Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL
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HOSER
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4
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1/4
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.
2/4
Tytuł oryginału:
Reactivity of alveolar macrophages in lung cancer patients and healthy subjects: surface ICAM-1 after INF-ç stimulation in vitro.
Autorzy:
Hoser
G.,
Grubek-Jaworska
H.,
Droszcz
P.,
Domagała-Kulawik
J.,
Dąbrowska
M.,
Chazan
R.
Źródło:
Folia Histochem. Cytobiol. 2002: 40 (2) s.103-104, il., tab., bibliogr. 6 poz. - Konferencja pt. Cytometria przepływowa i ilościowa, mikroskopia w diagnostyce medycznej Poznań 21-22.05. 2001
Sygnatura GBL:
304,846
Hasła klasyfikacyjne GBL:
immunologia
farmacja
pulmonologia
onkologia
Typ dokumentu:
praca związana ze zjazdem
praca kazuistyczna
tytuł obcojęzyczny
Wskaźnik treści:
ludzie
in vitro
Streszczenie angielskie:
The linearity of ICAM-1 expression on alveolar macrophages (AM) before and after INF-ç stimulation in healthy and lung cancaer subjects were compared. AM were collected by bronchoalveolar lavage and incubated with/without INF-ç according to standard procedures. The harvested calls were analyzed by flow cytometry using mooclonal antibodies against leucocytes and macrophages. Only viable cells were analyzed. Stimulation with INF-ç revealed two AM subpopulations of similar size differentiated in the intensity of ICAM-1 expression. They were not distinctly marked in every studied case. our preliminary results did not confirm the previously reported decreasing reactivity of AMs after INF-ç stimulation in lung cancer patients.
3/4
Tytuł oryginału:
Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism.
Autorzy:
Feleszko
Wojciech,
Młynarczuk
Izabela,
Olszewska
Dominika,
Jalili
Ahmad,
Grzela
Tomasz,
Lasek
Witold,
Hoser
Grażyna,
Korczak-Kowalska
Grażyna,
Jakóbisiak
Marek
Źródło:
Int. J. Cancer 2002: 100 (1) s.111-118, il., tab., bibliogr. 37 poz.
Sygnatura GBL:
305,029
Hasła klasyfikacyjne GBL:
farmacja
onkologia
Typ dokumentu:
praca doświadczalna
praca opublikowana za granicą
tytuł obcojęzyczny
Wskaźnik treści:
ludzie
zwierzęta
Streszczenie angielskie:
Lovastatin, a drug successfully used in the clinic to prevent and to treat coronary heart disease, has recently been reported to decrease the incidence of melanoma in lovastatintreated patients. Lovastatin has also been proved to potentiate antitumor effects of both cisplatin and TNF-ŕ in murine melanoma models. Recently, an augmented therapeutic effect of lovastatin and doxorubicin has been reported in 3 tumor models in mice. In our preliminary study lovastatin caused retardation of melanoma growth in mice treated with doxorubicin (Feleszko et al. J. Nati Cancer Inst 1998;90:247-8). In the present report, we supplement our preliminary observations and demonstrate in 2 murine and 2 human melanoma cell lines that lovastatin effectively potentiates the cytostatic/cytotoxic activity of doxorubicin in vitro via an augmentation of apoptosis (estimated with PARP-cleavage assay, annexin V assay and TUNEL). The combined antiproliferative activity of lovastatin and doxorubicin was evaluated using the combination index (CI) method of Chou and Talalay, revealing synergistic interactions in melanoma cells exposed to lovastatin and doxorubicin. In BI6FI0 murine melanoma model in vivo, we have demonstrate significantly increased sensitivity to the combined treatment with both lovastatin (5 mg/kg for 14 days) and doxorubicin (4 x I mg/kg) as compared with either agent acting alone. Lovastatin treatment resulted also in significant reduction of the number of experimental metastasis in doxorubicin-treated mice The results of our studies suggest that lovastatin may enhance the effectiveness of chemotherapeutic agents in the treatment of malignant melanomas.
4/4
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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