Secretory carcinoma of breast (SCB) is a rare salivary gland-type malignant tumor of the breast. This study reports two female patients with SCB admitted between 2019 and 2023, both presenting with breast masses. Breast ultrasonography indicated a BI-RADS category Ⅲ heterogeneous hyperechoic nodule in one case and a BI-RADS category Ⅳa hypoechoic nodule in the other. Histopathological examination showed that the maximum tumor diameters were 13 mm and 14 mm, respectively, with grayish-white cut surfaces, moderate consistency, and well-defined margins. Tumor cells exhibited mild to moderate atypia, with round or oval nuclei and a single small nucleolus. The cytoplasm was eosinophilic or vacuolated, and cells were arranged in microcystic, solid, or papillary patterns, with some showing cystic, hypersecretory lesion morphology. Eosinophilic secretions were observed within the lumens, and stromal fibrous tissue hyperplasia with hyaline degeneration was noted. Immunohistochemistry showed tumor cell expression of S100, pan-TRK, CD117, CK5/6, and GATA3, with low expression of ER and AR, and no expression of GCDFP-15, PR, or HER2. The Ki-67 proliferation index was approximately 5%. Alcian blue staining and periodic acid-Schiff staining showed positively stained secretions both within the cytoplasm and extracellularly. Molecular testing showed ETV6-NTRK3 gene fusion in both patients. A literature review of Chinese and English publications from 2020 to 2024 revealed 438 reported SCB cases, among which 80 had relatively complete clinicopathological and immunophenotypic data. This study summarized the clinicopathological characteristics, immunophenotypes, and molecular alterations of the 80 cases together with the two cases from our hospital, totaling 82 cases. The results showed expression rates of S100, pan-TRK, and GATA3 at 97%, 95%, and 100%, respectively. Approximately 50% of the cases showed low to moderate ER expression, about 20% showed low PR expression, and HER2 was generally negative. Molecular testing indicated that 98% of the cases had the characteristic ETV6-NTRK3 gene fusion, and two cases also had TERT promoter or PDGFR mutations.