Abstract
Metaplastic breast carcinoma (MBC) is a heterogeneous group of infrequent triple negative (TN) invasive carcinomas with poor prognosis. MBCs have a different clinical behavior from other types of triple negative breast cancer (TNBC), being more resistant to standard chemotherapy. MBCs are an example of tumors with activation of epithelial–mesenchymal transition (EMT). The mechanisms involved in EMT could be responsible for the increase in the infiltrative and metastatic capacity of MBCs and resistance to treatments. In addition, a relationship between EMT and the immune response has been seen in these tumors. In this sense, MBC differ from other TN tumors showing a lower number of tumor-infiltrating lymphocytes (TILS) and a higher percentage of tumor cells expressing programmed death-ligand 1 (PD-L1). A better understanding of the relationship between the immune system and EMT could provide new therapeutic approaches in MBC.
Highlights
There is a close relationship between the immune system and the development of cancer
Five histological subtypes are recognized in the new WHO classification of breast tumors: squamous cell carcinoma (SqCC), spindle cell carcinomas (SpCC), Metaplastic breast carcinoma (MBC) with heterologous mesenchymal differentiation (MBCHMD), low-grade adenosquamous carcinoma (LGASC), and fibromatosis-like MBC (FLMBC) [12]
We focus on HG-MBC
Summary
There is a close relationship between the immune system and the development of cancer. Five histological subtypes are recognized in the new WHO classification of breast tumors: squamous cell carcinoma (SqCC), spindle cell carcinomas (SpCC), MBC with heterologous mesenchymal differentiation (MBCHMD), low-grade adenosquamous carcinoma (LGASC), and fibromatosis-like MBC (FLMBC) [12]. Pure SqCC does not represent a typical example of EMT, we have included this subtype in this review since most tumors with squamous cell differentiation carry some degree of spindle cell or heterologous differentiation. The clinical response to systemic therapies is limited due to partial resistance of MBC to conventional chemotherapy For this reason, despite there being some new approaches such as mTOR inhibitors, check-point inhibitors, or PARP inhibitors, new targeted therapies based on specific molecular features or immunomodulation are required
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