Background: Although lung cancer is the most common malignancy diagnosed in patients with venous thromboembolism (VTE), data regarding pulmonary embolism (PE) in lung cancer patients are limited. Objectives: To investigate the clinicoradiological features, clinical course and survival of lung cancer patients with PE. Methods: We performed a retrospective case-control study investigating the clinical course and survival of 40 lung cancer patients with PE (PE group). The control group (non-PE group) consisted of 80 lung cancer patients without VTE, treated during the same period. Results: Adenocarcinoma (45.0%, n = 18) was the most common histological type of lung cancer and when PE was diagnosed, the majority of the lung cancer patients were in stages IIIB (37.5%, n = 15) and IV (47.5%, n = 19). Thirty-four patients (85.0%) were diagnosed with PE within 12 months of the diagnosis of lung cancer. The median survival from the diagnosis of PE was 3.5 months in the PE group, but the survival rates revealed no significant difference between the two groups (p = 0.249). In both groups, the most common cause of death was lung cancer progression (76.9 and 80.3%, respectively), followed by chemotherapy-related septic shock (19.2 and 16.7%, respectively). Conclusions: In lung cancer patients, PE may not be the main cause of death, but one of the various complications of lung cancer, despite suggesting a poor prognosis.

Background: Cyclooxygenase-2 (COX-2) plays an important role in the development of lung cancer. DNA sequence variations in theCOX-2gene may lead to altered COX-2 production and/or activity, and so they cause inter-individual differences in the susceptibility to lung cancer. To test this hypothesis, we investigated the association between the8473T>Cpolymorphism in the 3'-untranslated region of theCOX-2gene and the risk of lung cancer in a Korean population.Methods: TheCOX-2genotypes were determined using PCR-based primer-introduced restriction analysis in 582 lung cancer patients and in 582 healthy controls that were frequency-matched for age and gender.Results: The distribution of theCOX-2 8473T>Cgenotypes was not significantly different between the overall lung cancer cases and the controls. However, when the cases were categorized by the tumor histology, the combined8473 TC+CCgenotype was associated with a significantly decreased risk of adenocarcinoma as compared with the8473 TTgenotype (adjusted OR = 0.64; 95% CI = 0.46–0.90,P= 0.01). On the stratification analysis, the protective effect of the combined8473 TC+CCgenotype against adenocarcinoma was statistically significant in the males, older individuals and ever-smokers (adjusted OR = 0.59; 95% CI = 0.39–0.91,P= 0.02; adjusted OR = 0.55; 95% CI = 0.33–0.93,P= 0.03; and adjusted OR = 0.57; 95% CI = 0.37–0.87,P= 0.01, respectively).Conclusion: These findings suggest that theCOX-2 8473T>Cpolymorphism could be used as a marker for the genetic susceptibility to adenocarcinoma of the lung.

Background: Polymorphisms in Epidermal Growth Factor Receptor (EGFR) gene may influence EGFR production and/or activity, thereby modulating susceptibility to lung cancer. To test this hypothesis, we investigated the association between polymorphisms in theEGFRgene and the risk of lung cancer in a Korean population.Methods: We first examined the frequencies of 39 candidate polymorphisms in theEGFRgene in 27 healthy Korean individuals. After then, we genotyped five polymorphisms (127378C>T, 142285G>A, 162093G>A, 181946C>T and 187114T>C) that have variant allele frequencies greater than 10%, in 582 lung cancer patients and in 582 healthy controls.Results: Of the 5 polymorphisms, the 181946C>T genotype distribution was significantly different between the cases and controls (P= 0.04). Compared with the 181946 CC + CT genotype, the 181946 TT genotype was associated with a significantly decreased risk of lung cancer (adjusted OR = 0.63, 95% CI = 0.45–0.88,P= 0.007). When the analyses were stratified by smoking status, the protective effect of the TT genotype was statistically significant in ever-smokers (adjusted OR = 0.59, 95% CI = 0.41–0.86,P= 0.007), but not in never-smokers (adjusted OR = 0.89, 95% CI = 0.45–1.75,P= 0.73;P= 0.08, test for homogeneity). Consistent with the results of the genotyping analysis, the CGGCT haplotype with the 181946C allele was associated with a significantly increased risk of lung cancer compared to the CGGTT haplotype carrying the 181946T allele (adjusted OR = 1.50, 95% CI = 1.09–2.07,P= 0.012 and Bonferroni correctedP-value = 0.048).Conclusion: These results suggest that theEGFRpolymorphisms, particularly the 181945C>T polymorphism, could be used as markers for the genetic susceptibility to lung cancer.