Prognostic significance of Naples prognostic score in non-small-cell lung cancer patients with brain metastases.

Aims: The authors aimed to evaluate the prognostic value of Naples prognostic score (NPS) in advanced non-small-cell lung cancer patients with brain metastases. Materials & methods: A total of 186 consecutive advanced non-small-cell lung cancer patients were retrospectively analyzed. Kaplan-Meier survival analysis and Cox proportional regression models were used to assess the significance of NPS in overall survival and disease-free survival. Results: Multivariate Cox proportional regression analysis revealed that NPS was a significant independent predictive indicator for overall survival (hazard ratio: 1.897; 95% CI: 1.184-3.041; p = 0.008) and disease-free survival (hazard ratio: 2.169; 95% CI: 1.367-3.44; p = 0.001). Conclusion: NPS was a powerful prognostic indicator for outcome in advanced non-small-cell lung cancer patients with brain metastases.

Non-small-cell lung cancer (NSCLC) accounts for approximately 80­85% of all lung cancers. Survival rates in NSCLC patients with brain metastases without treatment are very poor. Radiation therapy is typically an effective treatment strategy. However, poor clinical outcomes pose a significant challenge after radiation therapy for NSCLC with brain metastases. Therefore, a reliable indicator is needed to predict outcomes in NSCLC patients with brain metastases and identify the specific subgroups of patients who will benefit from aggressive, individualized treatment. Recently, a novel Naples prognostic score (NPS) index has received considerable interest because it comprehensively reflects the patient's inflammatory and nutritional status in prognostic assessment. However, the prognostic significance of NPS is unknown for patients with stage IV NSCLC with brain metastases. The aim of this study was to explore the prognostic significance of NPS for NSCLC patients with brain metastases. The results confirmed that NPS was a powerful prognostic indicator for outcome in advanced NSCLC patients with brain metastases.

Cholesterol Enhances Colorectal Cancer Progression via ROS Elevation and MAPK Signaling Pathway Activation.

BACKGROUND/AIMS: Elevated serum cholesterol levels were linked to a higher risk of colorectal adenoma and colorectal cancer (CRC), while the effect of cholesterol on CRC metastasis has not been widely studied. METHODS: CRC patients were enrolled to evaluate the association between low-density lipoprotein cholesterol (LDL) and CRC metastases, and LDL receptor (LDLR) level of the CRC tissue was assessed by immunohistochemistry. The effects of LDL on cell proliferation, migration and stemness were assessed in CRC cells in vitro, and the effects of high fat diet (HFD) on tumor growth and intestinal tumorigenicity were investigated in vivo. ROS assays, gene expression array analysis and western blot were used to explore the mechanisms of LDL in CRC progression. RESULTS: The level of LDL was positively correlated with liver metastases, and a higher level of LDL receptor (LDLR) expression was associated with advanced N and M stages of CRC. In vitro, LDL promoted the migration and sphere formation of CRC cells and induced upregulated expression of "stemness" genes including Sox2, Oct4, Nanog and Bmi 1. High-fat diet (HFD) significantly enhanced tumor growth in vivo, and was associated with a shorter intestinal length in azoxymethane/dextran sodium sulfate (AOM/DSS)-treated mice. Furthermore, LDL significantly elevated reactive oxygen species (ROS) levels and Whole Human Genome Microarray found 87 differentially expressed genes between LDL-treated CRC cells and controls, which were largely clustered in the MAP kinase (MAPK) signaling pathway. CONCLUSIONS: LDL enhances intestinal inflammation and CRC progression via activation of ROS and signaling pathways including the MAPK pathway. Inflammation is strongly associated with cancer initiation, and the role of LDL in intestinal tumorigenicity should be further explored.