Aspirin plus clopidogrel is more effective in venous graft patency than aspirin alone in the short term after CABG, but further, long-term study is needed. (The Clopidogrel and Aspirin After Surgery for Coronary Artery Disease; NCT00776477).

BackgroundThe BRAF V600E and telomerase reverse transcriptase (TERT) promoter mutations have been reported in papillary thyroid carcinoma (PTC). The aim of this retrospective cross-sectional study was to add further information regarding the prevalence of the BRAF V600E and TERT promoter mutations in Chinese PTC and their clinicopathological associations.MethodsWe detected the BRAF V600E mutation and TERT promoter mutations in 455 Chinese PTC patients and analyzed the association of these mutations with several clinicopathological features.ResultsThe BRAF V600E mutation was detected in 343 (75.4%) of 455 cases and was significantly associated with older age (p<0.001) and conventional subtype (p = 0.003). TERT promoter mutations were detected in 19 (4.4%) of 434 PTCs and were associated with older age (p<0.001), larger tumor size (p = 0.024), and advanced TNM stage(p<0.001). Of the 19 patients that were positive for TERT promoter mutations, 18 (94.7%) also harbored the BRAF V600E mutation.ConclusionWe determined the prevalence and clinicopathological associations of BRAF V600E and TERT promoter mutations in Chinese PTC patients. TERT promoter mutations but not the BRAF V600E mutation were associated with more advanced TNM stage upon diagnosis.

BACKGROUND Hepatoma specific γ‐glutamyl transferase (HS‐GGT) bands were expressed in the development of hepatocellular carcinoma (HCC) and were associated with a high incidence of HCC diagnosis. The objectives of this study were to determine the levels of HS‐GGT quantitatively in the sera of patients with different liver diseases. The methylational status of GGT gene CCGG sites was analyzed in hepatoma tissues. METHODS The HS‐GGT concentrations were quantitatively analyzed in the sera of 156 HCC patients and others with liver diseases or extrahepatic tumors. In 20 hepatoma tissues, the GGT enzyme proteins were purified, the activities of GGTs of different molecular form were examined, total RNAs were extracted and amplified by using a nested polymerase chain reaction (PCR) assay, and the methylational status of CCGG site (M3) in the 5′‐noncoding region of GGT genes was investigated with the restriction enzyme Hpa II. RESULTS Total GGT activities in patients with liver diseases and extrahepatic tumors were abnormally increased. The levels of serum HS‐GGT were significantly elevated (P < 0.001) in the HCC group; the incidence of HS‐GGT over 5.5 IU/L was 86% in HCC patients and less than 3% in patients with other diseases. From liver cancer to distal noncancerous tissues, an increasing tendency (P < 0.05) of total RNA concentrations was found; the frequencies of amplified fragment and hypomethylated M3 site of GGT genes were 100% and 75% in HCC, 85% and 55% in paracancerous tissues, and 75% and 50% in noncancerous tissues, respectively. An inverse correlation was found between methylational degrees of GGT genes and expression levels of GGT. CONCLUSIONS The abnormal alteration of serum HS‐GGT level is a sensitive tumor marker for HCC diagnosis or differentiation, and the overexpression of GGT in HCC may be related to the hypomethylational status of CCGG sites of GGT genes. Cancer 2000;88:761–9. © 2000 American Cancer Society.

Tumor‐immune crosstalk within the tumor microenvironment (TME) occurs at all stages of tumorigenesis. Tumor‐associated M2 macrophages play a central role in tumor development, but the molecular underpinnings have not been fully elucidated. We demonstrated that M2 macrophages produce interleukin 1β (IL‐1β), which activates phosphorylation of the glycolytic enzyme glycerol‐3‐phosphate dehydrogenase (GPD2) at threonine 10 (GPD2 pT10) through phosphatidylinositol‐3‐kinase‐mediated activation of protein kinase‐delta (PKCδ) in glioma cells. GPD2 pT10 enhanced its substrate affinity and increased the catalytic rate of glycolysis in glioma cells. Inhibiting PKCδ or GPD2 pT10 in glioma cells or blocking IL‐1β generated by macrophages attenuated the glycolytic rate and proliferation of glioma cells. Furthermore, human glioblastoma tumor GPD2 pT10 levels were positively correlated with tumor p‐PKCδ and IL‐1β levels as well as intratumoral macrophage recruitment, tumor grade and human glioblastoma patient survival. These results reveal a novel tumorigenic role for M2 macrophages in the TME. In addition, these findings suggest possible treatment strategies for glioma patients through blockade of cytokine crosstalk between M2 macrophages and glioma cells.

Quercetin, a flavonoid found in many fruits and vegetables, belongs to an extensive class of polyphenolic compounds. Previous studies reported that quercetin inhibits the proliferation of various cancer cells and tumor growth in animal models. We investigated the growth inhibition and colony formation of quercetin on three bladder cancer cells (EJ, J82 and T24). The expression of tumor suppressor genes and oncogenes such as P53, Survivin, PTEN, as well as the methylation status of these genes was also evaluated. We observed that quercetin induced apoptosis in bladder cancer cells in a time- and dose-dependent manner. Quercetin (100 micromolars) significantly inhibited EJ, T24 and J82 cell growth accompanied by an increase in the G0/G1 phase. In all cell lines, quercetin decreased the expression of mutant P53 and Survivin proteins. However, there was no change in the level of PTEN protein. Moreover, the DNA methylation levels of the estrogen receptor (Er-beta), P16INK4a and RASSF1A were strongly decreased (from 35 to 70%) in the quercetin-treated group compared to the control. In conclusion, our study suggested that quercetin inhibits growth, colony formation and hypermethylation of bladder cancer cell lines. Quercetin-induced apoptosis might be associated with a decrease in mutant P53 and Survivin proteins.

No abstract

The purpose of this study was to evaluate the value of multi-detector computed tomography (MDCT) angiography for the diagnosis of congenital aortic arch anomalies and present the radiological images of congenital aortic arch anomalies in Chinese children. MDCT angiography and transthoracic echocardiography (TTE) were applied for the diagnosis of congenital aortic arch anomalies in 362 Chinese children between May 2006 and December 2011 (age ranges from 5 days to 12 years; mean age, 3.3 years). Surgery and/or catheter angiography (CA) were conducted in all patients to confirm the final diagnosis. In the 362 Chinese children with congenital heart anomalies, congenital aortic arch anomalies were definitely diagnosed in 198 children and 164 children ruled out by operation and/or (CA). Among the 198 children with anomalies, coarctation of aorta (CoA), interruption of aortic arch (IAA), right aortic arch, aberrant right subclavian artery and double aortic arch were diagnosed in 134, 32, 20, 10 and 2 children respectively, and there were 6 cases with uncommon congenital aortic arch anomalies: 2 had double aortic arch including 1 with five branches of the aortic arch, 2 had isolation of the right subclavian artery with two patent ductus arteriosus (PDA), 1 had an isolation of the common carotid artery with a PDA, and 1 had double PDA with a single ventricle and pulmonary artery atresia. Among the 32 children with IAA, 28 were of type A, and 4 were of type B. The diagnostic sensitivity, specificity and accuracy of MDCT angiography for congenital aortic arch anomalies were 100% (198/198), 98% (161/164) and 99% (359/362), respectively. The diagnostic sensitivity, specificity and accuracy of TTE were 92% (182/198), 81% (133/164) and 87% (315/362), respectively. In conclusion, MDCT angiography is a reliable, noninvasive imaging technique for the diagnosis of congenital aortic arch anomalies in children. Sometimes, even more information can be obtained from this technique than from conventional angiography.

A b s t r a c t Tissues of hepatocellular carcinoma (HCC) can express hepatoma-specific y-glutamyltransferase (GGT)and secrete GGT into circulating blood. Serum GGT was separated into several bands (up to 11), including hepatoma-specific bands (HSBs, V,11, and IV) y-Glutamyltransferase (GGT; Enzyme Commission number 2.3.2.2) is a membrane-bound ectoenzyme that catalyzes the degradation of glutathione and other y-glutamyl compounds by hydrolysis of the y-glutamyl moiety or by its transfer to a suitable acceptor.