Even within an individual, the same drug can have differing effects during different stages of cancer. Multidrug resistance (MDR) is considered as one of the main disturbances

affecting chemotherapeutic effects. Drug-resistant protein that induces MDR was always over-expressed within medication, shown to render chemotherapeutics unable to enter the effector target (i.e., the nucleus), selleck screening library leading to the failure of chemotherapy. Currently, platinum family is the powerful chemotherapy drug widely used in clinical. Cisplatin (CDDP) showed excellent therapeutic effects on various tumors in several organs, including lung, ovary, bladder, pate, esophagus, cervix, endometrium and testis [1]. Additionally,

oxaliplatin (L-OHP) was regarded as a third generation novel type of platinum compounds following CDDP and carboplatin, replacing the amino group of cisplatin with a bulky diaminocyclohexane (DACH) ring [2] and showing specific properties of high efficiency and low toxicity [3, 4]. Moreover, L-OPH was shown to be effective in primary CDDP- and carboplatin-resistant colon carcinoma and some secondary CDDP-resistant malignant tumors [5–7]. Gastric cancer is this website a common alimentary canal malignant tumor, which shows both primary and secondary drug resistance. Chen et al. considered that the drug-resistant mechanisms of gastric cancer to L-OHP and CDDP were correlated with augmentation of DNA repair and ATP7A overexpression [8]. MDR mechanisms of gastric cancer cells were detected to aid in choosing Acyl CoA dehydrogenase effective anti-cancer drugs, and individualized treatment plans were made, resulting in improved gastric therapeutic effects. With the rapid developments in the field of tumor immunology, use of immune effector cells, including lymphokine-activated killer (LAK), tumor-infiltration lymphocyte (TIL), anti-CD3 antibody induced

activated killer (CD3AK) and cytolytic T lymphocyte (CTL) cells, on certain advanced-stage tumors has shown therapeutic effects [9], and this treatment could kill remnant chemotherapy-resistant tumor cells [10]. Cytokine-induced killer (CIK) cells are a novel type of immunocompetent cells with highly efficient and broad-spectrum anti-tumor activity. These cells have been shown to proliferate among and p38 MAPK activation directly kill CD3+CD56+ tumor cells in vitro [11–13]. Furthermore, CIK cells were shown to enhance cellular immune function in hosts [14, 15], and previous studies showed the killing activity of CIK cells on MDR tumor cells was similar or greater than that on parental drug-sensitive tumor cells [16, 17]. This treatment is thought to be effective for patients with recurrent tumors when combined with chemotherapy [10, 18–20].