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Wyszukujesz frazę "chronic" wg kryterium: Temat


Tytuł:
Atorvastatin improves tubular status in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study
Autorzy:
Renke, Marcin
Tylicki, Leszek
Rutkowski, Przemysław
Neuwelt, Alexander
Larczyński, Wojciech
Ziętkiewicz, Marcin
Aleksandrowicz, Ewa
Łysiak-Szydłowska, Wiesława
Rutkowski, Bolesław
Powiązania:
https://bibliotekanauki.pl/articles/1040322.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
proteinuria
kidney
tubular injury
chronic kidney disease
Atorvastatin
Opis:
Background. There is evidence that dyslipidemia is associated with chronic kidney disease (CKD) and it has been implicated in the progression of renal damage. Optimal management of dyslipidemia should therefore lead to renal benefits. A number of experimental models demonstrate a beneficial effect of statins in ameliorating renal damage. However, the exact mechanism by which statins protect against renal damage remains unclear. Methods. In a placebo-controlled, randomized, cross-over study we evaluated the influence of atorvastatin (ATO) 40 mg/day added to the renin-angiotensin-aldosterone systeme (RAAS) blockade on proteinuria and surrogate biomarkers of tubular damage or injury in 14 non-diabetic patients with proteinuria (0.4-1.8 g per 24 h) with normal or declined kidney function (eGFR 55-153 ml/min). In the eight-week run-in period, therapy using angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: ATO/washout/placebo or placebo/washout/ATO. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The primary end point of this study was a change in proteinuria measured as 24-h urine protein excretion (DPE). Secondary end points included urine N-acetyl-β-d-glucosaminidase (NAG) and α1-microglobulin (α1m) excretion. Results. The ATO therapy significantly reduced urine excretion of α1m (p=0.033) and NAG (p=0.038) as compared to placebo. There were no differences in proteinuria, blood pressure, eGFR and serum creatinine between the ATO and placebo groups. Conclusion. Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 547-552
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Endothelial progenitor cells participation in cardiovascular and kidney diseases: a systematic review
Autorzy:
Kiewisz, Jolanta
Kaczmarek, Monika
Pawlowska, Anna
Kmiec, Zbigniew
Stompor, Tomasz
Powiązania:
https://bibliotekanauki.pl/articles/1038766.pdf
Data publikacji:
2016
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
endothelial progenitor cells
chronic kidney diseases
cardiovascular diseases.
Opis:
Endothelial progenitor cells (EPCs) represent a small population of blood cells (5-40 cells/mm3), with an ability to differentiate into endothelial cells that form the lining of the blood vessels and contribute to postnatal angiogenesis. Abundant evidence shows that recruitment of EPCs from the bone marrow, the monocyte/macrophage lineage and the organs facilitate the endothelial regeneration and repair. Changes in the number of EPCs were observed in both, chronic kidney and cardiovascular diseases. Thus, these cells were tested for usage in diagnosis and therapy. In this paper, we review the current knowledge on the EPC biology and contribution of these cells to the kidney and cardiovascular diseases.
Źródło:
Acta Biochimica Polonica; 2016, 63, 3; 475-482
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:
The mutual cooperation of blood platelets and lymphocytes in the development of autoimmune thyroid diseases
Autorzy:
Tomczyńska, Małgorzata
Saluk-Bijak, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1038518.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
autoimmune thyroid diseases
autoantibodies
blood platelets
chronic inflammation
lymphocytes
Opis:
Autoimmune thyroid diseases include several distinct clinical entities, mainly Graves' disease and Hashimoto's thyroiditis. An incompetent immune response directed against the body's own tissues, and the production of antibodies against specific cell antigens accompanied by chronic inflammation, all occur in autoimmune thyroid diseases. The autoimmune process is induced by genetic and environmental factors that are difficult to identify and generates the development of concomitant diseases in other systems. Leukocyte activation and overproduction of inflammatory mediators, as well as improper levels of thyroid hormones, play an essential role in the chronic course of these diseases. The development of autoimmune thyroid diseases results from the impairment of the regulatory and suppressor functions of T-cells or NK cells and activation of B cells, or from the changes in the number of those cells. Many reports have shown the significant role of platelet-leukocyte interaction in inflammation. Autoantibodies react with target antigens in different kinds of cells, including blood platelets, and autoimmune processes can modulate the mutual cooperation of blood platelets and lymphocytes. The activity of blood platelets and lymphocytes is reciprocally regulated. It has been suggested that blood platelets can influence lymphocyte function by direct contact with receptors, and indirectly via soluble mediators. The interactions of platelet-immune cells (neutrophils, monocytes, lymphocyte and dendritic cells) can have a potent enhancing effect on immune cells functions.
Źródło:
Acta Biochimica Polonica; 2018, 65, 1; 17-24
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Inhibition of cell proliferation and induction of apoptosis in K562 human leukemia cells by the derivative (3-NpC) from dihydro-pyranochromenes family
Autorzy:
Rahimi, Roghayeh
Mahdavi, Majid
Pejman, Sina
Zare, Payman
Balalaei, Saeed
Powiązania:
https://bibliotekanauki.pl/articles/1039138.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
apoptosis
chronic myeloid leukaemia
dihydro-pyranochromenes
K562 cells
Opis:
Leukemia is a particular type of cancer characterized by the failure of cell death or disability in differentiation of hematopoietic cells. Chronic myelogenus leukemia (CML) is the most studied kind of this cancer. In this study, anti-cancer effect of dihydro-pyranochromenes derivatives were investigated in the human leukemia K562 cells. These compounds were found to be active cell proliferation inhibitors using MTT assay. Among these compounds, 3-NpC was determined as stronger compound with IC50 value of 100±3.1 µM and was chosen for further studies. Induction of apoptosis was analyzed by AO/EtBr staining, DNA fragmentation assay, Annexin V/PI double staining and cell cycle analysis. Furthermore, Western Blot analysis showed that treatment of the cells with 3-NpC led to up-regulation and activation of caspase-3. The results of this investigation clearly indicated that dihydro-pyranochromenes derivatives induce apoptosis in the K562 cell line. This information signalizes also that these compounds may prepare a new therapeutic approach for the treatment of leukemia.
Źródło:
Acta Biochimica Polonica; 2015, 62, 1; 83-88
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Dietary supplement use among patients with chronic kidney disease
Autorzy:
Jakimowicz-Tylicka, Marzena
Chmielewski, Michał
Kuźmiuk-Glembin, Izabella
Skonieczny, Piotr
Dijakiewicz, Grażyna
Zdrojewska, Grażyna
Rutkowski, Bolesław
Tylicki, Leszek
Dębska Ślizień, Alicja
Powiązania:
https://bibliotekanauki.pl/articles/1038410.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
dietary supplements
vitamins
minerals
chronic kidney disease
dialysis
toxicity
Opis:
Background. Dietary supplements (DS) are available over the counter, but patients with impaired renal function are specifically at risk for toxicity when consuming certain DS. The aim of this study was to evaluate the prevalence and characteristics of DS use in patients with chronic kidney disease (CKD). Material and methods. A cross-sectional, controlled DS use survey (22 questions) was conducted among 180 CKD patients (stage 1-5, dialysis, kidney transplant), with 60 patients without CKD serving as controls. Results. DS use did not differ significantly between subjects with and without CKD, unless the CKD patients were on dialysis. In the CKD group, 20% admitted to use DS regularly and 22% did not take the mat all. In the controls, DS consumption was 17% and 13%, respectively (NS). The DS use was higher among women ascompared to men (89% vs. 70%; p < 0.005), and people living in cities versus those living in the country side (81% vs. 63%; p < 0.05). DS most commonly used were: vitamins, minerals, and herbs. Major indications for DS use included: musculoskeletal issues, general health improvement and prevention of urinary tract infections. Subgroup analyses revealed that dialysis patients were characterized by a significantly higher DS use in comparison to CKD stage 1-5 subjects and renal transplant recipients. The decision to introduce DS was made by the physician in 54% of cases; by a pharmacist in 9% of cases, and by the patients themselves in 37%. Only 21% of patients with CKD, and 27% of subjects without CKD, declared knowledge of any possible side-effects associated with DS (NS). Conclusions. The use of DS among patients with CKD is similar to patients without CKD, with the exception of those on dialysis. Vitamins and minerals were the most commonly reported DS consumed. The knowledge on potential side-effectof DS was limited to approximately one-fourth of those surveyed.
Źródło:
Acta Biochimica Polonica; 2018, 65, 2; 319-324
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Diagnosis and treatment difficulties in 18-year-old male patient with hereditary hemochromatosis, chronic hepatitis B, Gilbert syndrome and ulcerative colitis
Autorzy:
Sikorska, Katarzyna
Liberek, Anna
Romanowski, Tomasz
Szlagatys-Sidorkiewicz, Agnieszka
Landowski, Piotr
Bielawski, Krzysztof
Powiązania:
https://bibliotekanauki.pl/articles/1039929.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
hereditary hemochromatosis
ulcerative colitis
chronic hepatitis B
Glibert syndrome
Opis:
Among possible causes of chronic hepatitis in adolescents most common are infections, autoimmune disorders and metabolic diseases. Thus, diagnostic procedures should be multidirectional. This study reports diagnosis and treatment difficulties in an 18-year-old male patient with hereditary hemochromatosis (HH), ulcerative colitis (UC), chronic hepatitis B (CHB) and Gilbert syndrome. The presented case illustrates problems in diagnostics related to the presence of numerous disease conditions in one patient. It should be taken into consideration that these diseases coexisting in one patient can mutually affect their symptoms creating specific diagnostic difficulties.
Źródło:
Acta Biochimica Polonica; 2011, 58, 2; 251-254
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Selenium supplementation to chronic kidney disease patients on hemodialysis does not induce the synthesis of plasma glutathione peroxidase
Autorzy:
Zachara, Bronislaw
Gromadzinska, Jolanta
Zbrog, Zbigniew
Swiech, Rafal
Wasowicz, Wojciech
Twardowska, Ewa
Jablonska, Ewa
Sobala, Wojciech
Powiązania:
https://bibliotekanauki.pl/articles/1040656.pdf
Data publikacji:
2009
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
hemodialysis
selenium supplementation
glutathione peroxidase
chronic kidney disease
plasma
Opis:
Background: Numerous authors have shown that selenium (Se) concentration and glutathione peroxidase (GSH-Px) activity in plasma of chronic kidney disease (CKD) patients are lower than in healthy subjects, but there are only few publications on the level of GSH-Px protein in those patients and no reports on the effect of Se supplementation to HD patients on the level of this enzyme. Subjects and Methods: Se concentration and GSH-Px protein level in plasma were measured in a group of 30 CKD patients on hemodialysis (HD) supplemented with 200 µg Se/day for 3 months, and 28 patients on HD administered with placebo. Se concentration was measured by graphite furnace atomic absorption spectrometry and plasma GSH-Px protein level by the sandwich ELISA method using polyclonal antibody specific for human plasma GSH-Px. Results: Se concentration in patients on placebo did not change throughout the 3-month study period, but increased significantly in Se supplemented group. Se supplementation to CKD patients on HD had no effect on the level of GSH-Px protein. Conclusions: The lack of GSH-Px protein in CKD patients on HD is not linked to Se deficiency since the level of this element increased after Se supplementation while enzyme protein level did not change. The damaged kidney of HD patients is unable to synthesize GSH-Px, even after induction with selenium.
Źródło:
Acta Biochimica Polonica; 2009, 56, 1; 183-187
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Selenium, glutathione and glutathione peroxidases in blood of patients with chronic liver diseases.
Autorzy:
Czuczejko, Jolanta
Zachara, Bronisław
Staubach-Topczewska, Ewa
Halota, Waldemar
Kędziora, Józef
Powiązania:
https://bibliotekanauki.pl/articles/1043405.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
selenium
glutathione peroxidase
chronic liver disease
glutathione
oxidative stress
Opis:
Disturbances in the antioxidant system could play a role in pathogenesis of chronic liver disease. The aim of our study was to evaluate the levels/activities of antioxidants in blood of patients with chronic liver disease. We estimated selenium and glutathione concentrations and glutathione peroxidase activities in blood of 59 patients with chronic hepatitis B or C virus infection (group 1) and 64 patients with alcoholic, autoimmune or cryptogenic chronic liver disease (group 2). The results were compared with 50 healthy controls. Whole blood and plasma selenium and red cell glutathione concentrations were significantly lower in the patients compared with the controls. Red cell glutathione peroxidase activity was slightly reduced in both subgroups of group 1 and in group 2 with normal alanine aminotransferase values. Plasma glutathione peroxidase activity was slightly but significantly higher in patients with elevated aminotransferase values. The findings suggest that disturbances in antioxidant parameters in blood of patients with chronic liver disease may be the cause of the peroxidative damage of cells.
Źródło:
Acta Biochimica Polonica; 2003, 50, 4; 1147-1154
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of pentoxifylline on proteinuria, markers of tubular injury and oxidative stress in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study
Autorzy:
Renke, Marcin
Tylicki, Leszek
Rutkowski, Przemysław
Knap, Narcyz
Ziętkiewicz, Marcin
Neuwelt, Alexander
Aleksandrowicz, Ewa
Łysiak-Szydłowska, Wiesława
Woźniak, Michał
Rutkowski, Bolesław
Powiązania:
https://bibliotekanauki.pl/articles/1040438.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
pentoxifylline
oxidative stress
kidney
chronic kidney disease
proteinuria
tubular injury
Opis:
Background: Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. Methods: In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: The PTE therapy reduced proteinuria (by 26%) as compared to placebo. There were no differences in α1-microglobulin, urine excretion of N-acetyl-β-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F2t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Conclusion: Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.
Źródło:
Acta Biochimica Polonica; 2010, 57, 1; 119-123
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Virological response to treatment with peginterferon alfa-2a in adolescents with chronic hepatitis B
Autorzy:
Pawlowska, Małgorzata
Halota, Waldemar
Kozielewicz, Dorota
Jendryczka, Ewa
Powiązania:
https://bibliotekanauki.pl/articles/1039657.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
peginterferon alfa-2a
thrombocytopenia
hepatitis B virus
chronic hepatitis B
Opis:
Background: There are few data on the efficacy and safety of pegylated interferon treatment in adolescents with chronic hepatitis B. Aim: We conducted a pilot study in 13 adolescents with chronic hepatitis B treated with peginterferon alfa-2a at 100 µg/m2 once weekly for 48 weeks. Methods: HBV DNA was assessed by qPCR method. Results: After four weeks of treatment six adolescents had undetectable HBV DNA (<12 IU/mL). Seven adolescents - including five HBV negatives at week 4 - had undetectable HBV DNA (<55 IU/mL) at week 24, and seven adolescents - including all HBV DNA negatives at week 4 - had undetectable HBV DNA at week 48 of treatment (<55 IU/mL). Five adolescents had undetectable HBV DNA (<55 IU/mL) after 24 weeks of follow-up (sustained viral response). HBeAg seroconversion was achieved in one patient. HBsAg loss was documented at the end of therapy in two of the six adolescents HBV DNA negative at week 4 of treatment. Three adolescents withdrew from the treatment (two because of adverse events, one because of withdrawal of parental consent). Leukopenia was reported in seven adolescents and three individuals experienced thrombocytopenia. Except for one patient who discontinued treatment due to leukopenia, no dose modifications for adverse events or laboratory abnormalities were required. Conclusion: This pilot study shows that 48 weeks of treatment with peginterferon alfa-2a can result in sustained HBV DNA suppression, HBeAg seroconversion and HBsAg loss in adolescents with CHB. Larger and longer trials are now required to better define the magnitude of the benefit in this group of patients.
Źródło:
Acta Biochimica Polonica; 2012, 59, 4; 587-591
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Red blood cell and plasma glutathione peroxidase activities and selenium concentration in patients with chronic kidney disease: A review
Autorzy:
Zachara, Bronisław
Gromadzińska, Jolanta
Wąsowicz, Wojciech
Zbróg, Zbigniew
Powiązania:
https://bibliotekanauki.pl/articles/1041155.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
hemodialysis
selenium
kidney transplantation
glutathione peroxidase
chronic kidney disease
antioxidants
plasma
Opis:
The metabolism of oxygen in aerobic organisms leads to generation of reactive oxygen species (ROS). These entities are able to oxidize almost all classes of macromolecules, including proteins, lipids and nucleic acids. The physiological level of ROS is usually regulated by antioxidant defense mechanisms. There are at least three groups of antioxidant enzymes: superoxide dismutases, catalases and glutathione peroxidases (GSH-Pxs) which neutralize ROS. The trace elements (copper, zinc and selenium) bound to the active sites of the above listed enzymes play an important role in the antioxidant defense system. In mammals, a major function of selenium (Se) and Se-dependent GSH-Pxs is to protect cells from oxidative stress. Selenium concentrations and GSH-Px activities are altered in blood components of chronic kidney disease (CKD) patients. The Se level is frequently lower than in healthy subjects and the concentration very often decreases gradually with advancing stage of the disease. Studies on red cell GSH-Px activity in CKD patients reported its values significantly lower, significantly higher and lower or higher, but not significantly as compared with healthy subjects. On the other hand, all authors who studied plasma GSH-Px activity have shown significantly lower values than in healthy subjects. The degree of the reduction decreases gradually with the progression of the disease. High inverse correlations were seen between plasma GSH-Px activity and creatinine level. A gradual decrease in plasma GSH-Px activity in CKD patients is due to the fact that this enzyme is synthesized predominantly in the kidney and thus the impairment of this organ is the cause of the enzyme's lower activity. Se supplementation to CKD patients has a slightly positive effect in the incipient stage of the disease, but usually no effect was observed in end-stage CKD. Presently, kidney transplantation is the only treatment that may restore plasma Se level and GSH-Px activity in patients suffering from end-stage CKD. A few studies have shown that in kidney recipients, plasma Se concentration and GSH-Px activity are restored to normal values within a period of 2 weeks to 3 months following surgery and thus it can be acknowledged that Se supplementation to those patients has a positive effect on plasma GSH-Px activity.
Źródło:
Acta Biochimica Polonica; 2006, 53, 4; 663-677
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:
Some aspects of the SOS response system - A critical survey.
Autorzy:
Janion, Celina
Powiązania:
https://bibliotekanauki.pl/articles/1044087.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
SOS response
error-prone DNA polymerases
chronic SOS induction
DNA-repair
adaptive mutations
DNA mutations
Opis:
The SOS system and SOS mutagenesis are frequently studied, or exploited to obtain an increase in mutagenicity of bacteria. Here a short survey is made of the phenomenon of SOS response with special attention to latest and less discussed data, especially the induction of the SOS system in response to cell starvation or mutation of certain genes and the role of inducible DNA polymerases.
Źródło:
Acta Biochimica Polonica; 2001, 48, 3; 599-610
0001-527X
Pojawia się w:
Acta Biochimica Polonica
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

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