Metformin use and survival from lung cancer: A population-based cohort study.

Preclinical evidence suggests that metformin, a widely prescribed anti-diabetic drug, may inhibit lung cancer progression. We investigated whether metformin use was associated with decreased risk of cancer-specific mortality in lung cancer patients. This study included newly diagnosed lung cancer patients (identified from English National Cancer Data Repository, 1998-2009) with type 2 diabetes (based on UK Clinical Practice Research Datalink prescriptions and diagnosis records). Lung cancer deaths occurring up to 2012 were identified using Office of National Statistics mortality data and the association between metformin use (before and after diagnosis) and risk of lung cancer-specific mortality was calculated using Cox regression models. In analysis of 533 patients, we found a weak non-significant reduction in lung cancer-specific mortality with metformin use after diagnosis (adjusted HR, 0.86; 95% CI, 0.68-1.09). No association was evident for metformin use before diagnosis and cancer-specific mortality in analysis of 1350 patients (adjusted HR, 0.97; 95% CI, 0.86, 1.11). Associations were similar by duration of use. In addition, after adjustment for potential confounders, there was little evidence of an association between the use of other anti-diabetic medications (either before or after diagnosis) and lung cancer-specific mortality; including sulfonylureas, insulin or other anti-diabetic medications (such as thiazolidinediones). Overall, the results from this population-based study provide little evidence of a protective association between metformin use and cancer mortality in lung cancer patients.

Low-dose aspirin and survival from lung cancer: a population-based cohort study.

BACKGROUND: Preclinical evidence suggests that aspirin may inhibit lung cancer progression. In a large cohort of lung cancer patients, we investigated whether low-dose aspirin use was associated with a reduction in the risk of lung cancer-specific mortality. METHODS: We identified lung cancer patients from English cancer registries diagnosed between 1998 to 2009 from the National Cancer Data Repository. Medication usage was obtained from linkages to the UK Clinical Practice Research Datalink and lung cancer-specific deaths were identified from Office of National Statistics mortality data. Hazard ratios (HR) and 95 % confidence intervals (CI) for the association between low-dose aspirin use (before and after diagnosis) and risk of lung cancer-specific mortality were calculated using Cox regression models. RESULTS: A total of 14,735 lung cancer patients were identified during the study period. In analysis of 3,635 lung cancer patients, there was no suggestion of an association between low-dose aspirin use after diagnosis and cancer-specific mortality (adjusted HR=0.96, 95% CI: 0.85, 1.09). Similarly, no association was evident for low-dose aspirin use before diagnosis and cancer-specific mortality (adjusted HR=1.00, 95% CI: 0.95, 1.05). Associations were comparable by duration of use and for all-cause mortality. CONCLUSION: Overall, we found little evidence of a protective association between low-dose aspirin use and cancer-specific mortality in a large population-based lung cancer cohort.

Continuing smoking between adolescence and young adulthood is associated with higher arterial stiffness in young adults: the Northern Ireland Young Hearts Project.

OBJECTIVES: To investigate the associations between smoking in adolescence and adulthood, and changes in smoking behaviour between these age periods, with arterial stiffness in young adults; and whether any such associations could be explained by concomitant smoking-related levels of inflammation and endothelial dysfunction. METHODS: We studied 424 individuals (216 women) in whom smoking status was assessed in adolescence (age 15 years) and again in young adulthood (mean age of 22.6 ± 1.6 years), along with aorto-iliac, aorto-radial, and aorto-dorsalis pedis pulse wave velocity (PWV), and markers of inflammation (i.e. C-reactive protein and fibrinogen) and endothelial dysfunction (i.e. von Willebrand factor and tissue-plasminogen activator antigen) in young adulthood only. RESULTS: Smoking in adolescence was associated with higher aorto-iliac PWV, as well as with inflammation and endothelial dysfunction levels (expressed as two scores), independently of other adolescent and adult lifestyles. Compared with never smokers, continuing smokers, but not starters nor quitters, showed higher aorto-iliac PWV, independent of changes in other lifestyle variables: +0.157 m/s (95% confidence interval 0.026-0.288). This difference was attenuated to 0.124 m/s (-0.009 to 0.257) after adjustment for changes in traditional biological risk factors, but was not materially affected when adjusted for the inflammation and endothelial dysfunction scores, despite the continuing smoking-related higher levels of inflammation and endothelial dysfunction. Smoking was not associated with aorto-radial and aorto-dorsalis pedis PWV. CONCLUSION: Starting to smoke in adolescence and continuing to do so up to young adulthood is adversely associated with aortic stiffness. The continuing smoking-related aortic stiffness was not explained by concomitant higher inflammation and endothelial dysfunction. Prevention of smoking should target the young to prevent arterial stiffness in young adults.