sFas levels increase in response to cisplatin-based chemotherapy in lung cancer patients.

The Fas/Fas Ligand (FasL) system and survivin have counteracting roles in cell survival. Therefore, we explored the role of circulating soluble Fas (sFas) and the tissue levels of Fas and survivin with regard to response to chemotherapy in lung cancer patients. Serum samples from 52 lung cancer patients and 54 control subjects (19 benign lung disease and 35 healthy control subjects) were collected prior to and 24 and 48 h after chemotherapy. sFas was statistically significantly higher in the cancer group than that in the control groups (p < 0.001). Baseline (before chemotherapy) sFas values showed a statistically significant inverse correlation with overall survival (r = -0.599, p < 0.001). There was a significant increase in serum sFas levels 24 h after treatment (p < 0.05). Contrarily, tissue levels of Fas and survivin were not changed following the chemotherapy (p > 0,05). In conclusion, increased sFas may be an indicator of poor outcome in lung cancer patients. However, cisplatin-based chemotherapy may not be effective via neither the Fas/FasL system nor survivin pathway. Indeed, larger sample size is required for further evaluation.

Soluble cytokeratin 18 biomarkers may provide information on the type of cell death during early ischemia and reperfusion periods of liver transplantation.

Hepatocellular damage takes place as a result of ischemia and reperfusion during liver transplantation (LT). To discriminate the type of cell death and quantitate its severity may provide new insights into the mechanisms of hepatocellular damage. Therefore, we investigated the type of cell death by ELISA-based assays in patient sera. Apoptosis was specifically assessed by measuring a novel soluble biomarker, the caspase-cleaved cytokeratin 18, while total cell death (apoptosis and necrosis) by cytokeratin 18 released from dead (necrotic and apoptotic) cells. Twenty-seven live (LDLT) and 14 deceased (DDLT) donor liver transplantations were analyzed before the operation, at the anhepatic stage, first, sixth and 24th hour after the reperfusion. Both apoptosis and total cell death have successfully been demonstrated although they have not been confirmed by the liver biopsy that is impossible to perform in this setting. Apoptosis was not induced in LDLT. Total cell death (primarily necrosis) only transiently appeared the first hour after the reperfusion in LDLT, while it sharply increased the first hour after the reperfusion and maintained its level in DDLT. Soluble cytokeratin 18 biomarkers seem to be useful to discriminate and quantitate the type of cell death during early ischemia and reperfusion periods of LT.

[The evaluation to relationship between serum vascular endothelial growth factor (VEGF) level, metastases and other tumor markers in patients with lung cancer]. / Akciger kanserli olgularda serum "vascular endothelial growth factor (VEGF)" düzeylerinin metastazlar ve diger tümör belirteçleri ile iliskisinin incelenmesi.

Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis. Increased expression of VEGF may be associated with advanced stage and poor prognosis in patients with lung cancer. We investigated the relationship between serum VEGF level and lung cancer stage. We also studied the correlation between serum VEGF level and some other tumor markers. Forty newly diagnosed lung cancer (31 non-small cell, 9 small cell) patients and 25 age-matched controls were enrolled in this study. Serum VEGF levels of lung cancer group (345.16 +/- 159.36 pg/mL) were significantly higher than that of the control group (230.36 +/- 47.87 pg/mL) (p< 0.001). The area under the ROC curve was 0.727 (p< 0.05) for serum VEGF threshold of 249.8 pg/mL predictive sensitivity and specificity, for lung cancer were respectively 70.0% and 76.0%. There were no significant relationship between serum VEGF level and age, gender, histologic type, lung cancer stage, distant metastases and site of metastases. In addition, there were no correlation between serum VEGF level and other tumor markers (NSE, CYFRA 21-1, CEA, CA125, LDH).

The involvement of IL-10, IL-6, IFN-gamma, TNF-alpha and TGF-beta gene polymorphisms among Turkish lung cancer patients.

Several genes encoding different cytokines may play crucial roles in host susceptibility to lung cancer, since cytokine production capacity varies among individuals and depends on cytokine gene polymorphisms. The association between cytokine gene polymorphisms with primary lung carcinoma was investigated. DNA samples were obtained from a Turkish population of 44 patients with primary lung cancer, and 59 healthy control subjects. All genotyping (IFN-gamma, TGF-beta1, TNF-alpha, IL-6 and IL-10) experiments were performed using sequence-specific primers (SSP)-PCR. When compared to the healthy controls, the frequencies of high/intermediate producing genotypes of IL-10 and low producing genotype of TNF-alpha were significantly more common in the patient group. It is noteworthy that lung cancer patients with the TGF-beta T/T genotype in codon 10 had statistically longer survival compared to those having the C/C genotype (Kaplan-Meier survival function test, log rank significance = 0.014). These results suggest that IL-10, TNF-alpha and TGF-beta1 gene polymorphisms may affect host susceptibility to lung cancer and the outcome of the patients.