Journal
CLINICAL BREAST CANCER
Volume 22, Issue 7, Pages 642-649Publisher
CIG MEDIA GROUP, LP
DOI: 10.1016/j.clbc.2022.06.004
Keywords
Estrogen receptor; Immunotherapy; PD-1; PD-L1
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Immunotherapy is less effective in hormone receptor-positive breast cancer due to immunosuppressive changes caused by estrogen receptor signaling in the tumor microenvironment. Hormone receptor-positive tumors have lower levels of programmed death-ligand 1 expression compared to triple-negative tumors and the signaling through estrogen receptor alters the immune microenvironment, rendering such tumors immunologically cold.
Immunotherapy is less effective in hormone receptor-positive breast cancer. Estrogen receptor signaling appears to cause immunosuppressive changes in the tumor microenvironment that might explain blunted antitumor responses to immune checkpoint inhibition. Anti-programmed cell death protein 1 immunotherapy has been incorporated in the treatment algorithm of triple-negative breast cancer (TNBC). However, clinical trial results for patients with hormone receptor (HR)-positive disease appear less compelling. HR-positive tumors exhibit lower levels of programmed death-ligand 1 expression in comparison with their triple-negative counterparts. Moreover, signaling through estrogen receptor alters the immune microenvironment, rendering such tumors immunologically cold. To explain differential responses to immune checkpoint blockade, this review interrogates differences between HR-positive and TNBC. Starting from distinct genomic features, we further present disparities concerning the tumor microenvironment and finally, we summarize early-phase clinical trial results on promising novel immunotherapy combinations.
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