ITPKB suppresses ER calcium release to promote CXCL9 expression and enhance immunotherapy sensitivity in triple-negative breast cancer
A new calcium-signaling pathway in breast cancer controls immune cell recruitment, suggesting a target to help immunotherapy work better.
ITPKB (inositol-trisphosphate 3-kinase B) was mechanistically linked to ER calcium homeostasis and CXCL9 chemokine regulation in triple-negative breast cancer, with loss of ITPKB reducing immunotherapy sensitivity. This identifies a novel ER-calcium–CXCL9 axis as a determinant of TNBC immune microenvironment and immunotherapy response.
What the study was
- Study design
- preclinical_in_vitro
- Category
- novel_therapeutics_immunotherapy_cart_targeted
- Maturity
- Exploratory
- Journal
- Drug Resistance Updates
Why it surfaced
Drug Resist Updat (high-IF) mechanistic study linking novel ITPKB-ER calcium-CXCL9 axis to immunotherapy resistance in TNBC. Core T6 hit; TNBC has extremely high unmet need.
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