PIK3CA-mutations in breast cancer

ddc:610 0303 health sciences Receptor, ErbB-2 Class I Phosphatidylinositol 3-Kinases 610 Breast Neoplasms 3. Good health Cohort Studies 03 medical and health sciences Preclinical Study Mutation Humans Female
DOI: 10.1007/s10549-022-06637-w Publication Date: 2022-10-24T13:03:12Z
ABSTRACT
Phosphatidylinositide-3-kinase (PI3K) regulates proliferation and apoptosis; somatic PIK3CA-mutations may activate these processes. Aim of this study was to determine the prevalence in a cohort early stage breast cancer patients association course disease.From an unselected 1270 (PiA, Prognostic Assessment routine application, NCT01592825) 1123 tumours were tested for three PIK3CA hotspot-mutations H1047R, E545K, E542K by qPCR. Primary objectives their tumour characteristics. Secondary objective recurrence-free interval (RFI) overall survival.PIK3CA-mutation rate 26.7% (300 1123). significantly more frequent steroid hormone-receptor (SHR)-positive HER2-negative (31.4%), G1 G2 (32.8%). Overall, we did not observe significant RFI. In SHR-positive BCs with PIK3CA-mutations, strong trend impaired RFI observed (adjusted HR 1.64, 95% CI 0.958-2.807), whilst SHR-negative insignificantly associated improved 0.49; 0.152-1.597). Of note, detrimental prognostic impact on SHR-positive, if only aromatase inhibitors administered as adjuvant therapy 4.44, 1.385-13.920), no tamoxifen treated patients.This speficies mutation cancer. The OS heterogeneous. Our results suggest that estrogen deprivation failes be active case PIK3CA-mutation.
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