J L Ethier1, A Ocaña2, A Rodríguez Lescure3, A Ruíz4, E Alba5, L Calvo6, M Ruíz-Borrego7, A Santaballa8, C A Rodríguez9, C Crespo10, M Ramos11, J Gracia Marco12, A Lluch13, I Álvarez14, M Casas15, M Sánchez-Aragó15, E Carrasco15, R Caballero15, E Amir16, M Martin17. 1. Department of Medical Oncology, Kingston Health Sciences Centre, Queen's University, Kingston, Ontario, Canada. 2. Complejo Hospitalario de Albacete, Albacete, Spain; GEICAM (Spanish Breast Cancer Group), Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Spain. 3. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Universitario de Elche, Elche, Spain. 4. GEICAM (Spanish Breast Cancer Group), Spain; Instituto Valenciano de Oncología, Valencia, Spain. 5. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Virgen de La Victoria, Málaga, Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Spain. 6. GEICAM (Spanish Breast Cancer Group), Spain; Complejo Hospitalario Universitario A Coruña, A Coruña, Spain. 7. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Univ. Virgen Del Rocío, Sevilla, Spain. 8. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Universitario La Fe, Valencia, Spain. 9. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Clínico Universitario de Salamanca, Salamanca (IBSAL), Spain. 10. GEICAM (Spanish Breast Cancer Group), Spain; Hospital Ramón y Cajal, Madrid, Spain. 11. GEICAM (Spanish Breast Cancer Group), Spain; Centro Oncológico de Galicia, A Coruña, Spain. 12. GEICAM (Spanish Breast Cancer Group), Spain; Hospital de Cabueñes, Gijón, Spain. 13. GEICAM (Spanish Breast Cancer Group), Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Spain; Hospital Clínico Universitario de Valencia, Biomedical Research Institute INCLIVA, University of Valencia, Valencia, Spain. 14. GEICAM (Spanish Breast Cancer Group), Spain; Hospital de Donostia, San Sebastián, Spain. 15. GEICAM (Spanish Breast Cancer Group), Spain. 16. Division of Medical Oncology and Hematology, Princess Margaret Cancer Centre, Toronto, Canada. 17. GEICAM (Spanish Breast Cancer Group), Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Spain; Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain. Electronic address: mmartin@geicam.org.
Abstract
BACKGROUND: Retrospective data suggest better outcomes for patients with double hormonal receptor (oestrogen [ER] and progesterone receptor [PgR])-positive (dHR+) early breast cancer, compared with single hormonal receptor-positive, sHR+, (ER+/PgR- or ER-/PgR+) disease. Here, we evaluate the classification according to intrinsic subtypes and clinical outcomes of sHR+ versus dHR+ in HER2-negative breast cancer patients enrolled in GEICAM/9906 study (NCT00129922). METHODS: Archival tumours were retrieved retrospectively for the analysis of ER, PgR and HER2 status and classified into intrinsic subtypes using the PAM50 gene expression assay. Disease-free survival (DFS) and overall survival (OS) were explored using a Cox proportional hazard analysis. RESULTS: Data on intrinsic subtypes were available in 571 (50%) patients with ER+ and/or PR+, and HER2-negative primary tumours. The incidence of luminal A and luminal B subtypes were 52%/36% in dHR+ tumours (ER+/PgR+), and 15%/58% in ER+/PgR-tumours. ER-/PgR+ tumours were mainly luminal A (52%). Compared with ER+/PgR+ patients, DFS was similar in ER-/PgR+ (hazard ratio [HR] 1.15, 95% confidence interval [CI] 0.57-2.34, p = 0.70) but worse in ER+/PgR- patients (HR 1.60, 95% CI 1.12-2.28, p < 0.01). Similar results were observed for OS (HR 1.50, p = 0.30 and HR 1.86, p < 0.01, respectively). CONCLUSIONS: The ER+/PgR- group is characterised by higher proliferation and worse outcomes. In spite of the ER-/PgR+ subgroup resembles ER+/PgR+ disease in terms of molecular subtypes and outcomes, the small number of patients in this subgroup prevents from drawing any conclusions. TRIAL REGISTRATION: EudraCT: 2005-003108-12 (retrospectively registered 28/06/2005). CLINICALTRIALS. GOV IDENTIFIER: NCT00129922 (retrospectively registered 10/08/2005).
BACKGROUND: Retrospective data suggest better outcomes for patients with double hormonal receptor (oestrogen [ER] and progesterone receptor [PgR])-positive (dHR+) early breast cancer, compared with single hormonal receptor-positive, sHR+, (ER+/PgR- or ER-/PgR+) disease. Here, we evaluate the classification according to intrinsic subtypes and clinical outcomes of sHR+ versus dHR+ in HER2-negative breast cancerpatients enrolled in GEICAM/9906 study (NCT00129922). METHODS: Archival tumours were retrieved retrospectively for the analysis of ER, PgR and HER2 status and classified into intrinsic subtypes using the PAM50 gene expression assay. Disease-free survival (DFS) and overall survival (OS) were explored using a Cox proportional hazard analysis. RESULTS: Data on intrinsic subtypes were available in 571 (50%) patients with ER+ and/or PR+, and HER2-negative primary tumours. The incidence of luminal A and luminal B subtypes were 52%/36% in dHR+ tumours (ER+/PgR+), and 15%/58% in ER+/PgR-tumours. ER-/PgR+ tumours were mainly luminal A (52%). Compared with ER+/PgR+ patients, DFS was similar in ER-/PgR+ (hazard ratio [HR] 1.15, 95% confidence interval [CI] 0.57-2.34, p = 0.70) but worse in ER+/PgR- patients (HR 1.60, 95% CI 1.12-2.28, p < 0.01). Similar results were observed for OS (HR 1.50, p = 0.30 and HR 1.86, p < 0.01, respectively). CONCLUSIONS: The ER+/PgR- group is characterised by higher proliferation and worse outcomes. In spite of the ER-/PgR+ subgroup resembles ER+/PgR+ disease in terms of molecular subtypes and outcomes, the small number of patients in this subgroup prevents from drawing any conclusions. TRIAL REGISTRATION: EudraCT: 2005-003108-12 (retrospectively registered 28/06/2005). CLINICALTRIALS. GOV IDENTIFIER: NCT00129922 (retrospectively registered 10/08/2005).
Authors: Ki-Tae Hwang; Young Jin Suh; Chan-Heun Park; Young Joo Lee; Jee Ye Kim; Jin Hyang Jung; Seeyeong Kim; Junwon Min Journal: Oncologist Date: 2021-09-02
Authors: Erik Kudela; Marek Samec; Lenka Koklesova; Alena Liskova; Peter Kubatka; Erik Kozubik; Tomas Rokos; Terezia Pribulova; Eva Gabonova; Marek Smolar; Kamil Biringer Journal: Int J Mol Sci Date: 2020-10-17 Impact factor: 5.923