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1

MicroRNA in pathogenesis of head and neck squamous cell carcinoma

100%
Szaumkessel M., Szyfter K.
Biotechnologia
|
2010
|
issue 3
64-74
EN
Head and neck squamous cell carcinoma (HNSCC) is the sixth cancer in regard of both incidence and poor effect of treatment therapies, manifested in low cure rates (5-year survival rate ? 50%). The molecular heterogeneity found in HNSCC is the main reason why the already published data has not been sufficient to develop reliable prognostic tests and efficient therapies. A novel group of small non-coding RNA molecules (microRNA or miRNA) has been identified and proved to be strongly involved in cancer. However, the existing data does not specifically address microRNA involvement in HNSCC development and progression. This report summarizes the state-of-art concerning miRNA research in head and neck cancer and provides a list of miRNAs potentially involved in HNSCC pathogenesis.
2

Differences between rats and mice in induction of 4S beta-naphthoflavone-binding protein expression by treatment with beta-naphthoflavone

81%
Brauze D., Januchowski R., Szyfter K.
Journal of Applied Genetics
|
2002
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vol. 43
|
issue 3
371-376
EN
Sprague-Dawley rats and several inbred strains of mice were compared with respect to the induction of 4S BNF-binding protein expression by treatment with beta-naphthoflavone (BNF), an aryl hydrocarbon receptor (AhR) ligand. Inbred strains of mice chosen for the study encompassed 3 allelic forms of AhR found in Mus musculus so far. As it was reported by us earlier, treating rats with BNF caused a significant induction of BNF-binding protein expression. By contrast, no BNF-binding protein was detected in mice treated with BNF in corn oil as a vehicle or with corn oil itself.
3

Association of arylamine N-acetyltransferase (NAT1 and NAT2) genotypes with urinary bladder cancer risk

81%
Jaskula-Sztul R., Sokolowski W., Gajecka M., Szyfter K.
|
|
issue 2
223-231
EN
Arylamines are known bladder carcinogens deriving from tobacco smoke and environmental pollution. Arylamines are metabolised by NAT1 and NAT2 polymorphic enzymes in reactions of carcinogen activation and detoxification. We analysed genetic polymorphisms in both NAT1 and NAT2 genes in 56 bladder cancer patients and 320 healthy patients. Peripheral blood lymphocytes were collected from each subject and genotyped for NAT1 (six alleles) and NAT2 (four alleles) by PCR-RFLP. A weak association between NAT1 and NAT2 genotypes and bladder cancer risk was found when the genotypes were estimated separately (odds ratio OR 1.2, 95%CI 0.7-2.0, and OR 1.3, 95%CI 0.7-1.9, respectively). Almost all NAT1 genotypes possessing at least one ?risk? *10 allele were more frequent in the bladder cancer group than in the control group. There was also an increased frequency of ?risk? genotypes along with increased cigarette smoking in bladder cancer patients. The coincidence of NAT1-fast/NAT2-slow appears as a potential risk factor for urinary bladder cancer (OR 1.5, 0.8-3.0), as compared with the other genotype combinations.
4

Genotoxicity of the volatile anaesthetic desflurane in human lymphocytes in vitro, established by comet assay

71%
Karpinski T. M., Kostrzewska-Poczekaj M., Stachecki I., Mikstacki A., Szyfter K.
Journal of Applied Genetics
|
2005
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vol. 46
|
issue 3
319-324
EN
The aim of the present study was to estimate the genotoxicity of desflurane, applied as a volatile anaesthetic. The potential genotoxicity was determined by the comet assay as the extent of DNA fragmentation in human peripheral blood lymphocytes in vitro. The comet assay detects DNA strand breaks induced directly by genotoxic agents as well as DNA fragmentation due to cell death. Another anaesthetic, halothane, already proved to be a genotoxic agent, was used as a positive control. Both analysed drugs were capable of increasing DNA migration in a dose-dependent manner under experimental conditions applied. The results of the study demonstrated that the genotoxicity of desflurane was comparable with that of halothane. However, considering the pharmacodynamics of both drugs, the genotoxic activity of desflurane may be connected with a less harmful effect on the exposed patients or medical staff.
5

Genotoxicity of inhalation anaesthetics: DNA lesions generated by sevoflurane in vitro and in vivo

61%
Szyfter K., Szulc R., Mikstacki A., Stachecki I., Rydzanicz M., Jaloszynski P.
|
|
issue 3
369-374
EN
A moderate genotoxic activity of halothane and isoflurane applied as volatile anaesthetics has already been shown. The aim of this work was to estimate a potential genotoxicity of sevoflurane, introduced to clinical practice later than halothane and isoflurane. A genotoxic activity of all three compounds was estimated by using the comet assay in human peripheral blood lymphocytes (PBL) proliferating in vitro. We demonstrated that in contrast to the previously studied anaesthetics, sevoflurane did not induce any increase in DNA migration in the studied conditions. To estimate a genotoxic effect of a prolonged exposure to halogenated anaesthetics in vivo, PBL taken from operating room personnel (n = 29) were tested for DNA degradation and compared with those from a control non-exposed group (n = 20). No significant differences were detected between the groups. We conclude that sevoflurane does not have genotoxic properties, both in vitro and in vivo.
6

Relation betwwn DNA replication and DNA repair in human lymphocytes proliferating in vitro in the presence and in absence of mutagen

52%
Szyfter K., Wiktorowicz K., Wielgosz M. S., Zajaczek S., Kujawski M., Jaloszynski P., Czub M., Markowska M.
Journal of Applied Genetics
|
1995
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vol. 36
|
issue 4
379-388
EN
The effects of mutagens on DNA replication and DNA repair were studied in peripheral blood lymphocytes (BPL) obtained 21 healthy subjects, 2 samples from healthy heterozygote of Xeroderma pigmentosum (XP) and 2 samples from patient with clinically recognized XP.Inter-individual variations were found in DNA replication and in the level of spontanous DNA repair measured under standard culture condition.Exposure of human PBL proliferating in vitro to B(a)P was followed by a partial inhibition of replicative DNA synthesis in all subjects and by induction of DNA repair in healthy subjects.In XP patients DNA repair sythesis remained at the level attributed to spontaneous DNA repair.The response to mutagen varied individually.Results were analysed statistically.It was established that the studied indices of DNA synthesis correlete well with each other.The highest correlation was found between the levels of spontaneous and B(a)P-induced DNA repair.It is concluded that the level of spontaneous DNA repair is predictive for an estimation of cells ability to repair DNA damage.Inter-individual variations in the inhibition of DNA replication and in DNA repair sythesis are also dependet on the type of mutagen as shown by effect of other mutagens.Different effects of mutagen exposure on the inhibition of DNA replicative sythesis and induction of DNA repair can be explained by genetically controlled differences in the activity of enzymes responsible for mutagen processing and lesion removal.
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