Abstract
Abstract Purpose: The aim of the present study was to assess the predictive value of intrinsic luminal subtypes in premenopausal hormone receptor-positive early breast cancer patients who received adjuvant endocrine treatment or chemotherapy. Patients and Methods: Intrinsic luminal breast cancer subtypes were centrally assessed by immunohistochemistry on whole tissue sections of breast cancer patients who had been enrolled in the Austrian Breast and Colorectal Cancer Study Group (ABCSG) Trial 5 and received either 3 years of goserelin plus 5 years of tamoxifen or six cycles of cyclophosphamide, methotrexate, and fluorouracil (CMF). Luminal A disease was defined as Ki67 <20%, Luminal B/HER2-negative subtype as Ki67≥20%. Luminal B/HER2-positive subtype displayed HER2 overexpression by IHC or amplification by ISH. Recurrence-free survival (RFS) and overall survival (OS) were analyzed using Cox models adjusted for clinical and pathological factors. Results: 155 (36%), 217 (50%) and 59 (14%) of 431 tumors were classified as Luminal A, Luminal B/HER2-negative and Luminal B/HER2-positive, respectively. Luminal B subtypes were associated with poor outcome. Patients with Luminal B tumors had a significantly shorter RFS (adjusted hazard ratio [HR] for recurrence: 2.29, 95% confidence interval [CI] 1.44-3.64, P < 0.001) and OS (adjusted HR for death: 3.97, 95% CI 1.94-8.08, P < 0.001) as compared to patients with Luminal A disease. No interaction between intrinsic luminal subtypes and treatment was observed (test for interaction: P = 0.42 for RFS; P = 0.32 for OS). Combination endocrine treatment with goserelin/tamoxifen tended to be more effective than CMF chemotherapy in both luminal A and luminal B subtypes. Conclusion: Intrinsic luminal subtype is an independent prognostic factor for recurrence and death in premenopausal women with early-stage, hormone receptor positive breast cancer but is not predictive for outcome of adjuvant treatment with either goserelin/tamoxifen or chemotherapy with CMF. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P1-08-13.
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