Abstract
Metaplastic breast cancer (MBC) is a rare subtype of invasive breast cancer that tends to have an aggressive clinical presentation as well as a variety of distinct histologic designations. Few systemic treatment options are available for MBC, as it has consistently shown a suboptimal response to standard chemotherapy regimens. These characteristics result in a worse overall prognosis for patients with MBC compared to those with standard invasive breast cancer. Due to its rarity, data focusing on MBC is limited. This review will discuss the clinical presentation, breast imaging findings, histologic and molecular characteristics of MBC as well as potential future research directions.
Highlights
Metaplastic breast cancer (MBC) is a rare and histologically diverse subtype of breast carcinoma
The co-expression of S-100, vimentin, and/or cytokeratin in both the carcinomatous component (CC) and the heterogeneous sarcomatous component (HSC) is evidence for a metaplastic process [38]. These findings suggest that the HSC have an epithelial or myoepithelial origin and undergo subsequent metaplastic changes, but definitive genetic evidence for a monoclonal origin is still very limited [36,39,40]
This finding has been supported by the work of Hayes et al which showed evidence of Wnt pathway activation, which results in Epithelial-Mesenchymal transition (EMT), in most primary metaplastic carcinomas [54]
Summary
Metaplastic breast cancer (MBC) is a rare and histologically diverse subtype of breast carcinoma. The substantial decrease in miR-200f expression levels was found to be accompanied by an upregulation of EMT transcriptional inducers, further demonstrating the association between EMT and MBC [53] This finding has been supported by the work of Hayes et al which showed evidence of Wnt pathway activation, which results in EMT, in most primary metaplastic carcinomas [54]. MBC are poorly responsive to conventional chemotherapy or hormone therapy regimens and that tumors with EGFR amplification are reported to be sensitive to EGFR tyrosine kinase inhibitors, these findings indicate that further studies are warranted to explore EGFR tyrosine kinase inhibitors as potential therapeutic agents for metaplastic breast carcinomas harboring amplification of 7p11 [65,68]. This and other agents targeted against these receptors or pathways could potentially be an area of further research to develop novel therapeutic options for patients with MBC [76]
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