOI: 10.1038/s41523-026-00998-x
Martin Widschwendter, Rita Schmutzler, Nora Pashayan, Jelle Wesseling, Marc Tischkowitz, Michal Zikan, Miranda Steenbeek, Marike Gabrielson, Christian F Singer, Cathrin Brisken, Rebecca Gomperts, Sharon Cameron, Dafydd Gareth Evans, Andri Papakonstantinou, Marc Buyse, Kerstin Rhiem, Mateja Krajc, Charlotte Vavourakis, Elisa Redl, Chiara Herzog, James Barrett, Mohammed Fatih Rasul, Deborah Utjés, Kiriaki Papaikonomou, Angelique Flöter Rådestad, Athanasios Zouzos, Twana Alkasalias, Kristina Gemzell-Danielsson
{"title":"Individualised progesterone receptor modulator prevention strategies for triple-negative breast cancer in BRCA1 pathogenic variant carriers.","authors":"Martin Widschwendter, Rita Schmutzler, Nora Pashayan, Jelle Wesseling, Marc Tischkowitz, Michal Zikan, Miranda Steenbeek, Marike Gabrielson, Christian F Singer, Cathrin Brisken, Rebecca Gomperts, Sharon Cameron, Dafydd Gareth Evans, Andri Papakonstantinou, Marc Buyse, Kerstin Rhiem, Mateja Krajc, Charlotte Vavourakis, Elisa Redl, Chiara Herzog, James Barrett, Mohammed Fatih Rasul, Deborah Utjés, Kiriaki Papaikonomou, Angelique Flöter Rådestad, Athanasios Zouzos, Twana Alkasalias, Kristina Gemzell-Danielsson","doi":"10.1038/s41523-026-00998-x","DOIUrl":"10.1038/s41523-026-00998-x","url":null,"abstract":"<p><p>Women with germline BRCA1 pathogenic variants face a very high risk of early-onset triple-negative breast cancer (TNBC), with risk-reducing mastectomy currently the only established preventive option. Emerging evidence suggests aberrant progesterone signalling contributes to TNBC risk, while preclinical studies indicate progesterone receptor modulators such as mifepristone may substantially reduce cancer development. DNA methylation-based markers reflecting field cancerization and replicative age could enable real-time monitoring of preventive efficacy and support an individualised primary prevention approach.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-24DOI: 10.1038/s41523-026-00982-5
Yifei Chen, Binliang Liu, Zhanhong Chen, Ping Huang, Xiaohong Wu, Ying Zhang, Tao Sun, Fangyuan Dong, Tao Wu, Hong Zong, Lu Gan, Bin Shao, Quchang Ouyang
{"title":"Anlotinib-containing regimens in HR+ advanced breast cancer after prior CDK4/6 inhibitor progression.","authors":"Yifei Chen, Binliang Liu, Zhanhong Chen, Ping Huang, Xiaohong Wu, Ying Zhang, Tao Sun, Fangyuan Dong, Tao Wu, Hong Zong, Lu Gan, Bin Shao, Quchang Ouyang","doi":"10.1038/s41523-026-00982-5","DOIUrl":"10.1038/s41523-026-00982-5","url":null,"abstract":"<p><p>This retrospective study (NCT06734533, registered in ClinicalTrials.gov on November 3, 2024) evaluated the efficacy and safety of anlotinib-containing regimens in patients with HR + /HER2- advanced breast cancer who have progressed on prior CDK4/6 inhibitor therapy. From January 2020 to March 2025, 80 patients were included. With a median follow-up of 9.2 months, the median progression-free survival was 6.4 months (95% CI, 5.2-7.1). Age ≥ 60 years and bone metastasis were identified as poor predictors of PFS, whereas prior treatment with CDK4/6 inhibitor for ≥ 6 months was a favorable predictor. The objective response rate and disease control rate were 30.0% (95% CI, 19.6-42.1) and 87.1% (95% CI, 77.3-93.1), respectively. Grade 3-4 adverse events were observed in 10 patients (12.5%), with the most common being neutropenia (3.8%) and aspartate aminotransferase increased (3.8%). Given the retrospective design and potential confounding of this analysis, these findings should be interpreted with caution. Anlotinib-containing regimens showed potential clinical activity in this patient population and warrant further evaluation.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multimodal imaging and artificial intelligence for response assessment to neoadjuvant therapy in breast cancer: a comprehensive review.","authors":"Linlin Shao, Mingyu Zhang, Lili Zhang, Fangfang Sun, Hongyu Li, Jiangbo Shao, Yansong Liu, Xinyue Liu, Feng Hu, Lirong Zhao","doi":"10.1038/s41523-026-00995-0","DOIUrl":"10.1038/s41523-026-00995-0","url":null,"abstract":"<p><p>This narrative review explores the latest advancements in various imaging modalities combined with artificial intelligence (AI) for monitoring response to neoadjuvant therapy (NT) and predicting pathological complete response (pCR). We provide a detailed analysis of the principles, evaluation metrics, strengths, and limitations of each technique. The integration of multimodal imaging and AI is reshaping the paradigm for evaluating NT efficacy in breast cancer, offering robust support for precision medicine.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-22DOI: 10.1038/s41523-026-00994-1
Clara Bodelon, Mohamed Amgad, James M Hodge, Maha A T Elsebaie, Mariah Landry, Cheng Peng, Rulla M Tamimi, Peter Kraft, Lauren E McCullough, Mark E Sherman, Mia M Gaudet, Alpa V Patel, Lee A D Cooper, Lauren R Teras
{"title":"Effects of breast cancer risk factors on the tumor microenvironment: a morphological deep-learning analysis of three prospective cohorts.","authors":"Clara Bodelon, Mohamed Amgad, James M Hodge, Maha A T Elsebaie, Mariah Landry, Cheng Peng, Rulla M Tamimi, Peter Kraft, Lauren E McCullough, Mark E Sherman, Mia M Gaudet, Alpa V Patel, Lee A D Cooper, Lauren R Teras","doi":"10.1038/s41523-026-00994-1","DOIUrl":"10.1038/s41523-026-00994-1","url":null,"abstract":"<p><p>Emerging evidence suggests a critical role of the tumor microenvironment (TME) in breast cancer (BC) development and outcomes, yet factors that modify the TME are poorly understood. We investigated the relationship between BC etiological factors and the tumor and TME using 110 histological features of the epithelium, stroma, and immune infiltration, computationally quantified in 3724 H&E slides from three prospective cohort studies. Age, race, hormonal, and lifestyle factors were associated with features of the breast TME. Menopausal hormone therapy was associated with epithelial and stromal features found in less aggressive tumors, while higher body mass index (BMI) was associated with two histological features not captured by grade, and both were associated with poor prognosis. These two features mediated the BMI and BC-specific mortality association by 18.1%. Our findings provide novel insights into the role of etiological factors on the TME including modifiable factors that have implications for prevention and outcomes.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-20DOI: 10.1038/s41523-026-00990-5
Jee Eun Choi, Qi Yan, Jianmin Wang, Nicholas J Salgia, Jason B Muhitch, Cameron R MacDonald, Nathan T Roberts, Caitlin M James, Philip L McCarthy, Hemn Mohammadpour, Saeed Daneshmandi, Elizabeth A Repasky
{"title":"The suppressive function of ILC2 cells is regulated by β2-adrenergic receptor signaling in breast cancer.","authors":"Jee Eun Choi, Qi Yan, Jianmin Wang, Nicholas J Salgia, Jason B Muhitch, Cameron R MacDonald, Nathan T Roberts, Caitlin M James, Philip L McCarthy, Hemn Mohammadpour, Saeed Daneshmandi, Elizabeth A Repasky","doi":"10.1038/s41523-026-00990-5","DOIUrl":"10.1038/s41523-026-00990-5","url":null,"abstract":"<p><p>Type II innate lymphoid cells (ILC2s) have been implicated in both tumor-promoting and tumor-suppressive functions, but the mechanism(s) underlying this functional heterogeneity is not clear. Here, we tested the hypothesis that signaling through β2-adrenergic receptor (β2-AR) drives the pro-tumor functions of ILC2s within the tumor microenvironment. Using global (β2AR<sup>-</sup>/<sup>-</sup>) and ILC2-specific conditional knockout (IL5<sup>Cre</sup>β2AR<sup>fl/fl</sup>) mouse models, we examined how β2-AR deficiency affects ILC2 function in breast cancer. We studied the impact of β2-AR function on ILC2 phenotype, gene profile, anti-tumor T cell response and breast tumor growth. β2AR inhibition resulted in an enrichment of KLRG1⁺ ILC2s with elevated GATA3 and ST2 expression in breast tumor. Loss of β2-AR signaling in ILC2s reduced their pro-tumorigenic activity and resulted in suppressed tumor growth. Additionally, β2-AR inhibition in ILC2s was associated with increased CD4⁺ T cell infiltration in breast tumors and a greater TNF-α<sup>+</sup> CD8<sup>+</sup> T cell response. β2-AR deficiency reprograms ILC2s toward a more immunostimulatory phenotype, promoting T cell-mediated anti-tumor immunity. These findings identify activity of the β2-AR as a key regulator of ILC2 plasticity and suggest β2-AR blockade as a promising strategy to enhance cancer immunotherapy.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Predicting early-stage breast cancer disease-free survival and adjuvant therapy benefit from multimodal information using deep learning.","authors":"Yifan Yu, Zeyan Xu, Zejun Zhu, Jiayi Liao, Xu Huang, Kexin Chen, Zaiyi Liu, Ying Wang, Changhong Liang, Lei Wu","doi":"10.1038/s41523-026-00991-4","DOIUrl":"10.1038/s41523-026-00991-4","url":null,"abstract":"<p><p>Accurate prediction of disease-free survival (DFS) is essential for tailoring adjuvant regimens and improving clinical outcomes in early-stage breast cancer (EBC). A multimodal deep learning model (Mu-model) based on deep canonical correlation analysis (DCCA) integrating multiparametric magnetic resonance imaging (MRI)-including dynamic contrast-enhanced MRI (DCE-MRI) and diffusion-weighted imaging (DWI)-with clinical text data is developed to predict DFS and identify patients likely to benefit from adjuvant therapy. This multicenter retrospective study includes 1,120 patients with EBC (training cohort, n = 459; external validation cohort, n = 661). The Mu-model achieves concordance index (C-index) values of 0.742 (95% confidence interval [CI]: 0.662-0.821) in the training cohort (TC) and 0.735 (95% CI: 0.667-0.803) in the external validation cohort (EVC) for DFS. The Mu-model score (MuS) remains an independent prognostic factor after adjustment for clinicopathologic variables (all P < 0.05). In human epidermal growth factor receptor 2 (HER2)-positive, hormone receptor (HR)-positive, and T2-stage subgroups, a significant survival benefit associated with adjuvant therapy was observed in patients with low MuS, whereas no statistically significant association was detected in patients with high MuS. Transcriptomic analysis in 19 patients indicates that high MuS is associated with immune activation and enrichment of cell-cycle and purine-metabolism pathways. The Mu-model provides non-invasive DFS prediction and recurrence risk stratification, while preliminarily exploring its potential to identify patients who may derive differential benefits from adjuvant therapy.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-17DOI: 10.1038/s41523-026-00993-2
Laia Monserrat, Judith García-García, Cristina Molina, Andreu Òdena, Taras Yuziv Duda, Irene Agustí-Barea, Gilles Flamen, Cristina Viaplana, Aerica Nagornyuk, Ruth Maldonado-Padrol, Claudia Yáñez-Bartolomé, Flaminia Pedretti, Marta Guzmán, Olga Rodríguez, Fara Brasó-Maristany, Eduardo García-Galea, Rodrigo Dienstmann, Motoki Takaku, Aleix Prat, Sarat Chandarlapaty, Julia Ponomarenko, Cristina Saura, Mafalda Oliveira, Lara Nonell, Meritxell Bellet, Guillermo P Vicent, Violeta Serra
{"title":"Exploiting androgen receptor agonism as a treatment strategy in estrogen receptor-positive metastatic breast cancer.","authors":"Laia Monserrat, Judith García-García, Cristina Molina, Andreu Òdena, Taras Yuziv Duda, Irene Agustí-Barea, Gilles Flamen, Cristina Viaplana, Aerica Nagornyuk, Ruth Maldonado-Padrol, Claudia Yáñez-Bartolomé, Flaminia Pedretti, Marta Guzmán, Olga Rodríguez, Fara Brasó-Maristany, Eduardo García-Galea, Rodrigo Dienstmann, Motoki Takaku, Aleix Prat, Sarat Chandarlapaty, Julia Ponomarenko, Cristina Saura, Mafalda Oliveira, Lara Nonell, Meritxell Bellet, Guillermo P Vicent, Violeta Serra","doi":"10.1038/s41523-026-00993-2","DOIUrl":"10.1038/s41523-026-00993-2","url":null,"abstract":"<p><p>The androgen receptor (AR) is expressed in 75% of estrogen receptor-positive (ER+) breast cancers (BC). Selective AR modulators (SARMs), like EP0062, present a promising therapeutic strategy for ER + BC, particularly in patients who cannot tolerate endocrine therapy (ET) or whose tumors have developed resistance. We aimed to study the antitumor activity of EP0062 in ER+ patient-derived xenograft (PDX) models. EP0062 displayed comparable antitumor efficacy to selective ER degraders (SERDs), including in PDXs with ESR1, PIK3CA, or PTEN mutations. Tumors sensitive to SARMs were enriched in GATA3 mutations. EP0062 treatment induced AR-target genes across all models tested. A transcriptional signature associated with SARM sensitivity was identified, primarily driven by proliferation-related processes, consistent with a significant decrease in S-phase cell cycle proteins upon treatment in EP0062-sensitive models. In some EP0062-resistant tumors, the combination with palbociclib enhanced the antitumor effect of EP0062, suggesting a potential strategy for metastatic patients with acquired ET resistance.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-15DOI: 10.1038/s41523-026-00992-3
Cezary Cybulski, Wojciech Kluźniak, Dominika Wokołorczyk, Neda Zamani, Klaudia Stempa, Katarzyna Gliniewicz, Tomasz Huzarski, Michal Falco, Ping Sun, Jacek Gronwald, Jan Lubiński, Steven Narod, Mohammad R Akbari
{"title":"PCSK9 rs562556 variant and survival in BRCA1 mutation carriers and mutation-negative familial breast cancer.","authors":"Cezary Cybulski, Wojciech Kluźniak, Dominika Wokołorczyk, Neda Zamani, Klaudia Stempa, Katarzyna Gliniewicz, Tomasz Huzarski, Michal Falco, Ping Sun, Jacek Gronwald, Jan Lubiński, Steven Narod, Mohammad R Akbari","doi":"10.1038/s41523-026-00992-3","DOIUrl":"10.1038/s41523-026-00992-3","url":null,"abstract":"<p><p>Breast cancer etiology involves a complex interplay of various risk factors, with genetic alterations playing a significant role in susceptibility to the disease. While mutations in genes such as BRCA1 and BRCA2 are well established in elevating breast cancer risk, their potential role in predicting metastatic progression remains unclear. A recent study by Mei et al. suggested that a common germline variant in the PCSK9 gene (rs562556) may increase metastasis risk and lower survival rates in breast cancer patients. To investigate this association, we evaluated the relationship between the PCSK9 rs562556 variant genotypes and survival outcomes in two cohorts: patients with BRCA1 mutations and those with familial breast cancer lacking mutations in known susceptibility genes. Our study included 1052 BRCA1 mutation carriers, 467 familial breast cancer patients of unknown genetic etiology, and 1404 controls. Genotyping was performed using TaqMan genotyping and whole-exome sequencing. Survival analyses were conducted using Kaplan-Meier survival curves and Cox proportional hazards models. We found no significant association between PCSK9 rs562556 variant and breast cancer mortality or time to death following distant recurrence in either cohort. This finding does not support PCSK9 prognostic impact in breast cancer that may be modified by additional genetic or environmental factors.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148259074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-12DOI: 10.1038/s41523-026-00986-1
S A Wander, C M Weipert, L Cabel, J Liao, N Zhang, A Safonov, A Bardia, P Razavi
{"title":"Real-world cell-free circulating tumor DNA (ctDNA) analysis identifies CDK4/6 inhibitor resistance and tumor evolution in HR+ advanced breast cancer.","authors":"S A Wander, C M Weipert, L Cabel, J Liao, N Zhang, A Safonov, A Bardia, P Razavi","doi":"10.1038/s41523-026-00986-1","DOIUrl":"https://doi.org/10.1038/s41523-026-00986-1","url":null,"abstract":"<p><p>A large clinical-genomic database was used to assess circulating tumor DNA (ctDNA) pre- and post-CDK4/6 inhibitor (CDK4/6i) plus endocrine therapy (ET) treatment in a cohort of patients with HR+/HER2- metastatic breast cancer (mBC). A panel of putative resistance alterations to CDK4/6i + ET (CDK4/6i+ET-R) was developed based upon previous studies. Patients with ≥1 baseline CDK4/6i + ET-R were compared to patients without CDK4/6i + ET-R, and univariate and multivariate analyses were performed to assess differences in real-world time to treatment discontinuation (rwTTD), real-world time to next treatment (rwTTNT), and overall survival (OS). ESR1 and RB1 alterations were significantly more frequent post-CDK4/6i. Patients with CDK4/6i + ET-R mutations prior to CDK4/6i treatment had significantly worse outcomes in terms of time on CDK4/6i and OS, suggesting that this resistance signature could prove useful in better refining personalized treatment selection in future clinical practice, though further exploration is needed.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NPJ Breast CancerPub Date : 2026-06-12DOI: 10.1038/s41523-026-00980-7
Ahmad Sami, Petra Seibold, Carsten Sticht, Frank A Giordano, Marlon R Veldwijk, Carsten Herskind
{"title":"Novel method for risk stratification of radiation-induced breast fibrosis: subgroup hypothesis verified by machine learning.","authors":"Ahmad Sami, Petra Seibold, Carsten Sticht, Frank A Giordano, Marlon R Veldwijk, Carsten Herskind","doi":"10.1038/s41523-026-00980-7","DOIUrl":"10.1038/s41523-026-00980-7","url":null,"abstract":"<p><p>Breast fibrosis (BF) after radiotherapy remains one of the most dreaded late toxicities in breast cancer care, yet multiple additive predictors struggle to capture its underlying biological complexity. Radiation-induced lymphocyte apoptosis (RILA) has recently been associated with the risk of fibrosis more than 10 years post-RT. Here, we show that a combination of five independent factors, RILA, two SNPs in the CTGF and NBS1 genes, and two clinical variables (body-mass index and hypertension) exhibits several important interactions. Partition analysis identified six partly nested subgroups, which could be consolidated into three clinically meaningful risk groups. Machine-learning modelling verified and refined these groups, demonstrating a five-fold variation (17-83%) in BF risk with an AUC = 0.735 in ROC analysis using only these five features. Our study provides proof-of-concept that a biologically realistic subgroup-based approach sharpens predictive performance and may enable clinical identification of a subgroup of breast cancer patients highly susceptible to BF.</p>","PeriodicalId":19247,"journal":{"name":"NPJ Breast Cancer","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13279946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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