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    Wyświetlanie 1-7 z 7
    Tytuł:
    Original vs generic drugs in treatment of chronic myeloid leukaemia
    Autorzy:
    Rusicka, Patrycja
    Powiązania:
    https://bibliotekanauki.pl/articles/1065667.pdf
    Data publikacji:
    2014
    Wydawca:
    Medical Education
    Tematy:
    chronic myeloid leukaemia
    generic drug
    generic imatinib
    imatinib
    the original drug
    Opis:
    The beginning of the twenty-first century saw a breakthrough in haematology, oncology and general medicine driven by the introduction of imatinib (Glivec) to the treatment of chronic myeloid leukaemia. For the first time, a neoplastic disease was successfully treated by a therapy targeting the genetic cause of the disease. At present, targeted therapy based on imatinib is the first one to enter a new stage which is the launch of generic drugs. Poland is the first country in the European Union which, from the beginning of July 2014, introduced generic imatinib. Hence, there is no reliable data on its use except for results from bioequivalence tests. The only data available comes from developing countries where other preparations are used, without reliable bioequivalence studies. However, all generic drugs of imatinib registered in Poland have successfully passed such tests. Undoubtedly, it is necessary to appropriately monitor patients with chronic myeloid leukaemia receiving generic drugs in order to ensure their safety and provide information to other countries where therapy based on generic drugs will be introduced in the following years.
    Źródło:
    OncoReview; 2014, 4, 3; A126-131
    2450-6125
    Pojawia się w:
    OncoReview
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    The Outcome of Targeted Therapy in Advanced Gastrointestinal Stromal Tumors (Gist) with Non-Exon 11 Kit Mutations
    Autorzy:
    Osuch, Czesław
    Rutkowski, Piotr
    Brzuszkiewicz, Karolina
    Bylina, Elżbieta
    Limon, Janusz
    Siedlecki, Janusz A.
    Powiązania:
    https://bibliotekanauki.pl/articles/1395799.pdf
    Data publikacji:
    2014-07-01
    Wydawca:
    Index Copernicus International
    Tematy:
    GIST
    KIT mutations
    imatinib
    Opis:
    GIST is the most common mesenchymal tumour of gastrointestinal tract arising from mutation of KIT or PDGFRA gene. Surgery is the primary method of treatment, however a targeted therapy with imatinib is necessary due to recurrence. The aim of the study was to evaluate efficacy of the targeted chemotherapy in advanced gastrointestinal stromal tumours with non-exon 11 KIT mutations. Material and methods. Data from 279 patients with advanced GIST treated with imatinib between 2001 and 2011 were analysed in the study. Exon 11 KIT mutation was found in 192 patients (68.7%), non-exon 11 KIT mutation was found in 87 patients (31.3%): this group included lack of mutation - wild-type, exon 9 KIT mutations, exon 18 PDGFRA D842V mutations, non-D842V PDGFRA mutations as well as non-exon 9 and 11 KIT mutations. Analysis of progression-free survival and overall survival were done for the entire group of patients and for patients with particular mutations, and then effects on progression-free survival and overall survival of such factors as sex, age, imatinib dose were evaluated. Results. Occurrence of non-exon 11 KIT mutation increases the risk of disease progression by 20% in comparison to the presence of exon 11 KIT mutation, however it does not increase the risk of patient’s death. Percentage of 5-year progression-free survivals is the greatest in the case of PDGFRA mutation other than D842V mutation. Percentage of 5-year survivals in case of the presence of D842V PDGFRA mutation is more than twice worse than in the case of the other mutations. Lesion location in the gastrointestinal tract affected the risk of death, with the greatest percentage of 5-year survival for lesions located in the stomach. Such factors as sex, age at diagnosis (<50, ≥50 years) and imatinib dose did not affect the risk of disease progression and the risk of patient’s death. Conclusions. The ratio of overall survival of patients with advanced GIST with a mutation other than exon 11 KIT mutation treated with imatinib is similar to the ratio of overall survival of patients with GIST with exon 11 KIT mutation. An exception is the group of patients with GIST in whom the presence of D842V PDGFRA mutation was found. In general, longer survival has been found in patients with GIST located in the stomach in comparison to the small intestine or other less frequent locations. Percentage of 5-year progression-free survivals is the greatest in the case of PDGFRA mutation other than D842V mutation.
    Źródło:
    Polish Journal of Surgery; 2014, 86, 7; 325-332
    0032-373X
    2299-2847
    Pojawia się w:
    Polish Journal of Surgery
    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:
    PURITY DETERMINATION OF THE STARTING MATERIALS USED IN THE SYNTHESIS OF PHARMACEUTICAL SUBSTANCES
    Autorzy:
    Groman, Aleksandra
    Stolarczyk, Elżbieta
    Mucha, Mariola
    Powiązania:
    https://bibliotekanauki.pl/articles/895661.pdf
    Data publikacji:
    2019-02-28
    Wydawca:
    Polskie Towarzystwo Farmaceutyczne
    Tematy:
    quality control
    Imatinib
    BOSENTAN
    gas chromatography
    method validation
    Opis:
    High requirements on the API quality mean that the quality control of the starting material is crucial to the manufacturing process of drug substances. Three sensitive methods for the purity determination of the following starting materials: ethylene glycol (method I), 3-acetylpyridine (method II) and 4-chloromethyl-5-methyl-1,3-dioxol-2-one (method III) used in the synthesis of selected drug substances were developed using GC-FID techniques. All the methods were validated according to the International Conference on Harmonization guidelines. The correlation coefficient values were found about 0.99. The obtained RSD values from the replicate injections in the range of 20 - 120% of the nominal concentration ensured the precision.
    Źródło:
    Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 1; 29-35
    0001-6837
    2353-5288
    Pojawia się w:
    Acta Poloniae Pharmaceutica - Drug Research
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Adjuvant imatinib after resection of gastrointestinal stromal tumour – systematic review and meta-analysis
    Imatynib w terapii adiuwantowej pacjentów po zabiegu usunięcia nowotworów podścieliskowych przewodu pokarmowego (GIST) – przegląd systematyczny badań klinicznych i metaanaliza
    Autorzy:
    Kawalec, Paweł
    Kryst, Joanna
    Laczewski, Tomasz
    Martyna, Lech
    Powiązania:
    https://bibliotekanauki.pl/articles/1065969.pdf
    Data publikacji:
    2013
    Wydawca:
    Medical Education
    Tematy:
    GIST
    adjuvant therapy
    gastrointestinal stromal tumour
    imatinib
    systematic review
    Opis:
    Background: Adjuvant therapy is recommended for the population of patients with high risk of recurrence of gastrointestinal stromal tumour after resection. The aim of the study: Evaluation of the clinical efficacy and safety profile of imatinib used in adjuvant therapy in patients after complete resection of a gastrointestinal stromal tumour. Material and methods: A systematic review of the literature published up to 30.03.2012 was performed, and a meta-analysis of identified studies was carried out. Databases were searched: PubMed, EMBASE, The Cochrane Library and others. Results: Two randomised clinical trials regarding comparisons of: imatinib vs. placebo and 12 months of adjuvant imatinib vs. 36 months of adjuvant imatinib as well as 20 non-randomised trials fulfilled the established criteria. Adjuvant imatinib statistically significantly improves recurrence-free survival compared with placebo. Patients with high risk of recurrence benefit most from assigned treatment. Three years of adjuvant imatinib therapy improves recurrence-free state and overall survival compared with 1 year of imatinib in patients after resection of a gastrointestinal stromal tumour. The safety profile of imatinib in the analyzed population is acceptable. Conclusions: For patients with a significant risk of recurrence adjuvant therapy with imatinib should be considered for every patient, due to the clinical benefits it brings.
    Wstęp: Zastosowanie terapii adiuwantowej jest zalecane u pacjentów ze znaczącym ryzykiem nawrotu choroby po zabiegu usunięcia nowotworu podścieliskowego przewodu pokarmowego. Cel pracy: Ocena skuteczności klinicznej i profilu bezpieczeństwa imatynibu stosowanego w ramach terapii adiuwantowej u pacjentów po zabiegu całkowitej resekcji nowotworu podścieliskowego przewodu pokarmowego. Materiał i metody: Przeprowadzono systematyczny przegląd literatury opublikowanej do 30 marca 2012 r. oraz metaanalizę zakwalifikowanych do opracowania badań. Przeszukano następujące bazy danych: PubMed, EMBASE, The Cochrane Library oraz inne. Wyniki: Odnaleziono 2 randomizowane badania kliniczne, dotyczące porównania: imatynibu z placebo oraz imatynibu stosowanego przez 12 miesięcy z imatynibem podawanym przez 36 miesięcy, oraz 20 nierandomizowanych badań klinicznych dotyczących stosowania imatynibu w analizowanym wskazaniu. Zastosowanie imatynibu w terapii adiuwantowej prowadzi do istotnego statystycznie wydłużenia przeżycia wolnego od nawrotu choroby względem placebo. Największe korzyści z zastosowanej terapii odnoszą chorzy z wysokim ryzykiem nawrotu choroby. Przedłużenie 12-miesięcznej terapii imatynibem do 36 miesięcy zwiększa prawdopodobieństwo przeżycia wolnego od progresji choroby oraz przeżycia całkowitego pacjentów po zabiegu resekcji nowotworu podścieliskowego przewodu pokarmowego. Profil bezpieczeństwa imatynibu w analizowanej populacji okazał się korzystny. Wnioski: U pacjentów o znaczącym ryzyku nawrotu terapia adiuwantowa imatynibem powinna być rozpatrywana w przypadku każdego pacjenta ze względu na korzyści kliniczne, jakie przynosi.
    Źródło:
    OncoReview; 2013, 3, 4; 232-342, 343-354
    2450-6125
    Pojawia się w:
    OncoReview
    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
      Wyświetlanie 1-7 z 7

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