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Abstract: Introduction: Patients with chronic obstructive pulmonary disease (COPD) frequently experience concurrent comorbidities; therefore, risk assessment for major adverse cardiovascular events (MACEs) is very important. Objectives: We explored the association between COPD and risk of MACEs with three common clinical events: acute myocardial infarction (AMI), ischemic stroke (IS), and cardiovascular death (CVD). Methods: We evaluated the predictive value of the CHA2DS2‐VASc score (congestive heart failure [C], hypertension [H], age [A], diabetes [D], stroke [S], and vascular disease [VASc]) for MACEs in COPD patients. In this observational study, we retrospectively reviewed the records of 29 258 patients with COPD between 2005 and 2009 in relation to MACE risk using the CHA2DS2‐VASc score. We calculated the hazard ratios (HR) and 95% confidence intervals (CI) using a significance level of .05. Results: Patients with COPD had significantly (P < .001) increased risk of MACEs, and a high prevalence of CHA2DS2‐VASc scores ≥ 6, predicting MACEs (16.1%), AMI (3.3%), IS (8.7%), and CVD (4.0%). A good discrimination was found for MACEs, IS events, and CVD events (AUC = 0.740, 0.739, and 0.778, respectively) but poorer discrimination for AMI events (AUC = 0.697). Conclusion: Early lifestyle modifications and antithrombotic therapy may be essential for COPD patients at a high risk of MACEs, that is, those with CHA2DS2‐VASc scores ≥ 6. [ABSTRACT FROM AUTHOR]

Introduction. Epidermal growth factor receptor (EGFR) mutations are known as oncogene driver mutations and with EGFR mutations exhibit good response to the EGFR tyrosine kinase inhibitor Gefitinib. Some studies have shown that activation of estrogen and estrogen receptor α or β (ERα/β) promote adenocarcinoma. We evaluated the relationship between the two receptors and the potential therapeutic benefit with Gefitinib and Tamoxifen. Methods. We assessed the association between EGFR mutations as well as ERα/β expression/location and overall survival in a cohort of 55 patients with LAC from a single hospital. PC9 (EGFR exon 19 deletion mutant; Gefitinib-vulnerable cells) and A549 (EGFR wild type; Gefitinib-resistant cells) cancer cells were used to evaluate the in vitro therapeutic benefits of combining Gefitinib and Tamoxifen. Results. We found that the cytosolic but not the nuclear expression of ERβ was associated with better OS in LAC tumors but not associated with EGFR mutation. The in vitro study showed that combined Gefitinib and Tamoxifen resulted in increased apoptosis and cytosolic expression of ERβ. In addition, combining both medications resulted in reduced cell growth and increased the cytotoxic effect of Gefitinib. Conclusion. Tamoxifen enhanced advanced LAC cytotoxic effect induced by Gefitinib by arresting ERβ in cytosol. [ABSTRACT FROM AUTHOR]