ArticleActa neuropathologica communications2025
Genomic and immune profiling of breast cancer brain metastases.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- IRS2 as a driver and therapeutic target in brain metastases from colorectal cancer: a systematic review of mechanistic and translational evidence.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Spatial immune atlas of breast cancer brain metastasis reveals CD163Journal for immunotherapy of cancer · 2026Article
- MCLAM: a cost-effective deep learning model for predicting recurrence risk in HR+/HER2- breast cancer-a multi-center study in a Chinese cohort.Journal of the National Cancer Center · 2026Article
- Characterization, immune cell phenotyping and differential gene expression analysis of brain metastases and primary breast cancer samples.Scientific reports · 2026Article
- Breast Cancer Brain Metastases: Current Understanding and Future Directions.Current oncology reports · 2026Review
- Risk factors and predictive nomograms for early mortality in patients with thyroid cancer lung metastasis based on the SEER database and a Chinese population study.Gland surgery · 2025Article
- Novel treatment strategies and key research priorities for patients with breast cancer and central nervous system (CNS) metastases.NPJ breast cancer · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundBrain metastases (BrM) arising from breast cancer (BC) are an increasing consequence of advanced disease, with up to half of patients with metastatic HER2 + or triple negative BC experiencing central nervous system (CNS) recurrence. The genomic alterations driving CNS recurrence, along with contributions of the immune microenvironment, particularly by intrinsic subtype, remain unclear.
methodsWe characterized the genomic and immune landscape of BCBrM from a cohort of 42 patients by sequencing whole-exome DNA (WES) and total RNA libraries from frozen and FFPE BrM and FFPE extracranial tumors (ECT). Analyses included PAM50 intrinsic subtypes, somatic mutations, copy number variations (CNV), pathway alterations, immune cell type deconvolution, and associations with clinical outcomes
resultsIntrinsic subtype calls were concordant for the majority of BrM-ECT pairs (60%). Across all BrM and ECT samples, the most common somatic gene mutation was TP53 (64%, 30/47). For patients with matched FFPE BrM-FFPE ECT, alterations tended to be conserved across tissue type, although differential somatic mutations and CNV in specific genes were observed. Several genomic pathways were differentially expressed between patient-matched BrM-ECT; MYC targets, DNA damage repair, cholesterol homeostasis, and oxidative phosphorylation were higher in BrM, while immune-related pathways were lower in BrM. Deconvolution of immune populations between BrM-ECT demonstrated activated dendritic cell populations were higher in BrM compared to ECT. Increased expression of several oncogenic preselected pathways in BrM were associated with inferior survival, including DNA damage repair, inflammatory response, and oxidative phosphorylation
conclusionsCollectively, this study illustrates that while some genomic alterations are shared between BrM and ECT, there are also unique aspects of BrM including somatic mutations, CNV, pathway alterations, and immune landscape. A deeper understanding of differences inherent to BrM will contribute to the development of BrM-tailored therapeutic strategies. Additional analyses are warranted in larger cohorts, particularly with additional matched BrM-ECT.
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