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Recurrence‐free Survival Among Patients With ER+/PR+/HER2‐ Breast Cancers is Predicted by Expression of the Estrogen Response Signature
Author(s) -
Sandhu Rupninder,
Parker Joel,
Anders Carey,
Coleman William
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.926.2
Subject(s) - breast cancer , medicine , oncology , estrogen , estrogen receptor , immunohistochemistry , cancer , cancer research
ER+/PR+/HER2‐ breast cancers are frequently associated with good outcomes, but some patients experience disease progression/recurrence. We examined gene expression patterns among ER+/PR+/HER2‐ breast cancers (with known molecular subtypes) to identify those that express a 583‐gene estrogen response signature (ERS), indicating the presence of an intact ER/PR pathway. Unsupervised cluster analysis of 205 ER+/PR+/HER2‐ breast cancers identified two clusters (85 and 120 breast cancers). Kaplan‐Meier analysis of recurrence‐free survival (RFS) did not identify significant differences between these clusters. Correlation analysis against an ideal ERS identified two subsets among ER+/PR+/HER2‐ breast cancers: 44 breast cancers were negatively correlated and 161 breast cancers were positively correlated with this signature. Kaplan‐Meier analysis of RFS revealed a statistically significant difference between these patient subsets (P=0.0048), suggesting that ER+/PR+/HER2‐ breast cancers that express the ERS are associated with better RFS than those lacking this signature. Molecular subtypes of ER+/PR+/HER2‐ breast cancers that do not express the ERS include 5 basal‐like, 5 claudin‐low, 7 HER2‐enriched, 23 Luminal B, but only 2 Luminal A breast cancers. Among ER+/PR+/HER2‐ breast cancers lacking the ERS 28/44 (64%) relapsed, compared to 44% relapse among all other ER+/PR+/HER2‐ breast cancers. Lack of expression of the estrogen response signature predicts more aggressive disease among ER+/PR+/HER2‐ breast cancers.