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    Tytuł:
    Kinetic properties of the (Ca²+ + Mg²+)-ATPase bound to and extracted from the pig erythrocyte membrane
    Własności kinetyczne (Ca²+ + Mg²+)-ATPazy związanej z błonami erytrocytów świni i ekstrahowanej z nich
    Autorzy:
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/945007.pdf
    Data publikacji:
    1996
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1996, 11
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Partition coefficient of organophosphorus insecticides evaluated by fluorescence quenching
    Ocena współczynnika podziału insektycydów fosforoorganicznych metodą tłumienia fluorescencji
    Autorzy:
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/945008.pdf
    Data publikacji:
    1996
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Badając tłumienie fluorescenęji przez malation i metyloparation stwierdzono, że pierwszy związek nie tłumi iluorescencji żadnego ze stosowanych w badaniach znaczników (perylen i ANS). Opisując tłumienie za pomocą równania Stema-Volmera stwierdzono, że metyloparation wiązał się z liposomami utworzonymi z fasfatydylocholiny. Wiązanie to wykazywało silną zależność od stężenia insektycydu. Wiązanie insektycydu było znacznie słabsze, gdy liposomy tworzone były z różnych ilośd molowych fosfatydylocholiny i cholesterolu. Tłumienie iluorescencji było wyraźniejsze, gdy stosowano znacznik wiążący się z rdzeniem dwuwarstwy lipidowej (perylen), niż wówczas, gdy stosowano znacznik wiążący się z bardziej zewnętrznym obszarem dwuwarstwy (ANS). Uzyskane wyniki wskazują, że wiązanie niektórych insektycydów fosforoorganicznych może być zmieniane przez cholesterol.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1996, 11
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    The role of microRNA in metastatic colorectal cancer and its significance in cancer prognosis and treatment
    Autorzy:
    Tokarz, Paulina
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039629.pdf
    Data publikacji:
    2012
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    prognosis
    colorectal cancer
    metastasis
    prediction
    therapy
    miRNA
    Opis:
    microRNAs (miRNAs) are small, non-coding RNA molecules that regulate gene expression by targeting specific mRNAs. microRNAs play a role in several physiological processes in the cell, including migration, proliferation, differentiation and apoptosis. Apart from their role in regular metabolism, abnormal profiles of miRNA expression accompany cancer transformation, including colorectal cancer (CRC) metastasis. microRNAs may play a role in each phase of CRC metastasis including angiogenesis, invasion, intravasation, circulation, extravasation and metastatic colonization. microRNA levels may serve as a predictive CRC marker, which was confirmed by the serum level of miR-29a targeting KLF4, a marker of cell stemness, and the plasma level of miR-221 down-regulating c-Kit, Stat5A and ETS1, which are signal transducers and transcription factor, respectively. In turn, the level of miR-143 in CRC cells decreasing the amount of MACC1 (metastasis-associated in colon cancer-1) and oncogenic KRAS protein, may be utilized as a prognostic marker. Also, single nucleotide polymorphisms of genes encoding miRNAs, including miR-423 and miR-608, which correlate with tumor recurrence, may be useful as diagnostic, prognostic and predictive indicators in CRC metastasis. Pre-miR-34a and pre-miR-199a decreased the level of Axl, a tyrosine-protein kinase receptor, so they can be considered as drugs in antimetastatic therapy. On the other hand, miR-222 targeting ADAM-17, a disintegrin and metalloproteinase, and miR-328 interacting with ABCG2, an ABC transporter, may overcome drug resistance of cancer cells. microRNAs may be considered in wide-range application to facilitate CRC metastasis diagnosis, prognosis, prediction and therapy, however, further clinical, epidemiological and in vitro studies should be conducted to verify their utility.
    Źródło:
    Acta Biochimica Polonica; 2012, 59, 4; 467-474
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Non-homologous DNA end joining.
    Autorzy:
    Pastwa, Elżbieta
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1043360.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Ku proteins
    DNA-PK
    homologous recombination
    non-homologous end joining
    DSB; DNA repair
    DNA ligase IV
    DNA double-strand breaks
    NHEJ
    Opis:
    DNA double-strand breaks (DSBs) are a serious threat for the cell and when not repaired or misrepaired can result in mutations or chromosome rearrangements and eventually in cell death. Therefore, cells have evolved a number of pathways to deal with DSB including homologous recombination (HR), single-strand annealing (SSA) and non-homologous end joining (NHEJ). In mammals DSBs are primarily repaired by NHEJ and HR, while HR repair dominates in yeast, but this depends also on the phase of the cell cycle. NHEJ functions in all kinds of cells, from bacteria to man, and depends on the structure of DSB termini. In this process two DNA ends are joined directly, usually with no sequence homology, although in the case of same polarity of the single stranded overhangs in DSBs, regions of microhomology are utilized. The usage of microhomology is common in DNA end-joining of physiological DSBs, such as at the coding ends in V(D)J (variable(diversity) joining) recombination. The main components of the NHEJ system in eukaryotes are the catalytic subunit of DNA protein kinase (DNA-PKcs), which is recruited by DNA Ku protein, a heterodimer of Ku70 and Ku80, as well as XRCC4 protein and DNA ligase IV. A complex of Rad50/Mre11/Xrs2, a family of Sir proteins and probably other yet unidentified proteins can be also involved in this process. NHEJ and HR may play overlapping roles in the repair of DSBs produced in the S phase of the cell cycle or at replication forks. Aside from DNA repair, NHEJ may play a role in many different processes, including the maintenance of telomeres and integration of HIV-1 genome into a host genome, as well as the insertion of pseudogenes and repetitive sequences into the genome of mammalian cells. Inhibition of NHEJ can be exploited in cancer therapy in radio-sensitizing cancer cells. Identification of all key players and fundamental mechanisms underlying NHEJ still requires further research.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 4; 891-908
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Recognition and repair of DNA-cisplatin adducts.
    Autorzy:
    Woźniak, Katarzyna
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1043720.pdf
    Data publikacji:
    2002
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    DNA-protein crosslinks
    cisplatin
    DNA adducts
    DNA damage
    DNA repair
    cis-diamminedichloroplatinum
    Opis:
    Anticancer activity of cisplatin (cis-diamminedichloroplatinum) is believed to result from its interaction with DNA. The drug reacts with nucleophilic sites in DNA forming monoadducts as well as intra- and interstrand crosslinks. DNA-cisplatin adducts are specifically recognized by several proteins. They can be divided into two classes. One constitutes proteins which recognize DNA damage as an initial step of the nucleotide excision and mismatch repair pathways. The other class contains proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins from the HMG (high-mobility-group) family. They specifically recognize 1,2-interstrand d(GpG) and d(ApG) crosslinks of DNA-cisplatin adducts and inhibit their repair. Many HMG-domain proteins can function as transcription factors, e.g. UBF, an RNA polymerase I transcription factor, the mammalian testis-determining factor SRY and the human mitochondrial transcription factor mtTFA. Moreover, it seems that some proteins, which probably recognize DNA-cisplatin adducts non-specifically, e.g. actin and other nuclear matrix proteins, can disturb the structural and functional organization of the nucleus and whole cell. The formation of complexes between DNA and proteins in the presence of cisplatin and the changes in the cell architecture may account for the drug cytotoxicity.
    Źródło:
    Acta Biochimica Polonica; 2002, 49, 3; 583-596
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Role of anti-apoptotic pathways activated by BCR/ABL in the resistance of chronic myeloid leukemia cells to tyrosine kinase inhibitors
    Autorzy:
    Danisz, Katarzyna
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039432.pdf
    Data publikacji:
    2013
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    BCR/ABL
    chronic myeloid leukemia
    apoptotic signaling
    tyrosine kinase inhibitor
    imatinib
    drug resistance
    Opis:
    Chronic myeloid leukemia (CML) is a hematological stem cell disorder characterized by the excessive proliferation of the myeloid lineage. In its initial chronic phase, the myeloid progenitor cells expand and demonstrate apparently normal differentiation. The disease may then transform into the accelerated phase, usually associated with resistance to therapy, and finally, into acute leukemic progression phase - blast crisis. Abnormal myeloid cells produce progenitors, which have lost their ability to differentiate, but retain the capacity to proliferate. The molecular hallmark of CML is the Philadelphia chromosome, resulting from reciprocal chromosome translocation, t(9;22)(q34;q11), and containing the BCR/ABL fusion gene, producing the BCR/ABL protein with a constitutive tyrosine kinase activity. BCR/ABL-positive cells have faster growth and proliferation over their normal counterparts and are resistant to apoptosis. Introduction of imatinib (IM), a tyrosine kinase inhibitor, revolutionized the therapy of CML, changing it from a fatal disease into a chronic disorder. However, some patients show a primary resistance to IM, others acquire such resistance in the course of therapy. Therefore, a small number of leukemic stem cells retains self-renewal capacity under IM treatment. Because BCR/ABL is involved in many signaling pathways, some of them may be essential for resistance to IM-induced apoptosis. The PI3K/AKT, Ras and JAK/STAT signaling pathways are involved in resistance to apoptosis and can be activated by BCR/ABL. Therefore, they can be candidates for BCR/ABL-dependent pro-survival pathway(s), allowing a fraction of CML cells to withstand treatment with tyrosine kinase inhibitors.
    Źródło:
    Acta Biochimica Polonica; 2013, 60, 4; 503-514
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate.
    Autorzy:
    Błasiak, Janusz
    Kowalik, Joanna
    Powiązania:
    https://bibliotekanauki.pl/articles/1044192.pdf
    Data publikacji:
    2001
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    endonuclease III
    vitamin C
    Se-Pt conjugate [(NH3)2Pt(SeO3)]
    genotoxic effects of anticancer drugs
    DNA damage
    comet assay
    DNA repair
    Opis:
    Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing secondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since human diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, conjugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lymphocytes was examined using the trypan blue exclusion test and the alkaline comet assay, respectively. The conjugate evoked a concentration-dependent decrease in the cell viability, reaching nearly 50% at 250 μM. (NH3)2Pt(SeO3) at 1, 10 and 30 μM caused DNA strand breaks, measured as the increase in the comet tail moment of the lymphocytes. The treated cells were able to recover within a 30-min incubation in a drug-free medium at 37°C. Vitamin C at 10 and 50 μM diminished the extent of DNA damage evoked by (NH3)2Pt(SeO3) but had no effect on the kinetics of DNA repair. The vitamin did not directly inactivate the conjugate. Lymphocytes treated with endonuclease III, which recognises oxidised pyrimidines, displayed a greater tail moment than those untreated with the enzyme, suggesting that the damages induced by the drug have, at least in part, an oxidative origin. Vitamin C can be considered a potential protective agent against side effects of antitumor drugs, but further research with both normal and cancer cells are needed to clarify this point.
    Źródło:
    Acta Biochimica Polonica; 2001, 48, 1; 233-240
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Plasminogen activator inhibitor-1 (PAI-1) gene 4G/5G promoter polymorphism is not associated with breast cancer.
    Autorzy:
    Błasiak, Janusz
    Smolarz, Beata
    Powiązania:
    https://bibliotekanauki.pl/articles/1044431.pdf
    Data publikacji:
    2000
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    gene polymorphism
    PAI-1 gene
    prognostic marker
    plasminogen activator inhibitor-1 (PAI-1)
    breast cancer
    Opis:
    The antigen content of plasminogen activator inhibitor-1 (PAI-1) in primary breast cancer tissue extracts may be of strong prognostic value: high levels of PAI-1 in tumors predict poor prognosis for patients. The gene encoding PAI-1 is highly polymorphic and an insertion (5G)/deletion (4G) polymorphism in the PAI-1 gene promoter (the 4G/5G polymorphism), may have functional significance in PAI-1 expression. In the present work the distribution of genotypes and frequency of alleles of the 4G/5G polymorphism in subjects with breast cancer were investigated. Tumor tissues were obtained from 100 postmenopausal women with node-negative and node-positive ductal breast carcinoma with uniform tumor size. Blood samples from age matched healthy women served as control. The 4G/5G polymorphism was determined by PCR amplification using the allele specific primers. The distribution of the genotypes of the 4G/5G polymorphism in both control and patients did not differ significantly (P > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the genotype distributions and allele frequencies between node-positive and node-negative patients. The 4G/5G polymorphism may not be linked with elevated level of PAI-1 observed in breast cancer and therefore may not be associated with appearance and/or progression of breast cancer.
    Źródło:
    Acta Biochimica Polonica; 2000, 47, 1; 191-199
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Role of mitochondria in carcinogenesis
    Autorzy:
    Tokarz, Paulina
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039194.pdf
    Data publikacji:
    2014
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    cancer
    mitochondria
    mtDNA
    ROS
    anti-cancer therapy
    Opis:
    Mitochondria play the central role in supplying cells with ATP and are also the major source of reactive oxygen species (ROS) - molecules of both regulatory and destructive nature. Dysfunction of mitochondrial metabolism and/or morphology have been frequently reported in human cancers. This dysfunction can be associated with mitochondrial DNA (mtDNA) damage, which may be changed into mutations in mtDNA coding sequences, or the displacement-loop region, changes in the mtDNA copy number or mtDNA microsatellite instability. All these features are frequently associated with human cancers. Mutations in mtDNA can disturb the functioning of the ROS-producing organelle and further affect the entire cell which may contribute to genomic instability typical for cancer cells. Although the association between some mtDNA mutations and cancer is well established, the causative relationship between these two features is largely unknown. A hint suggesting the driving role of mtDNA mutations in carcinogenesis comes from the observation of tumor promotion after mtDNA depletion. Mitochondria with damaged DNA may alter signaling of the mitochondrial apoptosis pathway promoting cancer cell survival and conferring resistance to anticancer drugs. This resistance may be underlined by mtDNA copy number depletion. Therefore, mitochondria are considered a promising target in anticancer therapy and several mitochondria-targeting drugs are in preclinical and clinical trials. Some other aspects of mitochondrial structure and functions, including morphology and redox potential, can also be associated with cancer transformation and constitute new anticancer targets. Recently, several studies have disclosed new mechanisms underlying the association between mitochondria and cancer, including the protection of mtDNA by telomerase, suggesting new approaches in mitochondria-oriented anti-cancer therapy.
    Źródło:
    Acta Biochimica Polonica; 2014, 61, 4; 671-678
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Comparison of the DNA damaging activity of the organophosphorus insecticide m ethylparathion and its main metabolite
    Porównanie zdolności do uszkadzania DNA przez insektycyd fosforoorganiczny i jego główny metabolit
    Autorzy:
    Kowalik, Joanna
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/944951.pdf
    Data publikacji:
    1998
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Badano zdolność indukowania uszkodzeń DNA plazmidu pUC19 przez powszechnie stosowany insektycyd fosforoorganiczny metyloparation i jego główny metabolit metyloparaokson po 72 h inkubacji z tymi związkami. Stosowano metodę elektroforezy w żelu agarozowym i analizowano zmianę intensywności pasm odpowiadających dwóm formom konformacyjnym plazmidu - kolistej superskręconej (CCC) i kolistej otwartej (OC). Metyloparation, w przeciwieństwie do swego metabolitu, nie wywoływał zmian konformacyjnych plazmidowego DNA. Działanie metyloparaoksonu powodowało przejście konformacyjne DNA z formy CCC do OC. Otrzymane rezultaty wskazują na potencjalną zdolność metyloparaoksonu do wywoływania uszkodzeń DNA in vivo.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1998, 13
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Interaction between organophosphorus compounds and DNA assayed by the restriction endonuclease EcoRI
    Oddziaływanie pomiędzy związkami fosforoorganicznymi i DNA oceniane przy użyciu endonukleazy restrykcyjnej EcoRI
    Autorzy:
    Błasiak, Janusz
    Kowalik, Joanna
    Powiązania:
    https://bibliotekanauki.pl/articles/944953.pdf
    Data publikacji:
    1998
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Enzymy restrykcyjne ze względu na istotę swojego działania mogą być źródłem informacji na temat miejsca lub specyficzności sekwencyjnej wiązania substancji do DNA. Z drugiej strony, działanie enzymów może być zaburzone przez związki mające zdolność do metylacji zasad DNA. Cecha ta może być wykorzystywana do pierwotnej selekcji związków potencjalnie genotoksycznych. W pracy badano działanie enzymu restrykcyjnego £coRI na DNA, które było uprzednio inkubowane ze związkami fosforoorganicznymi. DNA plazmidu pUC19 0 stężeniu 78 μg/ml był inkubowany przez 72 h z insektycydami fosforoorganicznymi parationem i metyloparationem oraz z ich głównymi metabolitami, odpowiednio paraoksonem 1 metyloparaoksonem o stężeniu 300 μM. Po inkubacji nie związane insektycydy były usuwane przez ultrafiltrację, a DNA poddawano 1 h inkubacji z endonukleazą restrykcyjną EcoRI i analizowano przez elektroforezę w 0.8% żelu agarozowym. Związek fosforoorganiczny metyloparaokson powodowa! rozwinięcie superskręconego DNA plazmidu pUC19, a działanie EcoRI na ten DNA było zaburzone, co znalazło swe odbicie w zmienionym obrazie elektroforetycznym.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1998, 13
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells*.
    Autorzy:
    Blasiak, Janusz
    Widera, Kinga
    Pertyński, Tomasz
    Powiązania:
    https://bibliotekanauki.pl/articles/1043663.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    hyperthermia
    drug resistance
    K562 cells
    DNA repair
    Opis:
    Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37°C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 μM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37°C or 41°C. The lymphocytes incubated at 37°C needed about 60 min to remove completely the damage to their DNA, whereas at 41°C the time required for complete repair was shortened to 30 min. There was also a difference between the repair kinetics at 37°C and 41°C in cancer cells. Moreover, the kinetics were different in doxorubicin-sensitive and resistant cells. Therefore, hyperthermia may significantly affect the kinetics of DNA repair in drug-treated cells, but the magnitude of the effect may be different in normal and cancer cells. These features may be exploited in cancer chemotherapy to increase the effectiveness of the treatment and reduce unwanted effects of anticancer drugs in normal cells and fight DNA repair-based drug resistance of cancer cells.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 1; 191-195
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.
    Autorzy:
    Błasiak, Janusz
    Gloc, Ewa
    Warszawski, Mariusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1043821.pdf
    Data publikacji:
    2002
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    mitoxantrone
    oxidative DNA damage
    DNA damage
    idarubicin
    comet assay
    DNA methylation
    DNA repair
    Opis:
    Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assay we showed that the drugs at 0.01-10 μM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 μM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free radicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induce strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.
    Źródło:
    Acta Biochimica Polonica; 2002, 49, 1; 145-155
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Effects of some organophosphorus in secticides on calcium, potassium and chloride effux from isolated pig lymphocytes
    Wpływ insektycydów fosforoorganicznych na wypływ wapnia, potasu i chloru z izolowanych limfocytów św ini
    Autorzy:
    Błasiak, Janusz
    Walter, Zofia
    Gawrońska, Maria
    Powiązania:
    https://bibliotekanauki.pl/articles/944957.pdf
    Data publikacji:
    1992
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1992, 9
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Urokinase plasminogen activation system and its role in cancer invasion and metastasis
    Urokinazowy układ aktywacji plazminogenu i jego rola w inwazyjności nowotworów i ich zdolności do przerzutowania
    Autorzy:
    Błasiak, Janusz
    Smolarz, Beata
    Piestrzeniewicz, Dagmara
    Powiązania:
    https://bibliotekanauki.pl/articles/945065.pdf
    Data publikacji:
    1999
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Inwazyjność nowotworów i ich zdolność do przerzutowania są klinicznymi cechami progresji nowotworów i wymagają degradacji i migracji przez tkankę łączną przez komórki rakowe. Procesy te zależą od złożonego oddziaływania pomiędzy komórkami nowotworu i otaczającą macierzą zewnątrzkomórkową. Oddziaływania te są modyfikowane przez enzymy proteolityczne i ich receptory. Urokinazowy układ aktywacji plazminogenu odgrywa ważną rolę w inwazyjności nowotworów i ich zdolności do przerzutowania. Układ len zawiera urokinazowy aktywator plazminogenu (uPA), receptor urokinazowy (uPAR) i specyficzne inhibitory aktywatorów plazminogenu, PAI-1 i PAI-2. Receptor uPA może znajdować się na powierzchni komórek rakowych. uPA może być uwalniany zarówno przez komórki normalne jak i zmienione nowotworowo. Kompleks uPA-uPAR skupia aktywność proteolityczną na powierzchni komórek rakowych przez konwersję osoczowego białka plazminogenu d o proteazy serynowej plazminy. Plazmina degraduje macierz zewnątrzkomórkową w sąsiedztwie komórek rakowych ułatwiając w ten sposób inwazję nowotworów. uPA, uPAR i PAI-1 mogą być stosowane jak o markery prognostyczne w wielu typach raka.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1999, 14
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia
    Autorzy:
    Antoszewska-Smith, Joanna
    Pawlowska, Elzbieta
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1038675.pdf
    Data publikacji:
    2017
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    chronic myeloid leukemia
    reactive oxygen species
    DNA damage
    DNA repair
    cancer stem cells
    imatinib resistance
    Opis:
    Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be engaged in CML progression and TKI-resistance and warrant further study.
    Źródło:
    Acta Biochimica Polonica; 2017, 64, 1; 1-10
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Role of biochemical factors in the pathogenesis of keratoconus
    Autorzy:
    Wojcik, Katarzyna
    Blasiak, Janusz
    Szaflik, Jerzy
    Szaflik, Jacek
    Powiązania:
    https://bibliotekanauki.pl/articles/1039330.pdf
    Data publikacji:
    2014
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    keratoconus
    cornea
    collagen
    proteinases
    proinflammatory markers
    antioxidants
    Opis:
    Keratoconus (KC) is a corneal disease associated with structural abnormalities in the corneal epithelium, Bowman's layer and stroma and altered concentration of tear components. KC corneas show a different pattern of collagen lamellae than their normal counterparts. Also, a reduction of several collagen types in KC epithelium and stroma was observed. Altered expression and/or activity of lysyl oxidase, a critical enzyme of the biogenesis of connective tissue detected in KC corneas, may weaken covalent bonds between collagen and elastin fibrils, what may lead to biomechanical deterioration of the cornea. Increased activity of matrix metalloproteinases observed in KC may induce the degradation of the extracellular matrix causing damage to the cornea. Oxidative and nitrative stress play an important role in KC pathogenesis and KC corneas are characterized by the disturbed lipid peroxidation and nitric oxide pathways. Malfunctioning of these pathways may lead to accumulation of their toxic by-products inducing several detrimental effects, along with apoptosis of the corneal cells, which may result from the loss of β-actin or increased levels of cytokines, including interleukin-1 and -6. Change in the expression of genes associated with wound healing, including the nerve growth factor and the visual system homeobox 1, may contribute to increased susceptibility of KC corneas to injury. Consequently, biochemical changes may play an important role in KC pathophysiology and, therefore, can be considered in prevention, diagnosis, prognosis and in the therapy of this disease as well.
    Źródło:
    Acta Biochimica Polonica; 2014, 61, 1; 55-62
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Free radical scavengers can modulate the DNA-damaging action of alloxan.
    Autorzy:
    Blasiak, Janusz
    Sikora, Agnieszka
    Czechowska, Agnieszka
    Drzewoski, Józef
    Powiązania:
    https://bibliotekanauki.pl/articles/1043667.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    vitamin C
    spin trapping
    free radicals
    alloxan
    vitamin E
    DNA damage
    ebselen
    comet assay
    DNA repair
    diabetes mellitus
    Opis:
    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 μM 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 μM diminished the extent of DNA damage induced by 50 μM alloxan. Pre-treatment of the lymphocytes with a nitrone spin trap, α-(4-pyridil-1-oxide)- N-t-butylnitrone (POBN) or ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-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 alkylated 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.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 1; 205-210
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Genotoxicity of the organophosphorus compound methylparaoxon evaluated by the comet assay
    Autorzy:
    Trzeciak, Andrzej
    Błasiak, Janusz
    Wojewódzka, Maria
    Kowalik, Joanna
    Powiązania:
    https://bibliotekanauki.pl/articles/895975.pdf
    Data publikacji:
    2001
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Pesticides are widely used in agriculture, food production and household. Due to the broad spectrum of their activity, their biological action is extensively investigated. We assessed the genotoxidty of methylparaoxon - the main metabolite of commonly used organophosphorus insecticide, methylparathion. Freshly isolated human peripheral blood lymphocytes were incubated for 1 h with methylparaoxon at 37° C, and then, were incubated in methylparaoxon-free medium to examine DNA repair. Alkaline single cell gel electrophoresis (the comet assay) was used to assess DNA damage and repair. Methylparaoxon induced moderate DNA damages that were almost completely repaired after 60 min. Obtained results suggest that methylparaoxon could induce single-strand breaks in DNA both directly and by methylathion of DNA bases.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 2001, 15
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    The 4G /5G polymorphism in the promoter of the plasminogen activator in hibitor-1 (PAI-1) gene in subjects with cancer
    Polimorfizm 4G /5G obszaru promotorowego genu inhibitora aktywatorów plazminogenu typu 1 (PAI-1) u chorych na nowotwory złośliwe
    Autorzy:
    Błasiak, Janusz
    Smolarz, Beata
    Piestrzeniewicz, Dagmara
    Pytel, Jacek
    Powiązania:
    https://bibliotekanauki.pl/articles/945075.pdf
    Data publikacji:
    1999
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    Urokinazowy układ aktywacji plazminogenu zawiera enzymy proteolityczne mogące brać udział w inwazji komórek rakowych poprzez degradację macierzy zewnątrzkomórkowej i przerywaniu połączeń pomiędzy komórkami i macierzą. Wyniki znaczącej liczby eksperymentów wskazują, że zawartość przeciwciał dla jednego ze składników układu aktywacji plazminogenu inhibitora aktywatorów plazminogenu typu 1 (PAI-1), w ekstraktach z fragmentów pierwotnych guzów nowotworowych może mieć duże znaczenie prognostyczne: wysoki poziom PAI-1 źle rokuje dla pacjenta. Zademonstrowano także, że poziom PAI-1 w metastazie jest wyższy niż w guzach pierwotnych. Polimorfizm insercyjno/delecyjny 4G/5G w obszarze promotorowym genu PAI-1 może być związany z osoczowym poziomem PAI-1. W pracy badano ten polimorfizm we krwi 53 pacjentów cierpiących na różne rodzaje nowotworów (16 przypadków ra k a sutka, 12 jelita grubego, 9 żołądka, 9 czerniaków i 7 nowotworów głowy i szyi) oraz 53 odpowiednio dobranych osobników zdrowych. Częstości alleli 4G i 5G u chorych były odpowiednio: 0,53 i 0,47, podczas gdy w grupie kontrolnej wartości te wynosiły 0,43 i 0,57. Rozkłady genotypów w badanych grupach były znacząco różne - u chorych genotyp 4G/5G występował ze zwiększoną częstością niż w grupie kontrolnej. Konieczne są dalsze badania dla oceny częstości występowania danego genotypu polimorfizmu 4G/5G, jak również innych polimorfizmów, genu PAI-1 i stopniem ryzyka zapadnięcia na chorobę nowotworową.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1999, 14
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Expression of RUNX2 and its signaling partners TCF7, FGFR1/2 in cleidocranial dysplasia
    Autorzy:
    Pawłowska, Elżbieta
    Wójcik, Katarzyna
    Synowiec, Ewelina
    Szczepańska, Joanna
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039147.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    RUNX2
    Wnt signaling
    TCF7
    fibroblast growth factor signaling
    FGFR1
    FGFR2
    Opis:
    RUNX2 is a member of the PEBP2/CBF transcription factors family controlling the expression of genes whose products are essential for bone formation. Mutations in the RUNX2 gene may be associated with cleidocranial dysplasia (CCD), a rare skeletal disease characterized by stature aberrations, delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and multiple dental abnormalities. As RUNX2 is involved in many signaling pathways, we hypothesize that CCD may be associated with their changes. We determined the expression of RUNX2 and its signaling partners TCF7, involved in canonical Wnt signaling, and fibroblast growth factor receptors, FGFR1 and FGFR2 in periodontum of CCD patients and control individuals. We did not observe any differences between the level of RUNX2, TCF7 and FGFR1/2 mRNA, determined by real-time PCR, in CDD patients and controls. Therefore, RUNX2 signaling pathways with their partners TCF7 and FGFR1/2 may not be involved in CCD pathogenesis.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 1; 123-126
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Mitochondrial mutagenesis in BCR-ABL1-expressing cells sensitive and resistant to imatinib
    Autorzy:
    Blasiak, Janusz
    Hoser, Grazyna
    Bialkowska-Warzecha, Jolanta
    Pawlowska, Elzbieta
    Skorski, Tomasz
    Powiązania:
    https://bibliotekanauki.pl/articles/1038829.pdf
    Data publikacji:
    2016
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Imatinib
    chronic myeloid leukemia
    BCR-ABL1 gene
    Opis:
    Imatinib revolutionized the treatment of chronic myeloid leukemia (CML) with the expression of the BCR-ABL1 tyrosine kinase, but imatinib resistance is an emerging problem. Imatinib can hinder the inhibitory effects of BCR-ABL1 on mitochondrial apoptotic pathway, so mitochondrial mutagenesis can be important for its action. To explore the mechanisms of imatinib resistance we created a mouse-derived CML model cells consisting of parental 32D cells (P) and cells transfected with the BCR-ABL1 gene (S cells) or its variants with the Y253H or T315I mutations (253 and 315 cells, respectively), conferring resistance to imatinib. A fraction of the S cells was cultured in increasing concentrations of imatinib, acquiring resistance to this drug (AR cells). The 253, 315 and AR cells, in contrast to S cells, displayed resistance to imatinib. We observed that the T315I cells displayed greater extent of H2O2-induced mtDNA damage than their imatinib-sensitive counterparts. No difference in the sensitivity to UV radiation was observed among all the cell lines. A decrease in the extent of H2O2-induced mtDNA damage was observed during a 120-min repair incubation in all cell lines, but it was significant only in imatinib-sensitive and T315I cells. No difference in the copy number of mtDNA and frequency of the 3,867-bp deletion was observed and genotoxic stress induced by H2O2 or UV did not change this relationship. In conclusion, some aspects of mtDNA mutagenesis, including sensitivity to oxidative stress and DNA repair can contribute to imatinib resistance in BCR-ABL1-expressing cells.
    Źródło:
    Acta Biochimica Polonica; 2016, 63, 2; 365-370
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Antigen levels of urokinase-type plasminogen activator receptor and its gene polymorphism related to microvessel density in colorectal cancer
    Autorzy:
    Przybylowska, Karolina
    Szemraj, Janusz
    Kulig, Andrzej
    Dziki, Adam
    Ulanska, Joanna
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1040754.pdf
    Data publikacji:
    2008
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    plasminogen activation system
    urokinase type plasminogen activator receptor (uPAR)
    gene polymorphism
    colorectal cancer
    cancer progression
    angiogenesis
    microvessel density
    Opis:
    We determined the distribution of genotypes and frequencies of alleles of the (CA)n repeat polymorphism in intron 3 of the urokinase plasminogen activator receptor (uPAR) gene, uPAR antigen levels and microvessel density (MVD) in tumour and distant mucosa samples from 52 patients with colorectal cancer. The uPAR level was higher for patients with high MVD comparing to patients with lower MVD which may suggest that uPAR can be correlated with progression of colorectal cancer. The significant relationship between the high MVD and uPAR antigen level appeared to be independent of the (CA)n repeat polymorphism because no differences in the level of uPAR antigen between carriers of alleles were found. The received results, indicate that uPAR might be considered as a target in colorectal cancer patients' therapy.
    Źródło:
    Acta Biochimica Polonica; 2008, 55, 2; 357-363
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.
    Autorzy:
    Gloc, Ewa
    Warszawski, Mariusz
    Młynarski, Wojciech
    Stolarska, Małgorzata
    Hoser, Grażyna
    Skorski, Tomasz
    Błasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1043817.pdf
    Data publikacji:
    2002
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    oncogenic tyrosine kinase
    amifostine
    DNA damage
    idarubicin
    comet assay
    DNA repair
    TEL/JAK2
    Opis:
    The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13)) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. investigated the effects of amifostine on idarubicin-induced DNA damage and repair in murine pro-B lymphoid BaF3 cells and BaF3-TEL/JAK2-transformed cells using alkaline single cell gel electrophoresis (comet assay). Idarubicin induced DNA damage in both cell types but amifostine reduced its extent in control non-transformed BaF3 cells and enhanced it in TEL/JAK2-transformed cells. The transformed cells did not show measurable DNA repair after exposure to amifostine and idarubicin, but cells treated only with idarubicin were able to recover within a 60-min incubation. Because TEL/JAK2-transformed cells can be considered as model cells for certain human leukemias and lymphomas we anticipate an enhancement of idarubicin cytotoxicity by amifostine in these diseases. Moreover, TEL/JAK2 tyrosine kinase might be involved in cellular response to DNA damage. Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation.
    Źródło:
    Acta Biochimica Polonica; 2002, 49, 1; 121-128
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Analysis of the G/C polymorphism in the 5-untranslated region of the RAD51 gene in breast cancer.
    Autorzy:
    Blasiak, Janusz
    Przybyłowska, Karolina
    Czechowska, Agnieszka
    Zadrożny, Marek
    Pertyński, Tomasz
    Rykała, Jan
    Kołacińska, Agnieszka
    Morawiec, Zbigniew
    Drzewoski, Józef
    Powiązania:
    https://bibliotekanauki.pl/articles/1043672.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    genetic polymorphism
    RAD51 gene
    RFLP-PCR
    breast cancer
    Opis:
    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.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 1; 249-253
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Transferrin receptor levels and polymorphism of its gene in age-related macular degeneration
    Autorzy:
    Wysokinski, Daniel
    Danisz, Katarzyna
    Pawlowska, Elzbieta
    Dorecka, Mariola
    Romaniuk, Dorota
    Robaszkiewicz, Jacek
    Szaflik, Marta
    Szaflik, Jerzy
    Blasiak, Janusz
    Szaflik, Jacek
    Powiązania:
    https://bibliotekanauki.pl/articles/1039085.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    AMD
    gene polymorphism
    iron
    oxidative stress
    TFRC
    transferrin receptor
    Opis:
    The aim of the present study was to investigate the association of age related macular degeneration (AMD) risk with some aspects of iron homeostasis: iron concentration in serum, level of soluble transferrin receptor (sTfR), and transferrin receptor (TFRC) genetic variability. Four hundred and ninety one AMD patients and 171 controls were enrolled in the study. Restriction fragment length polymorphism PCR was employed to genotype polymorphisms of the TFRC gene, and colorimetric assays were used to determine the level of iron and sTfR. Multiple logistic regression was applied for all genotype/allele-related analyses and the ANOVA test for iron and sTfR serum level comparison. We found that the genotypes and alleles of the c.-253G > A polymorphism of the TFRC gene were associated with AMD risk and this association was modulated by smoking status, AMD family history, living environment (rural/urban), body mass index and age. The levels of sTfR was higher in AMD patients than controls, whereas concentrations of iron did not differ in these two groups. No association was found between AMD occurrence and the p.Gly142Ser polymorphism of the TRFC gene. The results obtained suggest that transferrin receptor and variability of its gene may influence AMD risk.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 2; 177-184
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
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