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Wyszukujesz frazę "chronic myeloid leukemia" wg kryterium: Temat


Wyświetlanie 1-11 z 11
Tytuł:
The effect of tyrosine kinase inhibitors used in the treatment of chronic myeloid leukemia on the cardiovascular system
Autorzy:
Sacha, Tomasz
Góra-Tybor, Joanna
Szmit, Sebastian
Powiązania:
https://bibliotekanauki.pl/articles/1035757.pdf
Data publikacji:
2019
Wydawca:
Medical Education
Tematy:
cardiovascular toxicity
chronic myeloid leukemia
tyrosine kinase inhibitors
Opis:
The use of tyrosine kinase inhibitors (TKIs) in the treatment of chronic myeloid leukemia has significantly improved the prognosis and outcomes for most patients. Clinical trials indicate that long-term CML therapy requires the introduction of second- or third-generation inhibitors in approximately 40–50% of cases. Effective in the case of imatinib resistance or intolerance, second generation TKI’s can also be used as a first-line treatment, leading to a faster, and deeper molecular response. TKIs, however, have also been observed to cause significant late adverse effects, including cardiovascular complications, which may raise certain safety concerns. The excellent treatment outcomes achieved with tyrosine kinase inhibitors have led to a gradual increase in the number and age of treated patients, and the associated higher incidence and severity of age-related co-morbidities such as diabetes, hypercholesterolemia, atherosclerosis, ischemic heart disease, hypertension, and congestive heart failure, which raise the risk of treatment-related cardiovascular complications. The article discusses the effects of individual TKIs on the pathogenesis of cardiovascular complications and presents the results of clinical trials that studied their impact on the incidence of such events.
Źródło:
OncoReview; 2019, 9, 1; 3-21
2450-6125
Pojawia się w:
OncoReview
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:
Deep molecular response (MR4.5) as a target of therapy with tyrosine kinase inhibitors. MR4.5 – goal of CML treatment
Autorzy:
Sacha, Tomasz
Powiązania:
https://bibliotekanauki.pl/articles/1065835.pdf
Data publikacji:
2014
Wydawca:
Medical Education
Tematy:
chronic myeloid leukemia
possibility cure
therapy targets
tyrosine kinase inhibitors
Opis:
Chronic myeloid leukemia (CML) accounts for 15% of diagnosed leukemias. The annual incidence in two Polish regions has been calculated for 0.7/100,000 of general population. Introduction of tyrosine kinase inhibitors (TKIs) have substantially improved not only the prognosis of CML, but also changed the treatment goals, and the expectations of patients and physicians. The goals of CML therapy include: to prevent the progression towards accelerated phase and blastic phase, to eliminate the risk of death from leukemia, to prolong the length of survival to comparable of healthy population and to attain a quality of life comparable to healthy people. Patients treated up-front with second generation TKIs (2GTKI) have a better chance to achieve faster and deeper response to therapy. Most of patients receiving 2GTKI in first line or e.g. nilotinib after initial phase of imatinib therapy can achieve very deep molecular response (MR4.5), which is a key criterion for discontinuation studies. The results of stop-trials suggest that substantial proportion of patient could achieve sustained treatment-free survival, and that the disease could be controlled despite of persistence of minimal residual disease, which does not require a clinical intervention. Patients group that could benefit most from discontinuation study include younger people, those who have achieved MR4.5 and patients reporting TKI – associated side effects. Achievement of MR4.5 could be considered as a target of CML therapy for considerable proportion of patients. The question of safe TKI dose reduction or therapy cessation should be addressed in the future planned clinical trials.
Źródło:
OncoReview; 2014, 4, 1; A27-32
2450-6125
Pojawia się w:
OncoReview
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
ANALYSIS OF CHRONIC MYELOID LEUKEMIA PHARMACOTHERAPY COSTS IN POLAND
Autorzy:
Paczkowska, Anna
Kus, Krzysztof
Nowicka, Monika
Kopciuch, Dorota
Zaprutko, Tomasz
Komarnicki, Mieczysław
Nowakowska, Elżbieta
Powiązania:
https://bibliotekanauki.pl/articles/895298.pdf
Data publikacji:
2019-02-28
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
poland
chronic myeloid leukemia
stem cell transplantation
pharmacotherapy cost analysis
Opis:
The aim of this study was to analyze pharmacotherapy cost of chronic myeloid leukemia from the society’s, the payer’s (National Health Fund), and the patient’s perspective. The study included 55 patients with a diagnosed and treated chronic myeloid leukemia at the selected hematology clinic in the city of Poznan. Retrospective study involved time horizon of one calendar year – 2013. The data required for economic evaluation were obtained from the patients’ case histories and the Department of Organization and Accounting of the selected health care facilities. The total cost of chronic myeloid leukemia pharmacotherapy for 55 patients from the society’s perspective in 2013 amounted to 1,483,416.88 EUR. Average annual cost of medication per patient in 2013 amounted to 26,971.22 EUR (Median – 32,854.22 EUR). Average cost of chronic myeloid leukemia pharmacotherapy for a patient without transplantation was 32,167.34 EUR (Median – 30,623.00 EUR), and for a patient after transplantation amounted to 413.13 EUR (Median – 378.40 EUR). The cost from the payer’s perspective is 99.93% of total costs from the society’s perspective. The cost from the patient’s perspective represents 0.07% of the total cost of chronic myeloid leukemia pharmacotherapy from the society’s perspective. Costs of chronic myeloid leukemia pharmacotherapy are very high and represent a significant burden to society. The highest costs associated with treatment of chronic myeloid leukemia are incurred by the society, and, subsequently, the public payer (NHF), and the patient.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 1; 175-183
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
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:
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:
Czy galusan epigallokatechiny może być skutecznym polifenolem w terapii skojarzonej z etopozydem w leczeniu przewlekłej białaczki szpikowej?
Can epigallocatechin gallate be an effective polyphenol in combination therapy with etoposide for the treatment of chronic myelogenous leukemia?
Autorzy:
Cierniak, Agnieszka
Skubal, Magdalena
Kalemba-Drożdż, Małgorzata
Powiązania:
https://bibliotekanauki.pl/articles/970179.pdf
Data publikacji:
2018
Wydawca:
Krakowska Akademia im. Andrzeja Frycza Modrzewskiego
Tematy:
apoptoza
EGCG
etopozyd
przewlekła białaczka szpikowa
uszkodzenia DNA
apoptosis
etoposide
chronic myeloid leukemia
DNA damage
Opis:
Wprowadzenie: Składnik zielonej herbaty – galusan epigallokatechiny (EGCG) – znany jest ze swoich właściwości chemoprewencyjnych i chemoterapeutycznych. Wykazuje silne właściwości antyoksydacyjne i przeciwzapalne, a w stosunku do komórek nowotworowych – działanie antyproliferacyjne lub proapoptotyczne. Etopozyd jest jednym z najczęściej stosowanych leków przeciwnowotworowych, wywołującym jednak wiele skutków ubocznych. Materiały i metody: W eksperymentach in vitro badano potencjalną rolę EGCG w terapii skojarzonej z etopozydem w leczeniu przewlekłej białaczki szpikowej. Komórki ustalonej linii białaczkowej K562 poddano działaniu etopozydu i/lub EGCG w celu określenia wpływu EGCG na przeżywalność komórek, poziom uszkodzeń DNA oraz częstość procesu apoptozy. Poziom uszkodzeń DNA mierzono przy pomocy elektroforezy pojedynczych komórek w żelu agarozowym (test kometowy), natomiast apoptozę oceniano pod mikroskopem fluorescencyjnym z użyciem barwnika Hoechst 33342. Wyniki: Uzyskane wyniki badań wskazują, że EGCG w stężeniu 50 i 100 μM uwrażliwia komórki białaczkowe na cytotoksyczne działanie etopozydu, zwiększając poziom uszkodzeń DNA i częstość apoptozy. Wnioski: Dane wskazują, że galusan epigallokatechiny może się okazać skutecznym polifenolem w terapii skojarzonej z etopozydem w leczeniu przewlekłej białaczki szpikowej
Introduction: Green tea ingredient – epigallocatechin gallate (EGCG) – is known for its chemopreventive and chemotherapeutic properties. It has strong antioxidant and anti-inflammatory properties, and antiproliferative or pro-apoptotic activity against cancer cells. Etoposide is one of the most commonly used anti-cancer drugs causing many side effects. Materials and methods: This study investigated the role of EGCG in combination therapy with etoposide in the treatment of chronic myeloid leukemia. K562 cells were treated with EGCG and / or etoposide to determine the effect of this polyphenol on cell survival, DNA damage or apoptosis. DNA damages were measured with single cell gel electrophoresis (comet assay) and the apoptosis were analyzed in fluorescence microscope with Hoechst 33342 staining. Results: Preliminary results suggest that EGCG at 50 and 100 μM sensitizes leukemic cells to the cytotoxic effect of etoposide, increases DNA damage that promotes removal cell and directs them to apoptosis. Conclusions: The data show that epigallocatechin gallate may prove to be an effective polyphenol in combination therapy with etoposide in the treatment of chronic myeloid leukemia. However, further research is needed to explain the EGCG interaction with chemotherapeutics.
Źródło:
Państwo i Społeczeństwo; 2018, 3; 9-28
1643-8299
2451-0858
Pojawia się w:
Państwo i Społeczeństwo
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Mechanism, detection and significance of some chromosomal rearrangements in chronic myeloid leukaemia [CML] and acute lymphoblastic leukaemia [ALL]
Autorzy:
Ladon, D
Witt, M.
Powiązania:
https://bibliotekanauki.pl/articles/2043432.pdf
Data publikacji:
2000
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
translocation
minimal residual disease
in situ
hybridization
fluorescence
chronic myeloid leukemia
chromosome aberration
mixed chimerism
detection
cytogenetic evolution
acute lymphoblastic leukemia
Źródło:
Journal of Applied Genetics; 2000, 41, 3; 187-197
1234-1983
Pojawia się w:
Journal of Applied Genetics
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Molecular follow up of donor lymphocyte infusion in CML children after allogeneic bone marrow transplantation
Autorzy:
Ladon, D
Pieczonka, A.
Jolkowska, J.
Wachowiak, J.
Witt, M.
Powiązania:
https://bibliotekanauki.pl/articles/2048295.pdf
Data publikacji:
2001
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
minimal residual disease
in situ
human genetics
bone marrow
hybridization
fluorescence
donor lymphocyte infusion
chronic myeloid leukemia
child
polymerase chain reaction
transplantation
Źródło:
Journal of Applied Genetics; 2001, 42, 4; 547-552
1234-1983
Pojawia się w:
Journal of Applied Genetics
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Aktywna postawa lekarza versus inercja pacjenta: wykrycie przewlekłej białaczki szpikowej podczas badań okresowych
Active physician attitude vs. patient inertia: detection of chronic myeloid leukemia during periodic examinations
Autorzy:
Marcinkiewicz, Andrzej
Powiązania:
https://bibliotekanauki.pl/articles/2152951.pdf
Data publikacji:
2022
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
przewlekła białaczka szpikowa
wczesne wykrywanie
komunikacja lekarz–pacjent
stosowanie się do zaleceń lekarskich
udział pacjenta
zdrowie pracujących
chronic myeloid leukemia
early detection
physycian–patient communication
compliance
patient participation
occupational health
Opis:
Opis przypadku dotyczy zapoczątkowanego podczas badań okresowych postępowania profilaktyczno-orzeczniczego, które doprowadziło do wczesnego wykrycia przewlekłej białaczki szpikowej. Szczególną uwagę zwrócono na skrócenie terminu ważności badania okresowego uzasadnione nieprawidłowością w stanie zdrowia, która nie miała bezpośredniego związku z warunkami zawodowymi, oraz na sposób komunikacji i wpływ na pracownika, aby zastosował się do zaleceń lekarskich. Wywnioskowano, że wprawdzie obligatoryjne i cykliczne badania profilaktyczne do celów Kodeksu pracy stwarzają możliwość wczesnego wykrycia nieuświadomionych stanów chorobowych, dając tym samym szansę na poprawę stanu zdrowia pacjentów, ale jednocześnie mogą być traktowane jako ingerencja w prawo do samostanowienia jednostki o własnym życiu i zdrowiu. Uznano, że w ocenie sytuacji kluczowe są postawa lekarza medycyny pracy oraz sposób komunikacji z badanym pracownikiem, które nie tyle zmuszą, ile przekonają – dla dobra pacjenta – do podjęcia diagnostyki lub interwencji prozdrowotnej.
The case report concerns the prophylactic and medical certification procedure initiated during periodic examinations, which led to the early detection of chronic myeloid leukemia. Particular attention was paid to the shortening of the period of validity of the periodic examination, justified by an abnormal health condition that is not directly related to the working conditions, as well as the method of communication and influencing the employee to comply with medical recommendations. The conclusions stated that, although obligatory and periodic preventive examinations for the purposes of the Labor Code create the possibility of early detection of unawereness of disease, thus giving a chance to improve health, but at the same time they can be treated as an interference with the individual’s right to self-determination about his life and health. It was noted that the key factor in assessing the situation would be the attitude of the occupational medicine physician and the manner of his communication with the employee, who would not be forced, but convinced – for his benefit, to undertake diagnostics or health interventions.
Źródło:
Medycyna Pracy; 2022, 73, 6; 485-490
0465-5893
2353-1339
Pojawia się w:
Medycyna Pracy
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Myeloid sarcoma associated with blast crisis in chronic myelogenous leukemia - case report
Autorzy:
Szymczyk, Agnieszka
Podhorecka, Monika
Tomczak, Waldemar
Szumiło, Justyna
Hus, Marek
Powiązania:
https://bibliotekanauki.pl/articles/972387.pdf
Data publikacji:
2016
Wydawca:
Instytut Medycyny Wsi
Tematy:
myeloid sarcoma
chronic myelogenous leukemia
blast crisis
Opis:
Introduction. Myeloid sarcoma (MS) is a rare extramedullary tumour which may precede or occur concomitantly with bone marrow involvement in acute myeloid leukemia, myelodysplastic syndrome, or blast crisis in chronic myeloproliferative disorder. Myeloid sarcoma is most commonly found in lymph nodes, skin, subcutaneous tissue and gums, while it is less common in bones, the retroperitoneal space and eye socket. Case Report. The case is reported of a 65-year-old woman with chronic myelogenous leukemia treated for about 20 years with hydroxyurea, 6-mercaptopurine and tyrosine-kinase inhibitors. During the treatment, the general condition of the patient progressively deteriorated, lymphadenopathy and splenomegaly worsened, and blast crisis was diagnosed. After the first cycle of induction chemotherapy, the patient’s lymph nodes were swollen and painful. One of the lymph nodes was subjected to histopathology, on the basis of which a diagnosis of MS was made. As the patient showed no response to the treatment, palliative care was initiated. Three months after the diagnosis of MS, the disease progressed. The patient died of infectious complications. Conclusions: A diagnosis of MS, which is considered an adverse prognostic factor, significantly reduces the chances of remission and overall survival in patients with acute myelogenous leukemia or blast crisis inchronic myeloproliferative disorders. It seems that early confirmation of the diagnosis and initiation of the treatment adjusted to the patient’s clinical condition may improve the prognosis and increase the response rates.
Źródło:
Journal of Pre-Clinical and Clinical Research; 2016, 10, 2; 136-139
1898-2395
Pojawia się w:
Journal of Pre-Clinical and Clinical Research
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-11 z 11

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