Epithelial Expressed B7-H4 Drives Differential Immunotherapy Response in Murine and Human Breast Cancer.
Elizabeth C WescottXiaopeng SunPaula I Gonzalez EricssonAnn HannaBrandie C TaylorVioleta SanchezJuliana BronziniSusan R OpalenikMelinda E SandersJulia D WulfkuhleRosa I GallagherHenry L GómezClaudine IsaacsVijaya BhartiJohn Tanner WilsonTarah Jean BallingerCesar A Santa-MariaPayal Deepak ShahElizabeth C DeesBrian D LehmannVandana G AbramsonGillian L HirstLamorna Brown SwigartLaura van 't VeerLaura J EssermanEmanuel F PetricoinJennifer A PietenpolJustin M BalkoPublished in: Cancer research communications (2024)
This translational study confirms the association of B7-H4 expression with a cold immune microenvironment in breast cancer and offers preclinical studies demonstrating a potential role for B7-H4 in suppressing response to checkpoint therapy. However, analysis of two clinical trials with checkpoint inhibitors in the early and metastatic settings argue against B7-H4 as being a mechanism of clinical resistance to checkpoints, with clear implications for its candidacy as a therapeutic target.
Keyphrases
- dna damage
- clinical trial
- cell cycle
- endothelial cells
- poor prognosis
- stem cells
- squamous cell carcinoma
- small cell lung cancer
- cell therapy
- signaling pathway
- induced pluripotent stem cells
- binding protein
- oxidative stress
- randomized controlled trial
- pluripotent stem cells
- mesenchymal stem cells
- replacement therapy
- breast cancer risk
- smoking cessation
- double blind
- placebo controlled