A novel mechanism of immunoevasion by ER+ breast cancer

Claudia Galassi; Lorenzo Galluzzi

doi:10.1016/j.it.2025.12.003

A novel mechanism of immunoevasion by ER⁺ breast cancer

Trends Immunol. 2026 Jan;47(1):6-8. doi: 10.1016/j.it.2025.12.003. Epub 2025 Dec 17.

Authors

Claudia Galassi¹, Lorenzo Galluzzi²

Affiliations

¹ Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA. Electronic address: clg4005@med.cornell.edu.
² Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address: deadoc80@gmail.com.

PMID: 41412836
DOI: 10.1016/j.it.2025.12.003

Abstract

Estrogen receptor (ER)⁺ breast malignancies are poorly infiltrated by immune cells, hence exhibiting limited sensitivity to immune checkpoint inhibitors (ICIs). Recent data from Palomeque et al. demonstrate that ER signaling actively contributes to such an immunoevasive phenotype by preventing the nuclear factor LCOR from establishing an ICI-sensitive tumor microenvironment.

Keywords: CD8(+) cytotoxic T lymphocytes; PD-1; antigen processing and presentation; endocrine therapy; immunotherapy; three Cs.

MeSH terms

Animals
Breast Neoplasms* / drug therapy
Breast Neoplasms* / immunology
Breast Neoplasms* / metabolism
Breast Neoplasms* / pathology
Female
Humans
Immune Checkpoint Inhibitors / therapeutic use
Receptors, Estrogen* / metabolism
Signal Transduction
Tumor Escape*
Tumor Microenvironment / immunology

Substances

Receptors, Estrogen
Immune Checkpoint Inhibitors