What question did this study set out to answer?

Investigate how ENTPD1/CD39 expression coordinates myeloid and T-cell immunosuppressive states and influences clinical outcomes in triple-negative breast cancer.

August 16, 2026Breast Cancer ResearchOpen Access

CD39-associated myeloid-T-cell coordination within an immunoregulatory neighborhood linked to treatment resistance in triple-negative breast cancer

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Authors

ZHZihan Hu HZHaoyu Zheng CJCheng Jin

Discussion

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Overview

Multi-omic profiling demonstrates that high CD39 expression drives immunosuppressive cellular interactions in triple-negative breast cancer, indicating a key mechanism of immunotherapy resistance.

Key Points

Investigate how ENTPD1/CD39 expression coordinates myeloid and T-cell immunosuppressive states and influences clinical outcomes in triple-negative breast cancer.
Re-analyzed single-cell RNA sequencing data from 156,120 immune cells across 27 tumor and metastatic samples from 14 patients with TNBC, validated with spatial transcriptomics and multiplex immunofluorescence.
Assessed CD39 protein expression and overall survival in an independent clinical cohort of 112 patients with TNBC using immunohistochemistry and multivariable Cox proportional hazards regression.
High macrophage ENTPD1 expression was associated with M2-like macrophage polarization, attenuated STING-type I interferon signaling, reduced antigen presentation, and preferential interactions with CD4+ CD39+ regulatory T cells.
Lymphotoxin signaling between CD4+ CD39+ T cells and myeloid populations was enriched in patients who did not respond to anti-PD-L1 plus chemotherapy.
High tissue-level CD39 protein expression was independently associated with shorter overall survival after adjusting for age group and AJCC stage.

Cite This Study

Hu et al. (2026) studied this question.

synapsesocial.com/papers/6a817a4cf2fb91fc834adf99 https://doi.org/10.1186/s13058-026-02375-9

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August 16, 2026Breast Cancer ResearchOpen Access

CD39-associated myeloid-T-cell coordination within an immunoregulatory neighborhood linked to treatment resistance in triple-negative breast cancer

View Full Paper

Ask AI

Bookmark

Authors

ZHZihan Hu HZHaoyu Zheng CJCheng Jin

Discussion

Member takes

Overview

Multi-omic profiling demonstrates that high CD39 expression drives immunosuppressive cellular interactions in triple-negative breast cancer, indicating a key mechanism of immunotherapy resistance.

Key Points

Investigate how ENTPD1/CD39 expression coordinates myeloid and T-cell immunosuppressive states and influences clinical outcomes in triple-negative breast cancer.
Re-analyzed single-cell RNA sequencing data from 156,120 immune cells across 27 tumor and metastatic samples from 14 patients with TNBC, validated with spatial transcriptomics and multiplex immunofluorescence.
Assessed CD39 protein expression and overall survival in an independent clinical cohort of 112 patients with TNBC using immunohistochemistry and multivariable Cox proportional hazards regression.
High macrophage ENTPD1 expression was associated with M2-like macrophage polarization, attenuated STING-type I interferon signaling, reduced antigen presentation, and preferential interactions with CD4+ CD39+ regulatory T cells.
Lymphotoxin signaling between CD4+ CD39+ T cells and myeloid populations was enriched in patients who did not respond to anti-PD-L1 plus chemotherapy.
High tissue-level CD39 protein expression was independently associated with shorter overall survival after adjusting for age group and AJCC stage.

Cite This Study

Hu et al. (2026) studied this question.

synapsesocial.com/papers/6a817a4cf2fb91fc834adf99 https://doi.org/10.1186/s13058-026-02375-9

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