RESUMO
BACKGROUND: Though methods for the diagnosis of pancreatic masses are various, such as ultrasonography (US), computed tomography (CT), endoscopic ultrasonography (EUS), and contrast-enhanced computed tomography (CE-CT), their sensitivity, specificity, and accuracy are not quite satisfying. Contrast-enhanced endoscopic ultrasonography (CE-EUS), as a new technique, has its own unique advantages in diagnosing pancreatic disease. However, its sensitivity, specificity, and accuracy are still controversial. OBJECTIVE: To evaluate the accuracy of CE-EUS for differential diagnosis between benign and malignant pancreatic mass lesions. DESIGN: Eighteen relevant articles systemically searched from PubMed, Web of Science, Ovid, Scopus, and MEDLINE were selected. The pooled results were calculated in a fixed effects model. MAIN OUTCOME MEASUREMENT: The pooled sensitivity, specificity, positive likelihood ratio (LR), negative likelihood ratio, diagnostic odds ratio (OR), and summary receiver operating characteristic (SROC) curve. RESULTS: The pooled sensitivity, specificity, and diagnostic odds ratio of CE-EUS for the differential diagnosis of pancreatic adenocarcinomas were 0.91 (95% confidence interval (CI), 0.89-0.93), 0.86 (95% CI, 0.83-0.89), and 69.50 (95% CI, 48.89-98.80), respectively. The SROC area under the curve was 0.9545. The subgroup analysis based on excluding the outliers showed that the heterogeneity was eliminated and the pooled sensitivity and specificity were 0.92 (95% CI, 0.90-0.93) and 0.87 (95% CI, 0.84-0.89), respectively. The SROC area under the curve was 0.9569. CONCLUSION: CE-EUS is a useful method to distinguish pancreatic adenocarcinoma from other pancreatic diseases. Compared with EUS elastography, it has higher specificity. However, it is still not superior to pathological diagnosis for the identification of pancreatic carcinomas.
RESUMO
The anticancer effect of MK-2206, an Akt inhibitor, has been explored in some types of cancers, but its effect on gastric cancer is unclear. In this study, we aimed to investigate its anticancer effect in gastric cancer cells. Cell viability and colony formation assays showed that MK-2206 effectively inhibited the proliferation of SGC-7901 and MKN45 cells. The 50% inhibitory concentration values after 24, 48, and 72 hours' treatment were 22.92, 13.68, and 8.55 µM in SGC-7901 cells and 19.21, 13.10, and 9.11 µM in MKN45 cells, respectively. Treatment with MK-2206 induced apoptosis in SGC-7901 cells as indicated by flow cytometry assay. The combination indexes of MK-2206 and doxorubicin were 0.59 in SGC-7901 cells and 0.57 in MKN45 cells, whereas for 5-fluorouracil (5-FU) the indexes were 0.17 in SGC-7901 cells and 0.73 in MKN45 cells, indicating that MK-2206 could work synergistically with doxorubicin or 5-FU to inhibit cell growth. Furthermore, a small dose (1 µM) of MK-2206 co-treatment with doxorubicin or 5-FU was sufficient for complete inhibition of chemotherapeutic alteration of phosphorylated Akt expression and significant enhancement of pro-apoptosis effect through the activation of caspase pathway. Therefore, MK-2206 effectively inhibits gastric cancer cell growth by attenuation of Akt phosphorylation and synergistically enhances the antitumor effect of doxorubicin and 5-FU via caspase-dependent apoptosis.