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Przyczyny zakażenia zarodnikami pleśni gazowanych wód do picia

100%
Urbanowicz A., Czechowska A.
Roczniki Państwowego Zakładu Higieny
|
1976
|
tom 27
|
nr 5
2

Inhibitor kinaz tyrozynowych STI571 - nadzieja na przelom w leczeniu bialaczek

100%
Czechowska A., Blasiak J.
Postępy Biochemii
|
2003
|
tom 49
|
nr 3
157-167
3

Eukariotyczne polimerazy DNA

100%
Czechowska A., Blasiak J.
Postępy Biochemii
|
2005
|
tom 51
|
nr 2
130-139
4

Cisplatin-evoked DNA fragmentation in normal and cancer cells

81%
Wozniak K., Czechowska A., Blasiak J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
5

Free radical scavengers can modulate the DNA-damaging action of alloxan

80%
Blasiak J., Sikora A., Czechowska A., Drzewoski J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 1
Alloxan can generate diabetes in experimental animals and its action can be associ­ated with the production of free radicals. It is therefore important to check how differ­ent substances often referred to as free radical scavengers may interact with alloxan, especially that some of these substance may show both pro- and antioxidant activities. Using the alkaline comet assay we showed that alloxan at concentrations 0.01-50 uM induced DNA damage in normal human lymphocytes in a dose-dependent manner. Treated cells were able to recover within a 120-min incubation. Vitamins C and E at 10 and 50 uM diminished the extent of DNA damage induced by 50 uM alloxan. Pre-treatment of the lymphocytes with a nitrone spin trap, a-(4-pyridil-1-oxide)- .-t-butylnitrone (POBN) or ebselen (2-phenyl-1,2-benzisoselenazol-3(2.H)-one), which mimics glutathione peroxides, reduced the alloxan-evoked DNA damage. The cells ex­posed to alloxan and treated with formamidopyrimidine-DNA glycosylase (Fpg) and 3-methyladenine-DNA glycosylase II (AlkA), enzymes recognizing oxidized and alkyl- ated bases, respectively, displayed greater extent of DNA damage than those not treated with these enzymes. The results confirmed that free radicals are involved in the formation of DNA lesions induced by alloxan. The results also suggest that alloxan can generate oxidized DNA bases with a preference for purines and contribute to their alkylation.
6

A single nucleotide polymorphism in the 5'untranslated region of RAD51 in breast cancer

51%
Blasiak J., Przybylowska K., Czechowska A., Zadrozny M., Rykala J., Kolacinska A., Morawiec Z., Drzewoski J.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
7

Analysis of the G-C polymorphism in the 5'-untranslated region of the RAD51 gene in breast cancer

51%
Blasiak J., Przybylowska K., Czechowska A., Zadrozny M., Pertynski T., Rykala J., Kolacinska A., Morawiec Z., Drzewoski J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 1
The breast cancer suppressor proteins BRCA1 and BRCA2 interact with RAD51, a protein essential for maintaining genomic stability by playing a central role in homology-dependent recombinational repair of the DNA double-strand breaks. Therefore, genetic variability in the RAD51 gene may contribute to the appearance and/or progression of breast cancer. A single nucleotide polymorphism in the 5 - un­translated region of RAD51 (a G to C substitution at position 135, the G/C polymor­phism) is reported to modulate breast cancer risk. We investigated the distribution of genotypes and frequency of alleles of the G/C polymorphism in breast cancer. Tumor tissues were obtained from postmenopausal women with node-negative and node-positive breast carcinoma with uniform tumor size. Blood samples from age matched healthy women served as control. The G/C polymorphism was determined by PCR-based MvaI restriction fragment length polymorphism. The distribution of the genotypes of the G/C polymorphism did not differ significantly (P > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the geno­type distribution and allele frequencies between node-positive and node-negative pa­tients. There were no significant differences between distributions of the genotypes in subgroups assigned to histological grades according to Scarf–Bloom–Richardson criteria and the distribution predicted by Hardy–Weinberg equilibrium (P > 0.05). Our study implies that the G/C polymorphism of the RAD51 gene may not be directly involved in the development and/or progression of breast cancer and so it may not be useful as an independent marker in this disease.
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