Inducible knockout of syncytin-a leads to poor placental glucose transport in mice.

INTRODUCTION: Cell-cell fusion of cytotrophoblasts into the syncytiotrophoblast layer is a key process in placental development. Syncytin, an endogenous retroviral envelope protein, is expressed in placental trophoblasts and specifically mediates syncytiotrophoblast layer formation. Syncytin deficiency has been observed in fetal growth-restricted placentas. Abnormal fetal growth, especially fetal growth restriction, is associated with the decreased expression of glucose transporters. Here, we aimed to determine the role of syncytin in fetal growth restriction in placental glucose transport capacity. METHODS: To better explore the function of syncytin in fetal growth-restricted placenta, we generated an inducible knockout mouse model of syncytin-a gene. The expression levels of glucose transporters in BeWo cells were measured before and after HERV-W knockdown. RESULTS: Syncytin-A disruption was associated with significant abnormalities in placental and fetal development in mice. Syncytin-A destruction causes extensive abnormalities in the maternal-fetal exchange structures in the labyrinth, including an extremely reduced number and dramatically irregular distribution of fetal vessels. Moreover, glucose transporter 1, glucose transporters 3, and connexin 26 expression levels decreased after E14.5. Consistently, low glucose transporter 1, glucose transporter 3, and connexin 26 levels were observed in HERV-W-silenced BeWo cells. DISCUSSION: Syncytin-A is crucial for both syncytiotrophoblast layer development and morphogenesis, suggesting that syncytin-A disruption leads to fetal growth restriction associated with abnormalities in the maternal-fetal exchange barrier and decreased glucose transport.

The treatment process of an extremely rare giant borderline phyllodes tumor of breast: case report and literature review.

Giant phyllodes tumors are rare fibroepithelial neoplasms, usually defined as >10 cm. It is often difficult for pathologists to distinguish fibroadenomas from phyllodes tumors and determine the malignant potential level. The current treatment principle is to ensure the extended resection of tumors with a margin of 1 cm or more. For patients with multiple local recurrences or large tumors after surgery, simple mastectomy is recommended. Axillary management should be considered when breast cancer is diagnosed at the same time. We now present a rare case: a female patient found a right breast mass in 2014, and the mass had continued to grow for more than 7 months, and she was ultimately diagnosed with a giant phyllodes tumor with a diameter of 30 cm. Extensive resection is a suitable method to treat smaller phyllodes tumors, but giant phyllodes tumors require mastectomy, so the patient in this case underwent a total mastectomy. We removed the mass completely without destroying the normal tissue and structure. The treatment effect was obvious, and no related adverse events occurred during or after the operation, the postoperative recovery was good, and the patient was discharged once she was verified to be in a stable condition. This case is the first reported case of a patient who had a giant borderline phyllodes tumor with a diameter of 30 cm, underwent total mastectomy, and was followed up for 6 months without recurrence. The long-term effect of the treatment will be further evaluated after 5 years.