Search

Uniportal video-assisted thoracoscopic surgery (UVATS) segmentectomy has emerged as an effective approach for managing early-stage non-small-cell lung cancer (NSCLC). Compared to conventional open and thoracoscopic surgeries, this minimally invasive surgical technique offers multiple benefits, including reduced postoperative discomfort, shorter hospital stays, expedited recovery, fewer complications, and superior cosmetic outcomes. Particularly advantageous in preserving lung function, UVATS segmentectomy is a compelling option for patients with compromised lung capabilities or limited pulmonary reserve. Notably, it demonstrates promising oncological results in early-stage NSCLC, with long-term survival rates comparable to those of lobectomies. Skilled thoracic surgeons can ensure a safe and effective execution of UVATS despite the potential technical challenges posed by complex tumor locations that may hinder visibility and maneuverability within the thoracic cavity. This study provided a comprehensive review of the literature and existing studies on UVATS segmentectomies. It delves into the evolution of the technique, its current applications, and the balance between its benefits and limitations. This discussion extends the technical considerations, challenges, and prospects of UVATS segmentectomy. Furthermore, it aimed to update advancements in segmentectomy for treating early-stage NSCLC, offering in-depth insights to thoracic surgeons to inform more scientifically grounded and patient-specific surgical decisions.

Defects in DNA repair pathways are emerging hallmarks of cancer. Accurate DNA repairs and replications are essential for genomic stability. Cancer cells require residual DNA repair capabilities to repair the damage from replication stress and genotoxic anti-tumor agents. Defective DNA repair also promotes the accumulation of genomic changes that eventually lead to tumorigenesis, tumor progression, and therapeutic resistance to DNA-damaging anti-tumor agents. Rad51 recombinase is a critical effector of homologous recombination, which is an essential DNA repair mechanism for double-strand breaks. Rad51 has been found to be upregulated in many malignant solid tumors, and is correlated with poor prognosis. In multiple tumor types, Rad51 is critical for tumor metabolism, metastasis and drug resistance. Herein, we initially introduced the structure, expression pattern of Rad51 and key Rad51 mediators involved in homologous recombination. Additionally, we primarily discussed the role of Rad51 in tumor metabolism, metastasis, resistance to chemotherapeutic agents and poly-ADP ribose polymerase inhibitors.