PI3K/AKT signaling is involved in Lewis y antigen-mediated proliferation of these cells

Another study revealed that PI3K/ AKT/mTOR signaling pathways serve as key regulators of platinum-based drug sensitivity of ovarian cancer cells. The present study found that expression of CD44 and Lewis y antigen was increased in tissue sections from drug-resistant ovarian cancer patients. Furthermore, multi-variable analysis demonstrated that CD44 and Lewis y antigen expression were both independent risk factors for development of drug-resistant ovarian cancer. Together with results from our preliminary studies, these findings suggest that the Lewis y antigen, as an important component of the molecular structure of CD44, promotes proliferation and inhibits apoptosis of ovarian cancer cells, leading to drug resistance via activation of PI3K/AKT signaling pathways. Our preliminary The tubs were placed at a common shelf height in a completely randomized design at the JARTU laborator studies also revealed that transfection with fucosyltransferase results in upregulated expression of Bcl-2, Topo-I, and Topo-II b in RMG-1-H cells, in addition to increased expression of the Lewis y antigen. Increased levels of the Lewis y antigen promoted the expression of Topo-I and Topo-II b through regulation of Bcl-2, resulting in enhanced DNA repair and inhibition of carboplatininduced apoptosis. These findings indicate that the Lewis y antigen can also promote development of drug resistance in tumor cells through topoisomerase-dependent pathways. Levels of the p38MAPK mRNA were also significantly increased by expression of the Lewis y antigen in transfected cells. In addition, levels of the p38MAPK and caspase-3 mRNAs were both increased in carboplatin-treated RMG-1-H cells, suggesting that Lewis y antigen-mediated apoptosis of ovarian cancer cells is associated with activation of the p38MAPK signaling pathway. In conclusion, we propose that the Lewis y antigen, as a structural component of CD44, integrins a5b1 and avb3, as well as EGFR, play a role in various cell adhesion processes that mediate both cell adhesion and drug resistance. In the current study, we analyzed drug-resistant clinical ovarian carcinoma samples and found that that Lewis y antigen and CD44 were associated with ovarian carcinoma drug resistance. In light of our previous studies, we consider that the Lewis y antigen represents a key molecule involved in CAM-DR with potential as a novel anti-apoptotic target for the treatment of drug resistant ovarian carcinomas. Since it was first introduced into clinical practice in 1980s, the transjugular intrahepatic portosystemic shunt has become an important and effective interventional procedure in the management of complications related to portal hypertension. Although the primary patency of TIPS has been greatly improved as its techniques improved, the long-term patency of TIPS is still suboptimal.The causes of TIPS dysfunction are multifactorial. The major reasons for limited long-term patency of TIPS are acute occlusion due to thrombosis and the development of pseudointimal hyperplasia in the TIPS or intimal hyperplasia in the hepatic venous outflow. Histologic studies have confirmed that either pseudointimal or true intimal hyperplasia results from migration and proliferation of venous smooth muscle cells sometimes related to cellular injury when the track is exposed to bile. Several studies have also demonstrated that the hepatic venous outflow is the primary site of stenosis when covered stent are used to construct the TIPS. To overcome this problem, the current practice is to extend the outflow ends of the stent-grafts from the TIPS tract into inferior vena cava.