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BACKGROUND AND AIMS: Microscopic detection of decoy cells is routinely performed in urine samples from renal transplant patients for the evaluation of polyomaviruses. However, they are scanty papers evaluated the diagnostic accuracy of decoy cells in urine samples. The aim of this study is to evaluate the diagnostic accuracy of decoy cells in urine samples and compare with plasma real-time polymerase chain reaction (RT-PCR) as a gold standard method. In addition, to compare the findings of this study with other similar studies. METHODS: A retrospective study over a period of four years from January 2014 to December 2017 was performed. A total of 89 urine samples from renal transplant patients were assessed for the presence of polyomaviruses and compared with plasma RT-PCR. The sensitivity, specificity, accuracy, positive predictive value (PPV) and negative predictive value (NPV) were measured. RESULTS: There were 29 males and 18 females. The mean patient age was 40.3 years. The sensitivity, specificity, accuracy, PPV and NPV were 86.6%, 67.5%, 70.7%, 35.1% and 96.1%, respectively. Other similar studies reported a sensitivity of 41.9-84.6%, specificity of 65.8-100% and accuracy of 69.9-82%. CONCLUSION: The findings of this study show that the detection of decoy cells in urine samples is a sensitive screening method for polyomaviruses. The findings of this study are compatible with other similar studies.

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BACKGROUND/AIM: p53 pathway is thought by many researchers to be critically involved in selenium's chemoprevention or in hepatocarcinogenesis. The aim of this study was to investigate the gene expression of p53, p21 and B-cell lymphoma-2 (bcl-2) using preventive and therapeutic approaches of selenium in chemically induced hepatocarcinogenesis in rats. MATERIALS AND METHODS: Rats were divided randomly into six groups: Negative control, positive control (diethyl nitrosamine +2-acetylaminofluorene), preventive group, preventive control (respective control for preventive group), therapeutic group and therapeutic control (respective control for therapeutic group). p53, p21 and bcl-2 genes on liver tissues were measured using real-time polymerase chain reaction. RESULTS: The expression of p53 was only significant in the therapeutic control. The expression of bcl-2 was insignificant in all the groups. p21 expression was significant in all the groups except the preventive group. CONCLUSIONS: The selenium molecular mechanism for liver cancer prevention is not through the p53 pathway. Also, the absence of p53 is not necessary for chemically induced liver cancer in rats.

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Selenium in the form of sodium selenite (SSE) is an essential micronutrient which known to possess antioxidant and anticancer properties. This study emphasizes the role of selenium on oxidative stress in experimental rats with N-diethylnitrosamine (DEN) initiated and 2-acetylaminofluorene (2-AAF) promoted multistage hepatocellular carcinogenesis (HCC). Rats were divided randomly into six groups: negative control, positive control (DEN+2-AAF), preventive group (pre-SEE 4 weeks+DEN), preventive control (respective control for preventive group), therapeutic group (DEN+post-SSE 12 weeks) and therapeutic control (respective control for therapeutic group). SSE (4 mg L(-1)) was given to animals before initiation and during promotion phase of HCC. The levels of total protein (TP), conjugated diens (CD), malondialdehyde (MDA), fluorescent pigment (FP), antioxidant activity (AOA) and DNA damage were measured. Supplementation of SSE before the initiation phase of carcinogenicity significantly increased TP and AOA level (p < 0.05) while it decreased the levels of CD, MDA, DNA damage and FP (p < 0.05). Supplementation of SSE during the promotion phase of carcinogenicity significantly decreased the DNA damage and FP level (p < 0.05) and there were negative correlation between the level of AOA and with the level of FP and CD. Thus, supplementation of SSE reduced the adverse changes which occur in liver cancer. However, the chemoprevention effect of SSE was more pronounced when it was supplemented before initiation phase of cancer when compared to promotion phase.

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BACKGROUND AND AIMS: Selenium's molecular mechanism for cancer chemoprevention remains unknown. We aimed to study the gene expression of nuclear factor-kappaB (NF-kappaB), tumor growth factor-alpha (TGF-alpha) and cyclin D1 and the effects of sodium selenite using preventive and therapeutic approaches in chemically-induced hepatocarcinogenesis in rats. METHODS: Rats were divided randomly into six groups: negative control, positive control (diethyl nitrosamine [DEN] + 2-acetylaminofluorene [2-AAF]), preventive group, preventive control (respective control for preventive group), therapeutic group and therapeutic control (respective control for therapeutic group). The relative gene expression of NF-kappaB, TGF-alpha and cyclin D1 in liver tissues were measured using real-time polymerase chain reaction. RESULTS: The findings showed that the gene expression of NF-kappaB in the preventive group and its respective control was significantly lower (P < 0.05) when compared with both the negative and positive controls. However, the expression of NF-kappaB in the positive controls and therapeutic group was significantly higher (P < 0.05) when compared with the negative controls. The expression of TGF-alpha and cyclin D1 was insignificant in all groups. CONCLUSION: The inhibition of the NF-kappaB pathway in the initiation phase of hepatocarcinogenesis could be a promising target for selenium chemoprevention. However, further studies are required.

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