BMC cancer · 2025
Transcriptomic profiles of endocrine-resistant breast cancer.
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Schagerholm Stanev Caroline, Sifakis Emmanouil G, Hases Linnea, Chen Xinsong, Williams Cecilia, Robertson Stephanie, Hartman Johan
Аннотация
BACKGROUND: The majority of breast cancer patients have tumors expressing estrogen receptor α (ER) and are treated with adjuvant endocrine therapy. However, nearly one-third relapse, most with retained ER expression.
METHODS: This study investigated patients with ER-positive and human epidermal growth factor receptor 2 (HER2)-negative primary breast cancer. Patients with ER-positive relapses within five years of ongoing endocrine therapy were defined as endocrine-resistant (N = 69). Patients with no disease progression after 10 years were defined as endocrine-sensitive (N = 77). RNA was extracted from archived tumor blocks, followed by gene expression analysis.
RESULTS: Significant differences were observed with higher tumor grades, intrinsic subtype risk scores, and upregulated cell-cycle gene sets in resistant compared to sensitive patients' primary tumors. Metabolism-associated gene sets were upregulated, and estrogen-response gene sets downregulated in resistant patients' relapse compared to primary tumors.
CONCLUSIONS: This study highlights gene sets associated with endocrine resistance and identifies transcriptomic and clinicopathological profiles that may serve as potential prognostic markers for therapy response.
METHODS: This study investigated patients with ER-positive and human epidermal growth factor receptor 2 (HER2)-negative primary breast cancer. Patients with ER-positive relapses within five years of ongoing endocrine therapy were defined as endocrine-resistant (N = 69). Patients with no disease progression after 10 years were defined as endocrine-sensitive (N = 77). RNA was extracted from archived tumor blocks, followed by gene expression analysis.
RESULTS: Significant differences were observed with higher tumor grades, intrinsic subtype risk scores, and upregulated cell-cycle gene sets in resistant compared to sensitive patients' primary tumors. Metabolism-associated gene sets were upregulated, and estrogen-response gene sets downregulated in resistant patients' relapse compared to primary tumors.
CONCLUSIONS: This study highlights gene sets associated with endocrine resistance and identifies transcriptomic and clinicopathological profiles that may serve as potential prognostic markers for therapy response.