The incidence of cancer-associated thrombosis has increased in recent years. While the association between venous thromboembolism (VTE) and chemotherapy is well established, there is no clear link between immune checkpoint inhibitors (ICIs) and VTE risk. Many risk assessment models (RAMs) have been developed to identify high-risk patients who need prophylaxis. However, these models are validated in patients undergoing chemotherapy, while they are scarce in those receiving immunotherapy. Moreover, the mechanisms linking ICIs to thrombosis are still a matter of debate. They include the upregulation of pro-inflammatory intracellular pathways, the release of cytokines, the activation of innate immune cells, the release of tissue factors and platelet activation, and the increase in adhesion molecules, thus resulting in the recruitment of agents involved in coagulation. Promising biomarkers are emerging to identify patients undergoing ICIs who are at high risk of developing VTE and need prophylaxis. In this review we investigate the possible causation between cancer-associated thrombosis (CAT) and immunotherapy and the underlying pathophysiological mechanisms. Thus, we suggest the most appropriate therapeutic approaches based on currently available data.

Background: Resectable or potentially resectable stage II–III NSCLC encompasses heterogeneous clinical scenarios. The introduction of neoadjuvant and perioperative strategies has expanded treatment options while increasing the complexity of multidisciplinary decision-making and the need to reassess treatment pathways over time. Methods: We conducted a single-centre retrospective descriptive analysis of 101 patients with clinical or pathological stage II–III NSCLC discussed within our thoracic multidisciplinary team (MDT) between 2023 and 2025. Using MDT meeting records supplemented by medical records, we analysed decision-making trajectories and the main reasons for changes in treatment strategy. Results: Three major decision points emerged: selection of preoperative treatment, reassessment of resectability and operability after preoperative treatment, and postoperative assessment of recurrence risk and feasibility of adjuvant treatment. Treatment pathways were modified according to disease response or progression, surgical feasibility, comorbidities, treatment-related toxicity, pathological findings, and postoperative recovery. Particularly challenging scenarios included heterogeneous stage II disease, borderline resectability, and discordant responses after induction therapy. Conclusions: Perioperative management of stage II–III NSCLC requires dynamic, longitudinal multidisciplinary decision-making rather than a single treatment decision at diagnosis. Integrated reassessment of clinical, pathological, and molecular disease characteristics, treatment response, patient fitness, and surgical feasibility may help individualise treatment pathways.