Epstein–Barr virus (EBV) is responsible for approximately 9% of stomach adenocarcinomas. EBV-encoded microRNAs have been reported as reducing the function of the class I major histocompatibility complex (MHC-I) antigen presentation apparatus, which could allow infected cells to evade adaptive immune responses. Using data from nearly 400 human gastric carcinomas (GCs), we assessed the impact of EBV on MHC-I heavy and light chain mRNA levels, as well as multiple other components essential for antigen processing and presentation. Unexpectedly, mRNA levels of these genes were as high, or higher, in EBV-associated gastric carcinomas (EBVaGCs) compared to normal control tissues or other GC subtypes. This coordinated upregulation could have been a consequence of the higher intratumoral levels of interferon γ in EBVaGCs, which correlated with signatures of increased infiltration by T and natural killer (NK) cells. These results indicate that EBV-encoded products do not effectively reduce mRNA levels of the MHC-I antigen presentation apparatus in human GCs.

Lymphedema is a common complication after breast cancer surgery, often causing functional limitations and reduced quality of life. Prophylactic compression sleeves have been suggested as a preventive strategy, but their effectiveness remains unclear. We conducted a systematic review of randomized controlled trials to evaluate whether early use of compression sleeves lowers the risk of lymphedema in this population. Comprehensive searches of major medical databases were performed, and eligible studies were analyzed. The findings showed that prophylactic compression sleeves did not significantly reduce the incidence of lymphedema compared with standard care. Some studies reported smaller increases in arm volume among sleeve users, but these results were inconsistent. Overall, compression sleeves appear to have limited value for lymphedema prevention, though they may provide modest benefit in reducing early swelling. Further high-quality research is needed to establish clear recommendations for clinical practice.

Background: Neoadjuvant partial breast irradiation using stereotactic body radiotherapy (SBRT) has emerged as a strategy to induce tumor and immune responses in early-stage, low-risk breast cancer. While prior studies have demonstrated encouraging response rates and evidence of immune modulation, the optimal radiotherapy regimen for immune priming remains unclear. SIGNAL 2.0 is a randomized phase II trial designed to compare the biological and immunological impact of a single-fraction versus three-fraction neoadjuvant SBRT. Materials and Methods: Sixty-one postmenopausal patients ≥ 50 years with unifocal, hormone positive, node-negative invasive ductal carcinoma < 3 cm were randomized 1:1 to receive either 21 Gy in one fraction or 30 Gy in three fractions, delivered to the tumor in the prone position. Core biopsies were collected pre-SBRT and 14–20 days post-SBRT at the time of surgery. Immune markers were assessed using tumor-infiltrating lymphocyte (TIL) scoring, NanoString nCounter PanCancer Immune Profiling, and NanoString GeoMx Digital Spatial Profiling (DSP). Results: Available tumor samples from 47 patients underwent paired tissue analysis. Three-fraction SBRT induced 200 differentially expressed genes, including enrichment of pathways related to adaptive immune activation, with significant increases in expression levels of macrophages, dendritic cells, neutrophils and CD8 T-cells. Proteomic profiling also identified a significant increase in the expression levels of neutrophils, Treg cells, macrophages, and NK cells in the tumor microenvironment of the samples from patients receiving the three-fraction regimen. Conclusions: Neoadjuvant SBRT induces measurable immune activation, with three-fraction regimens generating more extensive transcriptional, proteomic, and cellular immune changes than a single fraction. Three-fraction neoadjuvant SBRT may provide superior immune priming, providing a foundation for future trials integrating neoadjuvant radiotherapy with immunomodulatory therapies.

Breast cancer incidence increases with age, but the molecular features of cancers arising in older patients remain poorly characterized. We examined the age-associated differences in clinicopathologic characteristics, transcriptional pathways, and tumour microenvironment signatures using clinical and gene-expression data from three large cohorts. Patients were grouped as younger than 45, 45–64, or 65 years and older; the oldest group was further divided into 65–74, 75–84, and 85 years and older. Among the included 6323 patients, those younger than 45 had a higher proportion of hormone-receptor negative subtypes and grade 3 tumours with enrichment of proliferation-related pathways. Comparisons between patients aged 65–74 and 75–84 did not show a consistent shift towards markers of less aggressive tumour biology. Instead, metabolic-related differences such as in oxidative phosphorylation, glycolysis, and mechanistic target of rapamycin complex 1 signalling were noted. Immune cell signature differences were most evident in younger hormone-receptor positive tumours. These findings overall support evaluating tumour biology instead of chronological age in guiding future treatment strategies and research.