A 30-year retrospective study of rare ectopic seminal tract opening cases.

Ectopic seminal tract opening is a rare congenital malformation. Until recently, there has been a lack of comprehensive reporting on the condition. The purpose of this retrospective study is to summarize the experience of diagnosis and treatment of this condition based on 28 clinical practice cases throughout the past 30 years. We conducted auxiliary examinations on such patients including routine tests, imaging examinations, and endoscopy. Among these 28 cases, there were ectopic opening of vas deferens into enlarged prostatic utricles (6 cases); ejaculatory ducts into enlarged prostatic utricles, Müllerian ducts cysts, and urethras (18 cases, 2 cases, and 1 case, respectively); and ectopic opening of the unilateral vas deferens and the contralateral ejaculatory duct into enlarged prostatic utricle (1 case). The size of the enlarged prostatic utricle, the type of ectopic seminal tract opening, and the opening's location effectively assisted in the selection of clinical treatment methods, including transurethral fenestration of the utricle, transurethral cold-knife incision, open operation, laparoscopic operation, and conservative treatment. Satisfactory effect was achieved during follow-up. In conclusion, a definite diagnosis and personalized treatment are especially important for patients with ectopic seminal tract opening.

Targeting AXL overcomes resistance to docetaxel therapy in advanced prostate cancer.

Resistance to docetaxel is a major clinical problem in advanced prostate cancer. The overexpression of AXL receptor tyrosine kinase (AXL) has been correlated with chemotherapeutic drug resistance. However, the role of AXL expression in docetaxel resistance in prostate cancer is yet unclear. In this study, we demonstrate that AXL is overexpressed and activated independent of Gas6 in docetaxel-resistant prostate cancer cells (PC3-DR and DU145-DR). Moreover, we show that forced overexpression of AXL in PC3 and DU145 cells is sufficient to induce resistance to docetaxel in these cell lines. Notably, genetic or pharmacologic inhibition of AXL in the resistant models suppressed cell proliferation, migration, invasion, and tumor growth, and these effects were significantly augmented when AXL inhibition was combined with docetaxel treatment. Mechanistically, we found that AXL inhibition led to reversion of the epithelial-mesenchymal transition (EMT) phenotype and decreased the expression of ATP-binding cassette B1 (ABCB1). Overall, our results identify AXL as an important mediator of docetaxel resistance in prostate cancer. We propose that AXL-targeted therapy, in combination with docetaxel, has the potential to improve the response to docetaxel therapy and reduce resistance induced by prolonged docetaxel therapy in prostate cancer.