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Wyświetlanie 1-3 z 3
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:
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:
Adrenal Tumors - Diagnostics and the Factual Situation
Autorzy:
Krajewska, Ewa
Toutounchi, Sadegh
Fiszer, Patryk
Cieśla, Witold
Pogorzelski, Ryszard
Bednarczuk, Tomasz
Cieszanowski, Andrzej
Łoń, Izabela
Skórski, Maciej
Powiązania:
https://bibliotekanauki.pl/articles/1396721.pdf
Data publikacji:
2012-04-01
Wydawca:
Index Copernicus International
Tematy:
laparoscopic adrenalectomy
adrenalectomy
adrenal tumor
computer tomography
magnetic resonance
retroperitoneal space tumor
laparoscopic surgery
Opis:
The study presented three cases of patients diagnosed with adrenal tumors subject to surgical intervention during the past 6 months in our Department. The patients presented with radiological diagnostic difficulties, as to the character and location of the primary tumor.The aim of the study was to demonstrate differences between radiological examination results and the factual situation observed during the adrenalectomy. In all the presented cases patients' were subject to laparoscopic intervention. In two cases conversion to open surgery was necessary. The histopathological results of the surgically removed samples were as follows: leiomyoma, myoperycytoma and pheochromocytoma. In selected cases imaging examinations might be of limited value, especially when determining the character and location of the primary lesion of the adrenal gland.
Źródło:
Polish Journal of Surgery; 2012, 84, 4; 208-213
0032-373X
2299-2847
Pojawia się w:
Polish Journal of Surgery
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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