The number of immune cells, especially dendritic cells and cytotoxic tumor infiltrating lymphocytes (TIL), particularly Th1 cells, CD8 T cells, and NK cells is associated with increased survival of cancer patients. Such antitumor cellular immune responses can be greatly enhanced by adoptive transfer of activated type 1 lymphocytes. Recently, adoptive cell therapy based on infusion of ex vivo expanded TILs has achieved substantial clinical success. Cytokine-induced killer (CIK) cells are a heterogeneous population of effector CD8 T cells with diverse TCR specificities, possessing non-MHC-restricted cytolytic activities against tumor cells. Preclinical studies of CIK cells in murine tumor models demonstrate significant antitumor effects against a number of hematopoietic and solid tumors. Clinical studies have confirmed benefit and safety of CIK cell-based therapy for patients with comparable malignancies. Enhancing the potency and specificity of CIK therapy via immunological and genetic engineering approaches and identifying robust biomarkers of response will significantly improve this therapy.

Purpose To determine the long-term efficacy of adjuvant immunotherapy with autologous cytokine-induced killer (CIK) cells for locally advanced gastric cancer patients. Experimental design One hundred and fifty-one patients with stage III/IV gastric cancer who had undergone gastrectomy were enrolled, assigned to two groups (immunotherapy group versus no immunotherapy group/or control group), and followed. Results The 5-year overall survival (OS) and 5-year disease-free survival (DFS) rates for immunotherapy versus control group were 32.4 versus 23.4 % (P = 0.071) and 28.3 versus 10.4 % (P = 0.044), respectively. For patients with intestinal-type tumors, the 5-year OS and DFS rates were significantly higher for immunotherapy (OS, 46.8 vs. 31.4 % and P = 0.045; DFS, 42.4 vs. 15.7 % and P = 0.023). In the immunotherapy group, the mean CD3⁺ level, CD4⁺ level, and CD4⁺/CD8⁺ ratio increased from 50.8, 26.5, and 0.9 %, respectively, at baseline to 62.6, 35.0, and 1.4 %, respectively, 1 week after the first CIK-cell treatment, returned to baseline after 2 months, and maintained a higher level (60.7 ± 8.2 %, 34.2 ± 7.1 %, and 1.3 ± 0.3 %, respectively) 2 months after 3 cycles of immunotherapy. Conclusions Adjuvant immunotherapy with CIK cells prolongs DFS in patients with locally advanced gastric cancer and significantly improves OS in patients with intestinal-type tumors. Intestinal-type tumors could be selected as an important indication for CIK-cell therapy. This treatment may help improve T-lymphocyte subset distribution and improve the host’s immune functions, but multiple cycles are necessary for long-term therapeutic efficacy.

C-Jun NH2-terminal kinase/stress-activated kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38 MAPK) are important components of cellular signal transduction pathways, which have been reported to be involved in viral replication. However, little is known about JNK1/2 and p38 MAPK signaling pathways in enterovirus 71 (EV71)-infected immature dendritic cells (iDCs). Thus, iDCs were induced from peripheral blood mononuclear cells (PBMC) and performed to explore the expressions and phosphorylation of molecules in the two signaling pathways as well as secretions of inflammatory cytokines and interferons during EV71 replication.

Liver is one of the most important organs in energy metabolism. Most plasma apolipoproteins and endogenous lipids and lipoproteins are synthesized in the liver. It depends on the integrity of liver cellular function, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs, these processes are impaired and the plasma lipid and lipoprotein patterns may be changed. Liver cancer is the fifth common malignant tumor worldwide, and is closely related to the infections of hepatitis B virus (HBV) and hepatitis C virus (HCV). HBV and HCV infections are quite common in China and other Southeast Asian countries. In addition, liver cancer is often followed by a procession of chronic hepatitis or cirrhosis, so that hepatic function is damaged obviously on these bases, which may significantly influence lipid and lipoprotein metabolism in vivo. In this review we summarize the clinical significance of lipid and lipoprotein metabolism under liver cancer.