(1) Background: Liver kinase B1 (LKB1) is a tumor suppressor gene involved in cell growth and metabolism. However, its alterations are not routinely assessed for guiding therapy in clinical practice. We assessed LKB1 expression by immunohistochemistry as a potential biomarker. (2) Methods: This bicentric retrospective cohort study analyzed data from patients with advanced NSCLC who initiated platinum-based chemotherapy or epidermal growth factor receptor- tyrosine kinase inhibitor (EGFR-TKI) between January 2016 and December 2020. Kaplan–Meier and Cox regression models were used for survival curves and multivariate analysis. (3) Results: 110 patients were evaluated, and the clinical stage IV predominated the lung adenocarcinoma histology. LKB1 loss was observed in 66.3% of cases. LKB1 loss was associated with non-smokers, the absence of wood smoke exposure and an EGFR wild-type status. The median progression-free survival (PFS) and overall survival (OS) in the population were 11.1 and 26.8 months, respectively, in the loss group, compared with cases exhibiting a positive expression. After an adjustment by age, smoking status, Eastern Cooperative Oncology Group Performance Score (ECOG-PS), EGFR status and type of administered therapy, LKB1 loss was significantly associated with worse PFS and OS. (4) Conclusion: Patients with an LKB1 loss had worse clinical outcomes. This study warrants prospective assessments to confirm the prognostic role of the LKB1 expression in advanced NSCLC.

Introduction: Pulmonary hypertension (PH) is an increase in the normal value of systolic pressure of the pulmonary artery, frequently due to congenital heart diseases being its treatment the correction of this defects; alternatively, hyperbaric oxygen (HBO) has shown beneficial effects facilitating neovascularisation and decreased vascular resistance. An experimental study was designed to determine the effect of HBO on the alveoli-capillary unit in a murine model of irreversible pulmonary hypertension (IPAH) induced with monocrotaline.Material and methods: Four groups of 10 Wistar rats each were considered: A (control), B (HBO), C (IPAH), and D (IPAH+HBO). HBO was administered at 2 atm, 1 h daily, for 15 days. At the end of this time, systolic pulmonary artery pressure (PAP) was measured, followed by histologically quantification of the number of cells, vascular buttons, and neoformation vessels employing the immunochemistry detection of hypoxia-induced factor-1 (HIF-1), vascular endothelial growth factor (VEGF), and CD34, respectively.Results: Histologically, this matches with an increase of the average number of positive HIF-1 cells, and an increase in VEGF-positive vascular buttons in group D rats compared with those of group C. The number of CD34-positive neovessels was similar in groups C and D, but in the latter group the number of capillary vessels was more significant.Conclusions: This suggests that angiogenesis and vasculogenesis were induced by HIF-1, and it has been achieved due to an early effect of HBO therapy. Presumably, neovessels were formed between days 5 and 10 following HBO therapy, but more experimental studies are required to test this hypothesis.

Acute myocardial infarction has been placed in the leading cause of death in the world. Coronary interventionism is the gold standard in the treatment of AMI, however its therapeutic window is very limited. The decrease in the area of myocardial infarction and hemodynamic improvement have been reported with the use of HBO therapy in the ongoing AMI, as well as angiogenesis, decreased inflammation and useful as ischemic preconditioning. Methodology:An experimental study was designed to determine the effect of HBO on the rat cardiomyocyte after 6 hours of an AMI induced by ligation of the anterior descending coronary. The HBO was administered through a 100% hyperbaric chamber, at 2 ATA, for one hour daily. The size of the infarcted area was macroscopically measured, and antioxidant enzymes were evaluated. Six groups were compared. Results:A statistically significant decrease of the infarcted area was obtained from the 3rd session of HBO. Regarding oxidative stress, significant results were obtained for TBARS, TAS and 3-NT from the 5th session with HBO. Conclusion:Hyperbaric oxygen therapy shows a beneficial effect after 3 days of the induction of AMI, this is reflected by a decrease in the infarcted area; and after the 5th day reflected by a decrease in TBARS and 3-NT.