Keywords: Carcinoma, Renal Cell; FNDC5 protein, rat [Supplementary Concept]; Urologic Neoplasms

Background: The purpose of this study was to determine whether irisin is secreted by gastric tumor cells experimentally induced in mice, and also if it has any effect on cancer cachexia. Design and Methods : 12 out of 60 BALB/c mice were used as a control group, while N-nitroso-N-methylurea (MNU) was administered orally to the remaining 48. After 150 days, the surviving mice were sacrificed by decapitation, blood and stomach, skeletal muscle, brown and white adipose tissue specimens were collected. Following histopathological evaluation of the stomach tissues, it was decided to create four groups, one control group and three consisting of mice administered MNU, no cancer, pre-cancer and cancer. Gene expression analyses of fibronectin type III domain containing protein 5 (FNDC5) and some cachexia-related proteins were performed in tissue samples, while levels of irisin, and various inflammatory and tumor markers together with cachectic factors were determined in serum samples. Results : The levels of inflammatory, tumor markers and cachectic factors in serum samples were significantly higher in the cancer group compared with the control group. No expression of FNDC5 or zinc-α-2 glycoprotein, a cachectic factor, was observed in gastric tissues from the control and MNU groups, whereas significantly increased FNDC5 expression was determined in the both white and brown adipose tissues from the cancer group. Conclusion: Increased FNDC5 expression in white and brown adipose tissues may have a cachectic effect in mice with induced cancer. However, it is not possible to explain the mechanism of the relationship between irisin and gastric cancer development on the basis of the results of this study.

Cyclophosphamide (CP) is an antineoplastic drug that induces kidney damage via producing oxidative stress. Carvacrol (CAR) has antioxidative effect and we postulated that it can be protective against CP-induced nephrotoxicity. Six groups (n = 7) of rats (control, 100 mg/kg CP, CP+5 mg/kg CAR, CP+10 mg/kg CAR, 5 mg/kg CAR, and 10 mg/kg CAR) were injected intraperitoneally. Serum malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), creatinine (CRE), total antioxidant capacity (TAC), and total oxidant state (TOS) were measured, and oxidative stress indexes (OSI) were calculated. Kidneys were also analyzed histologically. In CP-alone group MDA, CRE, TOS, and OSI levels increased whereas GSH, SOD, CAT, and TAC levels decreased compared with control group. In CP plus CAR groups, MDA, TOS, and OSI levels decreased whereas GSH, SOD, CAT, and TAC levels increased compared with CP-alone group. However, CRE levels were similar in CP-alone and CP+5 CAR group whereas decreased in CP+10 CAR group. CP+10 CAR group was significantly different in all parameters (except TAC) from CP+5 CAR group. Kidney microscopy was showed lower tissue damage in CP plus CAR groups. In conclusion, 10 mg/kg CAR is more effective than 5 mg/kg CAR in prevention of CP-induced oxidative damage on kidney.

Key words: Carcinoma, Renal Cell; Biomarkers

Purposes: This study was intended to determine the diagnostic significance of signal peptide-CUB-EGF domain-containing protein 1 (SCUBE 1) levels in gastric cancer. Methods: This retrospective study was conducted with patients with gastric cancer. SC

Objectives: To determine the effect of royal jelly (RJ) on the oxidant-antioxidant balance in rats with N-methyl-N-nitrosourea (MNU) induced breast cancer and to compare this with the chemotherapeutic agent paclitaxel. Material and methods: Fifty-six female Sprague Dawley rats were divided into five groups. Except control group (n=8, Group I) others received MNU (50 mg/kg, a single dose, i.p.) to develop breast cancer: Group II (n=8) untreated, Group III (n=7) treated with paclitaxel (15 mg/kg/week, 3 times, i.p.), Group IV (n=7) with RJ (by oral gavage, 100 mg/kg/day, for 30 days), and Group V (n=7), with paclitaxel+RJ. At the end of 30 days, histopathological and biochemical parameters were evaluated in breast tissues. Results: Levels of protein carbonyl (PC) and 8-hydroxy-deoxyguanosine (8-OHdG) were higher in Group V than in Group II while malondialdehyde (MDA) levels were lower in groups IV and V compared to Group II (p<0.05). Levels of catalase (CAT) in Group V and glutathione (GSH) in Group III were higher than Group II (p<0.05). Glutathione peroxidase (GPx) and superoxide dismutase (SOD) levels did not significantly different. Decreasing effect of RJ on CA15-3 levels was relevant to histopathological results. Conclusion: Although RJ (with or without paclitaxel) had increasing effect of antioxidant status it was insufficient to reduce oxidative stress in breast cancer.