ArticleDiscover oncology2025
CCR5 expression and conformational stability as potential cooperative modulators of immune phenotypes and therapy response in breast cancer.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundCCR5 is a chemokine receptor involved in immune regulation and tumor progression. Its role in predicting therapy response in breast cancer remains unclear.
methodsWe evaluated CCR5 protein expression in a clinical cohort of 66 breast cancer patients treated with NAC, assessing its association with pathological complete response (pCR). Prognostic relevance was validated in the Kaplan-Meier Plotter database. We further investigated CCR5's predictive value in a cohort receiving chemo-immunotherapy (GSE173839). Immune-related transcriptional features were assessed via GSEA and deconvolution analysis. The structural impact of the V131I CCR5 variant was explored using AlphaFold modeling, molecular dynamics simulations, and AI-based protein stability prediction.
resultsHigh CCR5 expression was associated with reduced pCR rates in the NAC cohort (OR = 0.06, P = 0.012) and with poorer RFS, particularly in HER2-negative subtypes (P = 0.009). In contrast, CCR5-high tumors in the chemo-immunotherapy cohort exhibited significantly higher pCR rates (OR = 2.5, P = 0.046), suggesting a suppressed yet immune-infiltrated microenvironment potentially responsive to immune reactivation. GSEA analysis and immune cell infiltration profiling indicate a coexistence of immune activation and immunosuppression. Structural modeling of the V131I variant suggested increased conformational flexibility and reduced stability of CCR5, implying a potential sensitivity to subtle structural perturbations.
conclusionOur study supports a dual regulatory hypothesis, in which CCR5 expression may influence immune dynamics and therapeutic response, while its structural stability may serve as a potential modulatory factor. This hypothesis-generating observation suggests that CCR5 could represent a potential prognostic and predictive biomarker, particularly in NAC-refractory or immune-inflamed breast cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.