Combination Analysis of PCDHGA12and CDO1 DNA Methylation in Bronchial Washing Fluid for Lung Cancer Diagnosis

Background@#When suspicious lesions are observed on computer-tomography (CT), invasive tests are needed to confirm lung cancer. Compared with other procedures, bronchoscopy has fewer complications. However, the sensitivity of peripheral lesion through bronchoscopy including washing cytology is low. A new test with higher sensitivity through bronchoscopy is needed. In our previous study, DNA methylation of PCDHGA12 in bronchial washing cytology has a diagnostic value for lung cancer. In this study, combination of PCDHGA12 and CDO1 methylation obtained through bronchial washing cytology was evaluated as a diagnostic tool for lung cancer. @*Methods@#A total of 187 patients who had suspicious lesions in CT were enrolled. PCDHGA12methylation test, CDO1 methylation test, and cytological examination were performed using 3-plex LTE-qMSP test. @*Results@#Sixty-two patients were diagnosed with benign diseases and 125 patients were diagnosed with lung cancer. The sensitivity of PCDHGA12 was 74.4% and the specificity of PCDHGA12 was 91.9% respectively. CDO1 methylation test had a sensitivity of 57.6% and a specificity of 96.8%. The combination of both PCDHGA12 methylation test and CDO1 methylation test showed a sensitivity of 77.6% and a specificity of 90.3%. The sensitivity of lung cancer diagnosis was increased by combining both PCDHGA12 and CDO1 methylation tests. @*Conclusion@#Checking DNA methylation of both PCDHGA12 and CDO1 genes using bronchial washing fluid can reduce the invasive procedure to diagnose lung cancer.

Association between Promoter Polymorphisms of TFF1, TFF2, and TFF3 and the Risk of Gastric and Diffuse Gastric Cancers in a Korean Population

Gastric cancer is one of the most common cancers in the world. The aims of this study were to evaluate the association between polymorphisms in TFF gene family, TFF1, TFF2, and TFF3 and the risk of gastric cancer (GC) and GC subgroups in a Korean population via a case-control study. The eight polymorphisms in TFF gene family were identified by sequencing and genotyped with 377 GC patients and 396 controls by using TaqMan genotyping assay. The rs184432 TT genotype of TFF1 was significantly associated with a reduced risk of GC (odds ratio, [OR) = 0.45; 95% confidence interval, [CI] = 0.25-0.82; P = 0.009), more protective against diffuse-type GC (OR = 0.20; 95% CI = 0.05-0.89; P = 0.035) than GC (OR = 0.34; 95% CI = 0.14-0.82; P = 0.017) in subjects aged < 60 yr, and correlated with lymph node metastasis negative GC and diffuse-type GC (OR = 0.44; 95% CI = 0.23-0.86; P = 0.016 and OR = 0.20; 95% CI = 0.05-0.87; P = 0.031, respectively). In addition, a decreased risk of lymph node metastasis negative GC and diffuse-type GC was observed for rs225359 TT genotype of TFF1 (OR = 0.46, 95% CI = 0.24-0.88; P = 0.020 and OR = 0.21, 95% CI = 0.05-0.88; P = 0.033, respectively). These findings suggest that the rs184432 and rs225359 polymorphisms in TFF1 have protective effects for GC and contribute to the development of GC in Korean individuals.

Effects of Curcumin and Genistein on Phorbol Ester or Tumor Necrosis Factor-alpha-Induced Mucin Production from Human Airway Epithelial Cells / 결핵및호흡기질환

BACKGROUND: We investigated whether curcumin and genistein affect the MUC5AC mucin production from human airway epithelial cells that is induced by phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-alpha (TNF-alpha). METHODS: Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or TNF-alpha for 24 hours. MUC5AC mucin production was measured by an ELISA. RESULTS: (1) Curcumin dose-dependently inhibited the production of MUC5AC mucin that was induced by PMA or TNF-alpha; (2) Genistein inhibited PMA-induced MUC5AC mucin production. However, it did not decrease TNF-alpha-induced MUC5AC mucin production. CONCLUSION: These results suggest that curcumin and genistein inhibit the production of airway mucin induced by PMA.

Regulation of Tumor Necrosis Factor-alpha-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin / 결핵및호흡기질환

BACKGROUND: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells. METHODS: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-alpha for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. RESULTS: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-alpha; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-alpha. CONCLUSION: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-alpha, by directly acting on airway epithelial cells.