RESUMEN
Minimally invasive radical hysterectomy (MIRH) is widely performed as a treatment for early-stage cervical cancer. However, in 2018, a randomized controlled trial (RCT) called the Laparoscopic Approach to Cervical Cancer (LACC) trial showed that MIRH had poorer oncologic outcomes compared to laparotomy. Since then, several clinical studies have supported this finding, and most surgeons now perform MIRH with limited surgical indications. However, most of the reported studies evaluated laparoscopic radical hysterectomy rather than robotic radical hysterectomy (RRH). Robotic surgery has advantages for complex surgical procedures in the deep and narrow pelvic cavity in cervical cancer, making it necessary to evaluate the benefits and potential harms of RRH individually. Based on this systematic review, RRH is a safe and effective alternative to abdominal approach for early-stage cervical cancer. RRH offers significant perioperative benefits, including reduced blood loss, shorter hospital stays, and fewer complications, without compromising oncologic outcomes such as overall survival and progression-free survival. Additionally, surgeons should aim to minimize tumor cell spillage into the peritoneal cavity by eliminating the use of uterine manipulators or vaginal colpotomy. Ongoing RCTs will reveal whether we can perform RRH without oncologic compromise in cervical cancer.
RESUMEN
Smoking cigarettes is known to lower the risk of preeclampsia. The objective of this study is to evaluate the effect of smoking on the expression of soluble FMS-like tyrosine kinase-1 (sFlt-1), vascular endothelial growth factor (VEGF), and endoglin (sEng)-1 and the role of the aryl hydrocarbon receptor (AhR) in pregnant mice. We developed a smoking mouse model using a gas-filling system. One or two cigarettes per day were exposed to each of the five pregnant mice for five days a week throughout pregnancy. AhR agonist and antagonist were injected. Serum levels and expression in the placenta of sFlt-1, VEGF, and sEng-1 were analyzed and compared among the cigarette smoke and no-exposure groups after delivery. Compared to the no-smoke exposure group, the serum level of sFlt-1 was significantly decreased in the two-cigarette-exposed group (p < 0.001). When the AhR antagonist was added to the two-cigarette-exposed group, sFlt-1 levels were significantly increased compared to the two-cigarette group (p = 0.002). The levels of sFlt-1 in the AhR antagonist group did not change regardless of two-cigarette exposure (p = 0.064). With the AhR agonist, sFlt-1 decreased significantly compared to the control (p = 0.001) and AhR antagonist group (p = 0.002). The sFlt-1 level was significantly decreased after the injection of the AhR agonist compared to the control group (p = 0.001). Serum levels of VEGF were significantly decreased in the one-cigarette-exposed group compared to the control group; however, there was no difference between the control and the two-cigarette-exposed groups. The placental expression of sFlt-1, VEGF, and sEng were inconsistent. This study offers insights into the potential role of AhR on antiangiogenic sFlt-1 associated with preeclampsia. It may support the invention of a new treatment strategy for preeclampsia using AhR activation.
