ArticleOncoimmunology2025
PARP inhibitors accumulate B7-H3 on fibroblasts via blocking autophagic flux to potentiate immune evasion in ovarian cancer.
Article in Oncoimmunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Glutamine transporter SLC1A5 inhibits autophagy-mediated CD276 degradation to promote esophageal cancer progression.Cancer biology & therapy · 2026Article
- CD276 promotes lipid metabolic reprogramming and regulates ferroptosis in clear cell renal cell carcinoma by upregulating FASN expression via SREBP1.Human cell · 2026Article
- PIP4K2A Attenuates Cerebral Ischemia/Reperfusion Injury by Reducing the TRIB3-p62 Complex Burden and Modulating AKT/mTOR Signaling.Translational stroke research · 2026Article
- Low-affinity binding of anti-B7-H3 clone MJ18 to murine B7-H3 fails to induce tumor regression.Scientific reports · 2026Article
- The DDR-immune fitness score: a biomarker for guiding parp and immunotherapy synergy in extensive-stage small cell lung cancer.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
23 authors.
Funding
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Abstract
Besides targeting tumor cells via canonical synthetic lethality, poly(ADP-ribose) polymerase inhibitors (PARPis) can remodel tumor immune microenvironment (TIME), which then affects PARPis' anti-tumor capabilities. However, exact function of PARPis on TIME remains insufficiently explored. Here, by leveraging paired samples during neoadjuvant PARPi Niraparib treatment derived from a prospective clinical trial, we discovered that the expression of immune checkpoint ligand B7-H3 was induced by PARPis in cancer-associated fibroblasts (CAFs) of ovarian cancer. Depletion of B7-H3 in CAFs by using host
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