Abstract
Simple SummaryMesenchymal triple negative breast cancer subtype expresses genes involved in proliferation, epithelial to mesenchymal transition, stromal interaction and cell motility. Moreover, this subgroup is characterized by an immunosuppressive microenvironment. This review focuses on the intracellular pathways involved in tumorigenesis and cancer progression, as well as in the immune evasion mechanisms. Furthermore, we provide an overview of current clinical trials investigating the efficacy and safety of different therapeutic molecules for this aggressive subtype of triple negative breast cancer. The challenge is to restore immunocompetence by overcoming the chemo and immune-resistance profile of mesenchymal triple negative breast cancer to achieve a lasting response to therapy.The pathologic definition of triple negative breast cancer (TNBC) relies on the absence of expression of estrogen, progesterone and HER2 receptors. However, this BC subgroup is distinguished by a wide biological, molecular and clinical heterogeneity. Among the intrinsic TNBC subtypes, the mesenchymal type is defined by the expression of genes involved in the epithelial to mesenchymal transition, stromal interaction and cell motility. Moreover, it shows a high expression of genes involved in proliferation and an immune-suppressive microenvironment. Several molecular alterations along different pathways activated during carcinogenesis and tumor progression have been outlined and could be involved in immune evasion mechanisms. Furthermore, reverting epithelial to mesenchymal transition process could lead to the overcoming of immune-resistance. This paper reviews the current knowledge regarding the mesenchymal TNBC subtype and its response to conventional therapeutic strategies, as well as to some promising molecular target agents and immunotherapy. The final goal is a tailored combination of cytotoxic drugs, target agents and immunotherapy in order to restore immunocompetence in mesenchymal breast cancer patients.
Highlights
Introduction distributed under the terms andThe management of breast cancer (BC), the most common tumor in women [1] has improved since its sub-classification based on the expression of estrogen (ER), progesterone receptors (PR) [2] and human epidermal growth factor receptor-2 (HER2) [3]
This review summarizes the biological and clinical knowledge we have acquired to date in regards to the triple negative breast cancer (TNBC) M subgroup and the state of the art of clinical trials investigating the efficacy and safety of different molecules, either on their own or in combination, in the treatment of this aggressive and resistant subtype of breast cancer
Mesenchymal TNBC subtype is characterized by the expression of genes involved in ETM, stromal interaction, cell motility, proliferation and by immune evasion
Summary
Introduction distributed under the terms andThe management of breast cancer (BC), the most common tumor in women [1] has improved since its sub-classification based on the expression of estrogen (ER), progesterone receptors (PR) [2] and human epidermal growth factor receptor-2 (HER2) [3]. Four main molecular subtypes of BC have been identified so far, based on the analysis of its global conditions of the Creative Commons. Cancers 2021, 13, 1080 main molecular subtypes of BC have been identified so far, based on the analysis of its global gene expression: Luminal A, luminal B, HER2, basal-like, and the more recently gene expression: Luminal A, luminal. HER2, basal-like, and the more recently identified identified claudin-low tumor subtypeB,[4,5]. (TNBC) is defined by the lack of expression of ER, PR. Triple and negative breast is defined thedefinition lack of expression of PR and HER2 accounts forcancer about (TNBC) BCs [6].
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