Breast cancer is the most common cancer and the leading cause of cancer death among women worldwide, encompassing a wide heterogeneity of subtypes with different clinical features. Among them, Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor, progesterone receptor, and does not overexpress human epidermal growth factor receptor 2 (HER2), is characterized by a worse prognosis. It accounts for about 9–21 % of all breast cancers, affects more frequently young patients, and is represented by advanced stage, higher proliferative index, higher histologic grade, and significantly higher metastatic rates than all other subtypes.
Currently, the standard treatment for TNBC is cytotoxic chemotherapy, however many tumors encounter early therapeutic escape, leading to aggressive metastatic relapse quickly after treatment in the adjuvant setting, causing death in more than 90% of patients. Only in the last two years, some targeted therapies, including treatment with PARP-inhibitors (olaparib and talazoparib) and immunotherapy (anti-PD-L1, atezolizumab) have been approved by the US Food and Drug Administration. However, research of an efficient targeted therapy for TNBC, especially at the metastatic stage, still represents a serious clinical therapeutic challenge. A major reason for the therapeutic failure is the wide heterogeneity of TNBC that has been recently well-characterized at gene expression profiling level. Molecular subtypes of TNBC are associated with differences in survival and can potentially contribute to treatment selection. Hence, there is an urgent need to develop signatures to aid in the early diagnosis and better treatment stratification of TNBC patients.
In this Research Topic, we aim to present the recent advances in the diagnosis of TNBC. We are especially interested in innovative strategies with potential translation into clinical practice. We welcome Original Research and Review Articles. Topics of interest include, but are not limited to:
1) Aptamer-based targeted imaging and other new in-vivo imaging modalities for TNBC treatment evaluation.
2) MiRNAs and Lnc-RNAs as new biomarkers of TNBC.
3) The role of circulating tumor cells and cell-free DNA in the diagnosis of TNBC.
4) Developing organoids and other innovative in-vitro cell systems to investigate TNBC plasticity, and associated gene signatures, linked to therapeutic escape.
5) Targeted next-generation sequencing to identify clinical relevant TNBC subtypes.
6) Molecular profiling of the residual disease of TNBC after cytotoxic chemo- and/or targeted therapy.
Breast cancer is the most common cancer and the leading cause of cancer death among women worldwide, encompassing a wide heterogeneity of subtypes with different clinical features. Among them, Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor, progesterone receptor, and does not overexpress human epidermal growth factor receptor 2 (HER2), is characterized by a worse prognosis. It accounts for about 9–21 % of all breast cancers, affects more frequently young patients, and is represented by advanced stage, higher proliferative index, higher histologic grade, and significantly higher metastatic rates than all other subtypes.
Currently, the standard treatment for TNBC is cytotoxic chemotherapy, however many tumors encounter early therapeutic escape, leading to aggressive metastatic relapse quickly after treatment in the adjuvant setting, causing death in more than 90% of patients. Only in the last two years, some targeted therapies, including treatment with PARP-inhibitors (olaparib and talazoparib) and immunotherapy (anti-PD-L1, atezolizumab) have been approved by the US Food and Drug Administration. However, research of an efficient targeted therapy for TNBC, especially at the metastatic stage, still represents a serious clinical therapeutic challenge. A major reason for the therapeutic failure is the wide heterogeneity of TNBC that has been recently well-characterized at gene expression profiling level. Molecular subtypes of TNBC are associated with differences in survival and can potentially contribute to treatment selection. Hence, there is an urgent need to develop signatures to aid in the early diagnosis and better treatment stratification of TNBC patients.
In this Research Topic, we aim to present the recent advances in the diagnosis of TNBC. We are especially interested in innovative strategies with potential translation into clinical practice. We welcome Original Research and Review Articles. Topics of interest include, but are not limited to:
1) Aptamer-based targeted imaging and other new in-vivo imaging modalities for TNBC treatment evaluation.
2) MiRNAs and Lnc-RNAs as new biomarkers of TNBC.
3) The role of circulating tumor cells and cell-free DNA in the diagnosis of TNBC.
4) Developing organoids and other innovative in-vitro cell systems to investigate TNBC plasticity, and associated gene signatures, linked to therapeutic escape.
5) Targeted next-generation sequencing to identify clinical relevant TNBC subtypes.
6) Molecular profiling of the residual disease of TNBC after cytotoxic chemo- and/or targeted therapy.
![(A–F) Representative photomicrographs for expression of Ki-67, COX2, and Bcl2. Nuclear expression of Ki-67 (B); cytoplasmic expression of COX2 and Bcl-2 (C,D) with corresponding hematoxylin and eosin stained sections (A–C) [scale bar, 50 μm (original magnification, 10×); inserts: scale bar, 20 μm (original magnification, 20×)].](https://www.frontiersin.org/_rtmag/_next/image?url=https%3A%2F%2Fwww.frontiersin.org%2Ffiles%2FArticles%2F535969%2Ffonc-10-01083-HTML%2Fimage_m%2Ffonc-10-01083-g004.jpg&w=3840&q=75)
