(2026). Clinico-pathological and genomic features of HER2-low early Breast Cancer (eBC). Results of retrospective analysis of seven adjuvant trials by the Hellenic Cooperative Oncology Group (HeCOG). Clinical Cancer Research, 32(4_Supplement). https://doi.org/10.1158/1557-3265.sabcs25-ps4-01-20
Περίληψη
Background: HER2-low breast cancers are a mixture of luminal and triple negative tumors. Precise molecular characterization can help refine treatment strategies with novel antibody-drug conjugates and improve outcomes in this patient subgroup. Methods: We used central ER/PgR (HR) and HER2/ERBB2 IHC/FISH assessment to define HER2-low (IHC 1+ or 2+/FISH non-amplified), HER2-zero (IHC 0) and Luminal A/ Luminal B/ TNBC subtypes across 7 prospective adjuvant studies in which eBC patients were treated with dose dense sequential chemotherapy. Retrospective analysis of clinico-pathological data and IHC markers from tissue microarray cores was performed on N=2,751 cases, whereas DNA next generation sequencing (NGS) data were available in a subset of N=1,120 tumors. Heterogeneity was investigated by comparing HER2-low concordant (HER2-low_c) cases, when all cores were scored consistently as HER2-low (>0) and HER2-low discordant (HER2-low_d) cases, when at least one core was scored “0”. Results: First, HER2-low tumors were more likely to be HR + (p<0.001). Second, within HR + disease only, the proportion of Luminal B was higher in HER2-low (51%) than HER2-zero (41.6%), whereas Luminal A showed the opposite pattern (p< 0.001); PIK3CA mutations on the other hand were more common in HER2-zero (33.6% vs. 24.7%
- DOI
- 10.1158/1557-3265.sabcs25-ps4-01-20
- Τύπος
- Άρθρο σε Περιοδικό
- Έτος
- 2026
Σύνδεσμοι
BibTeX
@article{lakis2026clinico,
title = {Clinico-pathological and genomic features of HER2-low early Breast Cancer (eBC). Results of retrospective analysis of seven adjuvant trials by the Hellenic Cooperative Oncology Group (HeCOG)},
author = {Sotirios Lakis and Eleftheria Tsolaki and Nikolaos Korfiatis and A. Goussia and H. P. Kourea and A. Batistatou and Mattheos Bobos and Kyriaki Papadopoulou and Antonia Charchanti and M. Bai and Olympia Tzaida and K. Petraki and P. Arapantoni and T. Koletsa and D. Pectasides and A. Koutras and D. Kalapanida and F. Dimitrakopoulos and E. Aravantinou-Fatorou and N. Spathas and A. Psyrri and H. Gogas and Flora Zagouri and G. Fountzilas},
url = {https://doi.org/10.1158/1557-3265.sabcs25-ps4-01-20},
doi = {10.1158/1557-3265.sabcs25-ps4-01-20},
year = {2026},
date = {2026-01-01},
journal = {Clinical Cancer Research},
volume = {32},
number = {4_Supplement},
publisher = {American Association for Cancer Research},
address = {San Antonio, Texas},
abstract = {Background: HER2-low breast cancers are a mixture of luminal and triple negative tumors. Precise molecular characterization can help refine treatment strategies with novel antibody-drug conjugates and improve outcomes in this patient subgroup. Methods: We used central ER/PgR (HR) and HER2/ERBB2 IHC/FISH assessment to define HER2-low (IHC 1+ or 2+/FISH non-amplified), HER2-zero (IHC 0) and Luminal A/ Luminal B/ TNBC subtypes across 7 prospective adjuvant studies in which eBC patients were treated with dose dense sequential chemotherapy. Retrospective analysis of clinico-pathological data and IHC markers from tissue microarray cores was performed on N=2,751 cases, whereas DNA next generation sequencing (NGS) data were available in a subset of N=1,120 tumors. Heterogeneity was investigated by comparing HER2-low concordant (HER2-low_c) cases, when all cores were scored consistently as HER2-low (>0) and HER2-low discordant (HER2-low_d) cases, when at least one core was scored “0”. Results: First, HER2-low tumors were more likely to be HR + (p<0.001). Second, within HR + disease only, the proportion of Luminal B was higher in HER2-low (51%) than HER2-zero (41.6%), whereas Luminal A showed the opposite pattern (p< 0.001); PIK3CA mutations on the other hand were more common in HER2-zero (33.6% vs. 24.7%},
note = {Conference abstract PS4-01-20},
keywords = {},
pubstate = {published},
tppubtype = {article}
}