Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: WARSZAWSKI
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Tytuł oryginału: 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
Źródło: Acta Bioch. Pol. 2002: 49 (1) s.121-128, il., bibliogr. 30 poz. - 8 Międzynarodowe Sympozjum pt. Aspekty molekularne chemioterapii Gdańsk 09. 2001
Sygnatura GBL: 303,116

Hasła klasyfikacyjne GBL:
  • toksykologia
  • genetyka
  • hematologia
  • onkologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • in vitro

    Streszczenie angielskie: 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. We 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.


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    Tytuł oryginału: A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.
    Autorzy: Błasiak Janusz, Gloc Ewa, Warszawski Mariusz
    Źródło: Acta Bioch. Pol. 2002: 49 (1) s.145-155, il., bibliogr. 38 poz. - 8 Międzynarodowe Sympozjum pt. Aspekty molekularne chemioterapii Gdańsk 09. 2001
    Sygnatura GBL: 303,116

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • onkologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: 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 ćM 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 ćM 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 redicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extnt 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 induces 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.

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