Metaplastic breast carcinomas (MBC) first described by Huvos in 1973, they are rare tumors and account for approximately 0.25-1% of all breast malignancies. These tumors are histologically defined by the differentiation of the neoplastic epithelium into squamous or mesenchymal-like elements. The metaplastic component may occur with or without an in situ or invasive ductal component. In its formation, according to the theory of metaplastic differentiation, epithelial elements are considered to turn into sarcomatous elements According to the Who 2021 classification, low grade adenosquamous carcinoma ,fibromatosis like MBC,squamous cell carcinoma ,spindle cell carcinoma,MBC with mesenchymal differentiation (chondroid, osseous, and other types), and mixed MBC are divided into subtypes. 

Clinically, it is manifested by a rapidly growing mass in the breast, axillary metastases are rarely seen, the average age is 55 years. There is a mass image in mammography, the average diameter of the mass is 32 mm. Microcalcification is rarely seen in the presence of an in situ component. Immunohistochemically, ER, PR and Cerb-b2 are negative tumors. It is also positive for Vimentin, S100, P63 and high molecular weight cytokeratin (CK 5/6). PIK3CA/PIK3R1 mutations are high in their genetic characteristics (61%). TP53 mutation is seen in 64% and TERT promoter mutation in 25%. The presence of TERT mutations is also associated with poor response to chemotherapy, MBC are usually chemoresistant tumors. Metaplastic breast carcinomas have a worse prognosis than other triple-negative breast carcinomas, and have a high risk of distant metastases. They often metastasize to the lungs and bones. In some species, the risk of local recurrence is higher. While mastectomy or breast-conserving surgery is applied in the treatment, mastectomy is generally more preferred due to the large diameter of the tumor. Radiotherapy and chemotherapy are used in adjuvant therapy, studies have shown that the benefit of neoadjuvant chemotherapy is generally low. Immunotherapy and smart drug therapies are also used. Chemotherapy protocols are AC (doxorubucin, cyclophosphamide), weekly paclitaxel (12 weeks), TC (dosetaxel, cyclophosphamide), TAC (dosetaxel, doxorubucin, cyclophosphamide), CMF, EC. Capacitabine is used in the presence of residual disease after neoadjuvant chemotherapy.  Those who receive antihormonal therapy and anti-HER-2 therapy have better survival outcomes than those who do not. In the presence of residual disease after neoadjuvant CT, olaparib treatment can be used for 1 year in patients with positive BRCA mutation. In high-risk stage 2-3 patients, preoperative pembrolizumab-carboplatin-paclitaxel+preoperative pembrolizumab-cyclophosphamide-doxorubicin+adjuvant pembrolizumab treatment options are available.  PARP inhibitors and platinum-based agents can be used in tumors with positive DNA repair deficiency-PIK3/mTor pathway changes. Antibody-drug conjugation therapies are effective in patients with 2 (1 or 2 positive and negative in situ hybridization with IHC).  Since 98% of tumors with squamous differentiation are TROP2+ (sacituzumab, govetecon-antibody drug conjugate), it can be used. Studies have shown that the survival rate is higher when adjuvant RT is applied after lumpectomy (p<0.001). While the survival benefit of post-mastectomy adjuvant radiotherapy was present in T3-4/node-positive patients (p<0.001), the survival benefit was not shown in patients with T1-2N0 patients (p=0.259). One study covering 460 patients (Seer database) in 2019, a survival advantage (p<0.001) was shown in those who received adjuvant RT after mastectomy in multivariate analysis. The 5-year survival rate was 62.3% in patients with PMRT and 50.3% in patients without PMRT (p=0.001).