Open versus robot-assisted retroperitoneal tumors resection involving inferior vena cava, abdominal aorta, and renal hilum: a comparative study.

INTRODUCTION: Surgery is currently the only effective treatment for retroperitoneal tumors that do not involve any specific organ. The use of robots for removing both benign and malignant retroperitoneal tumors is considered safe and feasible. However, there is insufficient evidence to determine whether robotic retroperitoneal tumor resection (RMBRs) is superior to open retroperitoneal malignant resection (OMBRs). This study compares the short-term outcomes of robotic excision of benign and malignant retroperitoneal tumors with open excision of the same-sized tumors. METHODS: The study compared demographics and outcomes of patients who underwent robotic resection (n = 54) vs open resection (n = 54) of retroperitoneal tumors between March 2018 and December 2022. A 1:1 matching analysis was conducted to ensure a fair comparison. RESULTS: The study found that RBMRs resulted in reduced operative time (OT), estimated blood loss (EBM), and postoperative hospital stay (PSH) when compared to OBMRs. Additionally, RBMRs reduced EBL, PHS, and OT for patients with malignant tumor involvement in major vessels. No significant differences were found in tumor size, blood transfusion rate, and morbidity rate between the RBMRs and OBMRs groups. CONCLUSION: When comparing RMBRs to OMBRs, it was observed that RMBR was associated with lower (EBL), shorter postoperative hospital stays (PHS), and reduced operative time (OT) in a specific group of patients with both benign and malignant tumors.

UBC9 deficiency enhances immunostimulatory macrophage activation and subsequent antitumor T cell response in prostate cancer.

The role of tumor-associated macrophages (TAMs), along with the regulatory mechanisms underlying distinct macrophage activation states, remains poorly understood in prostate cancer (PCa). Herein, we report that PCa growth in mice with macrophage-specific Ubc9 deficiency is substantially suppressed compared with that in wild-type littermates, an effect partially ascribed to the augmented CD8+ T cell response. Biochemical and molecular analyses revealed that signal transducer and activator of transcription 4 (STAT4) is a crucial UBC9-mediated SUMOylation target, with lysine residue 350 (K350) as the major modification site. Site-directed mutation of STAT4 (K350R) enhanced its nuclear translocation and stability, thereby facilitating the proinflammatory activation of macrophages. Importantly, administration of the UBC9 inhibitor 2-D08 promoted the antitumor effect of TAMs and increased the expression of PD-1 on CD8+ T cells, supporting a synergistic antitumor efficacy once it combined with the immune checkpoint blockade therapy. Together, our results demonstrate that ablation of UBC9 could reverse the immunosuppressive phenotype of TAMs by promoting STAT4-mediated macrophage activation and macrophage-CD8+ T cell crosstalk, which provides valuable insights to halt the pathogenic process of tumorigenesis.