Metastatic dissemination defines a complex phenomenon driven by genetic forces and, importantly, determined by interaction between cancer cells and the surrounding stroma. Although the biologic and immune reactions which characterize the process have been widely and extensively evaluated, fewer data are available regarding the mechanical and physical forces to which circulating neoplastic clones are exposed. It should be hypothesized that this interaction can be modified in case of concomitant pathologic conditions, such as chronic vasculopathy, which frequently occurs in lung cancer patients. We here aim at analyzing and discussing the complex interplay between lung malignant transformation and arteriopathy, mainly focusing on the immune–inflammatory systemic reaction. Notably—in most instances—smoking-related fixed airflow obstruction, including but not limited to COPD, frequently coexists and contributes to both tumor progression and vascular complications. Attention is paid mainly to the analysis of the role of immune checkpoint inhibitors and their interaction with triple bronchodilation and antiaggregants. Understanding the biomechanical and molecular dynamics of lung cancer progression in altered vascular territories has several translational implications in defining risk stratification and in surgical planning and therapeutic targeting. Moreover, computational modeling of the physical forces which regulate the transit and extravasation of metastatic clones in altered contexts could be of help in deciphering the whole process and in determining more effective blockade strategies.

Metastatic dissemination defines a complex phenomenon driven by genetic forces and importantly determined by interaction between cancer cells and the surrounding stroma. Although the biologic and immune reactions which characterize the process have been widely and extensively evaluated, fewer data are available regarding the mechanic and physical forces to which circulating neoplastic clones are exposed. It should be hypothesized that this interaction can be modified in case of concomitant pathologic conditions, such as chronic vasculopathy which frequently occurs in lung cancer patients. We here aim at analysing and discussing the complex interplay between lung malignant transformation and artheriopathy, mainly focusing on the immune-inflammatory sistemic reaction. Notably - in most instances – smoking history and a consequent chronic obstructive pulmonary disease cohexists. A main attention is payed to the analysis of the role of immunecheckpoint inhibitors and their interaction with triple bronchodilation and antiaggreagants. Understanding the biomechanical and molecular dynamics of lung cancer progression in altered vascular territories has several translational implications in defining risk stratification, in surgical planning and therapeutic targeting: Moreover, computational modelling of the physical forces which regulate the transit and extravasation of metastatic clones in altered contexts could be of help in deciphering the whole process and in determining more effective blockade strategies.

Cancer progression is a multistep process driving by oncogenic forces and promoted by the close interaction between neoplastic cells and the surrounding microenviroment as well as the pre-metastatic niche. In this perspective the context of chronic arteriopathy represents a specific setting which can be associated with the arousal of lung cancer being and most often the both diseases share smoke as common risk factor. Within respect to the arterial disease we focused on the role of aneurysma dilations and on its impact on blood dynamics in cancer. Through a physical approach we defined a mathematical model which identifies altered viscosity as the physical variable linking cancer to aneurysm-related rheology. To further validate this theroretic approach an extensive screening of 976 patients carried diagnosis of cancer and arteriopaty from 2018 to 2024 was performed. From them a population of 120 cancer patients with concomitant aneurysmal disease was selected. The study cohort was subdivided based on primary site of origin into 3 groups: lung cancer (39 cases), other solid organ cancer (66 cases) and hematologic neoplasms (15 cases). Exaustive demographic, clinical and biologic data were available for each case. A close male gender-specificity was documented (83.3% of cases) as well as significant exposure to cigarette smoke. Quite surprisingly a reduced metastatic potential was reported in in all cancer types.

Background: Chronic obstructive pulmonary disease (COPD) is among the most relevant comorbidity associated with lung cancer. The advent of innovative triple treatment approaches for COPD has significantly improved patients’ quality of life and outcomes. Few data are available regarding the impact of triple inhaler therapy on patients featuring COPD and lung cancer. Methods: We retrospectively evaluated the impact of triple inhale bronchodilators in a cohort of 56 patients with treated COPD who underwent lung surgery for primary cancer. Results: Triple bronchodilation can help to relieve the symptoms of the disease and improve lung function, allowing people with lung cancer to reduce the risk of serious exacerbations and improve their quality of life. Conclusions: Within the limits of the study, it should be underlined that bronchodilators can effectively affect the outcome and performance status after thoracic surgery.