Abstract
Triple-negative breast cancer (TNBC) is one of the most heterogeneous diseases in solid tumors and has limited therapeutic options. Due to the lack of appropriate targetable markers, the mainstay therapeutic strategy for patients with TNBC has been chemotherapy for the last several decades. Indeed, TNBC tumors have no expression of estrogen receptor, progesterone receptor, or human epidermal growth factor receptor 2 (HER2); therefore, they do not respond to hormone therapy and HER2-targeted therapy. In this review paper, the molecular heterogeneities, possible therapeutic targets, and recently approved and upcoming drugs for TNBC will be summarized.
Highlights
The overall response rates (ORRs) was higher in the talazoparib group than in the standard chemotherapy group (62.6% vs. 27.2%; p < 0.001). The results of this trial showed that talazoparib had a significant benefit compared with the standard chemotherapy for patients with advanced breast cancer and germline BRCA mutations, which contributed to the U.S Food and Drug Administration (FDA)’s approval of talazoparib (Table 2)
This study showed that neoadjuvant chemotherapy plus pembrolizumab could significantly improve pathological complete response (pCR) in early triple-negative breast cancer (TNBC) patients, with statistically significant enhanced event-free survival [25]
The biggest obstacle in terms of drug development would be the heterogeneity of TNBC, leading to dissecting this 15% of whole breast cancers into small target populations to be studied in clinical trials
Summary
Hormone receptor-positive breast cancer, covering luminal A and luminal B subtypes (70–80%) in gene expression profiles, is quite dependent on the hormone receptor pathway, so its mainstream treatment is endocrine therapy with or without targeted agents to interrupt estrogen-signaling pathways and other critical pathways, such as cyclin-dependent kinase (CDK) 4/6 and phosphoinositide. Triple-negative breast cancer (TNBC) lacks these three receptors (estrogen receptor (ER), progesterone receptor (PR), and HER2) and, is a diagnosis of exclusion showing the basal subtype in molecular profiling. Most of the clinical trials with targeted agents for TNBC included all TNBC subtypes, even after full awareness of it as a heterogeneous disease [2,3].
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