Abstract
Triple-negative breast cancer (TNBC) is a heterogeneous group of tumors characterized by aggressive behavior, high risk of distant recurrence, and poor survival. Chemotherapy is still the main therapeutic approach for this subgroup of patients, therefore, progress in the treatment of TNBC remains an important challenge. Data derived from molecular technologies have identified TNBCs with different gene expression and mutation profiles that may help developing targeted therapies. So far, however, only a few of these have shown to improve the prognosis and outcomes of TNBC patients. Robust predictive biomarkers to accelerate clinical progress are needed. Herein, we review prognostic and predictive biomarkers in TNBC, discuss the current evidence supporting their use, and look at the future of this research field.
Highlights
Triple negative breast cancer (TNBC) is a subtype of breast cancer lacking expression of estrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER2) [1]
Results showed that the HR deficiency and homologous recombination deficiency (HRD) score in non-tmBRCA were predictors of response, the HRD assay failed to identify a subset of patients most likely to derive benefit from the addition of carboplatin [61]
The results showed that patients with Tumor mutational burden (TMB)-H in solid tumors who were treated with Pembrolizumab had a higher overall response rate (29%) compared to patients with TMB [137]
Summary
Triple negative breast cancer (TNBC) is a subtype of breast cancer lacking expression of estrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER2) [1]. Regarding sensibility to platinum agents of BRCAness phenotype in this setting, the phase II TBCR009 trial has shown a correlation between high HRD scores and their predictive response to platinum-based chemotherapy, beyond BRCA1/2 mutations, in advanced first and second line TNBC patients. Results showed that the HR deficiency (defined as HRD score 42 and/or presence of tmBRCA) and HRD score in non-tmBRCA were predictors of response, the HRD assay failed to identify a subset of patients most likely to derive benefit from the addition of carboplatin [61] In this context, the PrECOG 0105 phase II study of gemcitabine and carboplatin plus iniparib as neoadjuvant therapy for TNBC and BRCA1/2 mutation-associated breast cancer, revealed that combination of gemcitabine, carboplatin, and iniparib is active in the treatment of early-stage triple-negative and BRCA1/2 mutation-associated breast cancer. AZD6738 [85,86,87], leading to early phase clinical trials combining ATR inhibitors and PARPis in different cancers (NCT02723864, NCT03462342, NCT03682289, NCT02576444)
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