Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: SKORSKI
Liczba odnalezionych rekordów: 2



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Tytuł oryginału: Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis.
Autorzy: Nieborowska-Skorska Małgorzata, Hoser Grażyna, Kossev Plamen, Wasik Mariusz A., Skorski Tomasz
Źródło: Blood 2002: 99 (12) s.4531-4539, il., bibliogr. 68 poz.
Sygnatura GBL: 301,770

Hasła klasyfikacyjne GBL:
  • onkologia
  • hematologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • zwierzęta
  • myszy
  • in vitro

    Streszczenie angielskie: BCR/ABL oncogenic tyrosine kinase activates STAT5, which plays an important role in leukemogenesis. The downstream effectors of the BCR/ABL- STAT5 pathway remain poorly defined. We show here that expression of the antiapoptic protein A1, a member of the Bcl-2 family, and the serine/threonine kinase pim-1 are enhanced by CRB/ABL. This up-regulation requires activation of STAT5 by the signaling from SH3 + SH2 domains of the BCR/ABL. Enhanced expression of A1 and pim-1 played a key role in the BCR/ABL-mediated cell protection from apoptosis. In addition, pim-1 promoted proliferation of the BCR/ABL-transformed cells. Both A1 and pim-1 were required to induce interleukin 3-independent cell growth, inhibit activation of caspase 3, and stimulate cell cycle progression. Moreover, simultaneous up-regulation of both A1 and pim-1 was essential for in vitro transformation and in vivo leukemogenesis mediated by BCR/ABL. These data indicate that induction of A1 and pim-1 expression may play a critical role in the BCR/ABL - depenendent transformation.


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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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