RESUMEN
BACKGROUND: Ductal carcinoma in situ (DCIS) arising within fibroadenoma is a type of tumor that is rarely encountered in clinic, with only about 100 cases of carcinoma arising within a fibroadenoma reported in the literature. Here, we present two cases of breast DCIS arising within a fibroadenoma and discuss their clinical and imaging findings as well as treatment. CASE SUMMARY: The patients did not have cancer-related personal and family histories. Case 1 (a 49-year-old woman) was diagnosed with a bilateral breast nodule in May 2018 and was followed (preoperative imaging data including ultrasound and mammography) for 3 years; she underwent an excisional biopsy to address an enlargement in nodule size. Case 2 (a 37-year-old woman) was diagnosed with a left breast nodule in June 2021 and consequently received vacuum-assisted biopsy of the tumor which appeared as "irregularly shaped" and "unevenly textured" tissue on ultrasound. The pathological diagnosis was clear in both cases. Both patients underwent breast-conserving surgery and sentinel lymph node biopsy. The two cases received or planned to receive radiotherapy as well as endocrine therapy (tamoxifen). CONCLUSION: Breast DCIS arising within a fibroadenoma is rare, but patients treated with radiotherapy and endocrine therapy can have good prognosis.
RESUMEN
OBJECTIVE: Estrogen receptor-positive (ER+) breast cancers are the most often diagnosed subtype of breast tumors, in which the development of tamoxifen resistance remains a major impediment. The effect of long non-coding RNA (lncRNA) on therapy resistance is beginning to emerge. The lncRNA 91H, a recently identified lncRNA involved in tumorigenesis, is also overexpressed in breast cancer. The purpose of this study was to explore the role of 91H in the biological function and tamoxifen resistance of ER+ breast cancer cells. METHODS: MCF-7 and T47D cells were transfected for 91H silence. CCK-8 assay was performed to examine cell viability and drug sensitivity. Cell cycle and apoptosis were analyzed using flow cytometry. Cell migration capacity was determined by wound healing assay. The protein level was analyzed by Western blotting. RESULTS: MCF-7 and T47D cells with 91H knockdown exhibited lower capacities of cell proliferation and migration. In addition, knockdown of 91H resulted in significantly increased sensitivity to tamoxifen and a higher ratio of apoptosis induced by tamoxifen. Furthermore, the protein level of p-mTOR was notably inhibited through downregulating 91H expression. And the mTOR inhibitor together with tamoxifen presented synergistic effect on the inhibition of cell viability. CONCLUSION: Our study highlights that 91H might serve as a potential target for ER+ breast cancer patients who have acquired tamoxifen resistance.