Preoperative NLR for predicting survival rate after radical resection combined with adjuvant immunotherapy with CIK and postoperative chemotherapy in gastric cancer.

PURPOSE: The purpose of this study is to determine the efficacy of adjuvant immunotherapy with autologous cytokine-induced killer (CIK) for postoperative patients with gastric cancer and to investigate the impacts of the predictors on the efficacy of CIK immunotherapy. PATIENTS AND METHODS: Ninety-two gastric cancer patients who have accepted radical resection were enrolled. The CIK and control groups were established by 1:1 matching on their baseline. As prognosis indicators, preoperative blood cell counts, the neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) were analyzed, respectively. Statistical analyses were done using IBM SPSS Statistics ver.19.0. RESULTS: CIK treatment significantly prolonged disease-free survival (DFS) (p < 0.05) and there was a tendency of longer overall survival (OS) in the CIK group (p = 0.057). Preoperative NLR was an independent prognostic factor for DFS (p < 0.05). When patients were classified into low and high NLR groups using the cutoff value of 2.995, patients in the low NLR group had a better DFS (p < 0.05). Subset analysis showed that CIK immunotherapy significantly prolonged the DFS in the low NLR group (p = 0.017) but not in the high NLR group (p = 0.695) except that it did well clearly within 17 months. Compared to the low NLR group, lymphocyte decreased significantly, neutrophil increased steeply and white blood cell (WBC) elevated subsequently (p < 0.001in all cases) in the high NLR group. CONCLUSION: Adjuvant immunotherapy with the CIK cells prolongs DFS in postoperative patients with gastric cancer and the preoperative NLR is an independent prognostic factor for DFS. Low NLR predicts significant benefits from the CIK immunotherapy while high NLR forebodes the requirement of more cycles of CIK treatment or other stronger immunotherapy to improve the survival rate of patients.

N-terminal truncated carboxypeptidase E expression is associated with poor prognosis of lung adenocarcinoma.

Lung cancer is a malignant tumor with high morbidity and mortality rates. To date, no suitable molecular diagnostic tool to predict disease recurrence and metastasis has been identified. The current study aimed to evaluate the potential of N-terminal truncated carboxypeptidase E (CPEΔN) to predict the recurrence and metastasis of lung adenocarcinoma. Western blotting revealed the co-expression of CPE and CPEΔN in the surgically collected pathological and pericarcinoma tissues tissues of 62.1% (59/95) lung adenocarcinoma patients. The full length CPE protein was predominantly expressed in pericarcinoma tissues and CPEΔN expression was identified in the pericarcinoma normal tissues of only 5.26% (5/95) patients. The 3-year postoperative recurrence and metastasis rates were significantly higher in patients with positive CPEΔN expression than in patients with negative CPEΔN expression (P=0.009). Furthermore, the overall survival rate of patients with predominant nuclear CPE expression was lower than that of patients with predominant cytoplasmic CPE expression (46.3 vs. 64.7%); however, no statistically significant difference was identified (P=0.125). Thus, the results of the current study indicated that CPEΔN may present a novel molecular biomarker for predicting recurrence and metastasis of lung adenocarcinoma, which may aid with stratifying patients by risk and thus, may facilitate individualized therapy.

Osteopontin as a potential biomarker of proliferation and invasiveness for lung cancer.

PURPOSE: Lung cancer is one of the most malignant tumors and poses a significant threat to human health. Osteopontin (OPN) is a variably expressed, secreted glycophosphoprotein that mediates the growth and metastases of several carcinoma types. In this study, we aimed to understand the role of OPN in lung cancer cell proliferation and invasiveness. METHODS: Expression of OPN was examined using an immunohistochemical method in paraffin-embedded sections collected from 49 patients with lung cancer. We silenced OPN expression by lentivirus-mediated OPN-specific small interfering RNA (siRNA) and examined the proliferation and invasiveness of OPN-silenced lung cancer cell (A549) through MTT, BrdU, flow cytometry, and Matrigel assay. In addition, we tested the role of individual OPN splice variants in A549 cell growth and invasion by constructing OPN overexpression lentiviruses. RESULT: Downregulation of OPN inhibited A549 cell proliferation and in vivo tumor growth, abrogated augmentation of invasion, induced G1-phase cell cycle arrest, and induced cell late apoptosis and necrosis. Moreover, the proliferation and invasiveness was linked to different OPN splice variants, of which OPN-b affected the cell proliferation and OPN-c showed significant correlation with invasion behavior. CONCLUSIONS: Our data suggested that OPN served as a potential biomarker for invasive lung cancer and provided new molecular-targeted therapy for lung cancer based on lentivirus-mediated RNA interference.