ArticleCancer discovery2022
Tumor ENPP1 (CD203a)/Haptoglobin Axis Exploits Myeloid-Derived Suppressor Cells to Promote Post-Radiotherapy Local Recurrence in Breast Cancer.
Article in Cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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
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Who cites it
48 citing papers in PubMed, 63 citations in OpenAlex.
- From initial complete response to recurrence: ENPP1 mutation drives cisplatin resistance through STING/NF-κB/IL-6 axis in hypopharyngeal squamous cell carcinoma.British journal of cancer · 2026Article
- A mammary-specific microfluidic device for studying post-radiotherapy vascular-immune cell interactions.bioRxiv : the preprint server for biology · 2026Article
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- Beyond radiation: immunological potentials of boron neutron capture therapy.Cancer immunology, immunotherapy : CII · 2026Review
- PMN-MDSCs-derived exosomal S100A9 drives breast cancer progression by enhancing cancer stemness and CXCL5-mediated metastatic potential.Cell death discovery · 2026Article
- CTSC Confers Radioresistance in Hepatocellular Carcinoma by Regulating Myeloid-Derived Suppressor Cells.Journal of cellular and molecular medicine · 2026Article
- The cGAS-STING pathway in cancer: friend or foe.Cell death & disease · 2026Review
- Tanshinone IIA&Icaritin -MPs regulated vascular normalization and restored tumor-infiltrating T lymphocyte function to boost anti-PD-1 therapy in melanoma lung metastasis.Journal of nanobiotechnology · 2026Article
- Tumor-derived neutrophil extracellular trap-associated DNA impairs treatment efficacy in breast cancer via CCDC25-dependent epithelial-mesenchymal transition.The Journal of clinical investigation · 2026Article
- Targeting the tripartite axis of immune-metabolic-spatial crosstalk to overcome therapy resistance in breast cancer.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in tumor microenvironment for radiotherapy: friend or foe?Frontiers in immunology · 2026Review
- JUN-ENPP1-cGAS-STING axis mediates immune evasion and tumor progression in bladder cancer.Journal of translational medicine · 2025Article
- Neutrophils and neutrophil extracellular traps: double-edged swords in cancer pathophysiology and therapy resistance.Cell communication and signaling : CCS · 2025Review
- Circulating tumour cells for the prediction of the response to radiation therapy in prostate cancer.The British journal of radiology · 2025Review
- ENPP1 inhibitor with ultralong drug-target residence time as an innate immune checkpoint blockade cancer therapy.Cell reports. Medicine · 2025Article
- Neutrophil extracellular traps in tumor metastasis: mechanisms, and therapeutic implications.Discover oncology · 2025Review
- Target neutrophil heterogeneity and plasticity in cancer.Journal of hematology & oncology · 2025Review
- Dual ENPP1/ATM depletion blunts DNA damage repair boosting radioimmune efficacy to abrogate triple-negative breast cancer.Signal transduction and targeted therapy · 2025Article
- Co-targeting of epigenetic regulators and BCL-XL improves efficacy of immune checkpoint blockade therapy in multiple solid tumors.Molecular cancer · 2025Article
- Abnormal proportions and functions of myeloid-derived suppressor cells in peripheral blood of patients with diffuse large B-cell lymphoma.BMC cancer · 2025Article
Corrections and comments
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Authors and funding
32 authors at 7 institutions in 4 countries.
Funding
Abstract
abstractLocoregional failure (LRF) in patients with breast cancer post-surgery and post-irradiation is linked to a dismal prognosis. In a refined new model, we identified ectonucleotide pyrophosphatase/phosphodiesterase 1/CD203a (ENPP1) to be closely associated with LRF. ENPP1hi circulating tumor cells (CTC) contribute to relapse by a self-seeding mechanism. This process requires the infiltration of polymorphonuclear myeloid-derived suppressor cells and neutrophil extracellular trap (NET) formation. Genetic and pharmacologic ENPP1 inhibition or NET blockade extends relapse-free survival. Furthermore, in combination with fractionated irradiation, ENPP1 abrogation obliterates LRF. Mechanistically, ENPP1-generated adenosinergic metabolites enhance haptoglobin (HP) expression. This inflammatory mediator elicits myeloid invasiveness and promotes NET formation. Accordingly, a significant increase in ENPP1 and NET formation is detected in relapsed human breast cancer tumors. Moreover, high ENPP1 or HP levels are associated with poor prognosis. These findings unveil the ENPP1/HP axis as an unanticipated mechanism exploited by tumor cells linking inflammation to immune remodeling favoring local relapse. SIGNIFICANCE: CTC exploit the ENPP1/HP axis to promote local recurrence post-surgery and post-irradiation by subduing myeloid suppressor cells in breast tumors. Blocking this axis impairs tumor engraftment, impedes immunosuppression, and obliterates NET formation, unveiling new opportunities for therapeutic intervention to eradicate local relapse and ameliorate patient survival. This article is highlighted in the In This Issue feature, p. 1171.
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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.