Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: SZMIGIELSKA-KAPŁON
Liczba odnalezionych rekordów: 3



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Tytuł oryginału: Anthracyclines potentiate activity against murine leukemias L 1210 and P388 in vivo and in vitro.
Autorzy: Szmigielska-Kapłon Anna, Ciesielska Ewa, Szmigiero Leszek, Robak Tadusz
Źródło: Eur. J. Haematol. 2002: 68 (6) s.370-375, il., tab., bibliogr. 37 poz.
Sygnatura GBL: 304,912

Hasła klasyfikacyjne GBL:
  • farmacja
  • hematologia
  • onkologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: Abstract: The interactions of 2-chlorodeoxyadenosine (2-CdA, cladribine) and three anthracyclines: doxorubicin (DOX), idarubicin (IDA) and mitoxantrone (MIT) were evaluated on murine leukemias P 388 adn L 1210. Prolongation of survival time of animals receiving drugs in combination compared to mice tereated with drugs in monotherapy was tested. We have also evaluated interactions of the cytostatics on murine leukemias in vitro by measuring their inhibitory effects on P 388 and L 1210 cell proliferation. We have observed a synergistic effect of MIT and IDA in combination with 2-CdA on P 388 leukemia resulting in an increase of life span (ILS) = 226 p.c in case of MIT + 2-CdA and ILS = 126 p.c. in the case of IDA + 2-CdA, whereas 2-CdA used as a sole drug resulted in an ILS = 47 p.c. The survival time of animals inoculated with P 388 leukemic cells and treated with DOX + 2-CdA was similar to ILS gained by DOX monotherapy (178 p.c. and 200 p.c. respectively). The mice bearing L 1210 leukemia receiving combined chamotherapy lived significantly longer than the animals on single agent regiments. The animals treated with schedule 2-CdA + MIT lived significantly longer (P = 0.004) as compard to the groups receiving drugs in monotherapy (ILS of 2-CdA + MIT group = 60 p.c., ILS of MIT groups 33 p.c., and 2-CdA group 33 p.c.). Finally, combination of DOX or IDA with 2-CdA resulted in ILS = 73 p.c. (2-CdA + DOX regimen), and ILS = 60 p.c. in case of 2-CdA + IDA regimen, which is significantly higher than ILS gained on monotherapy schedules. In vitro tests revealed that all tested anthracyclines enhance the antiproliferative activity of 2-CdA against L 1210 and P 388 leukemic cells (p 0.05)...

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    Tytuł oryginału: Cytotxic effect of cyclosporin A alone and in combination with 2-chlorodeoxyadenosine against P388 murine leukemia in vivo.
    Autorzy: Józefowicz-Okonkwo Grażyna, Szmigielska-Kapłon Anna, Robak Tadeusz
    Źródło: Med. Sci. Monitor 2002: 8 (9) s.BR373-BR377, il., tab., bibliogr. 21 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • onkologia
  • farmacja
  • hematologia

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: Background: THe purpose of our study was to determine the antileukemic effects of cyclosporin A (CsA0 and its interaction with a new purine analogue, -chlorodeoxyadenosine (2-CdA, cladribine) on P388 murine leukemia in vivo. Material/methods: Mice were engrafted intraperitoneally (i.p.) with 10**6 P388 leukemia cells on day 0 of each step of the two-step experiment. ALl treatments were initiated on teh next day (day 1) as daily i.p. injections and lasted for five consecutive days. In the first part of the experiment, designed to establish the antileukemic effect of CsA, the mice received 10, 15, 20, 25 or 30 mg/kg of CsA. In the second part, where the interaction between CsA and 2-CdA was examined, the animals were administered CsA at a dose of 15 mg/gk, or 2-CdA at a dose of 20 mg/kg, or CsA combined with 2-CdA at the same doses as in monotherpay. Results: CsA did not influence the survival time of mice with P388 leukemia at any dose. ScA was used for the interaction study at a dosage of 15 mg/kg, as this was best tolerated by the animals. The mice treated with combination therapy using CsA and 2-CdA survived longer than those treated with 2-CdA monotehrapy (p = 0.00015). Conclusion: Our study revealed that CsA alone does not increase the survival time of mice with P388 leukemia, but it augments the antileukemic effect of 2CdA.

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    Tytuł oryginału: Acute lymphoblastic leukemia in adult first manifested as severe aplastic anemia - role of molecular analysis in correct diagnosis.
    Autorzy: Robak Tadeusz, Bartkowiak Jacek, Urbańska-Ryś Halina, Szmigielska-Kapłon Anna, Strzelecka Bogusława, Chojnowski Krzysztof
    Źródło: Leuk. Lymphoma 2002: 43 (5) s.1147-1152, il., bibliogr. 40 poz.
    Sygnatura GBL: 312,939

    Hasła klasyfikacyjne GBL:
  • genetyka
  • hematologia
  • onkologia

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

    Wskaźnik treści:
  • ludzie
  • dorośli 19-44 r.ż.
  • płeć męska

    Streszczenie angielskie: Aplastic anemia (AA) may sometimes precede the diagnosis of acute lymphoblastic leukemia (ALL) in children. Such presentation of ALL is externally rare in adults and until now only few such cases have been reported. We present a 40-year-old male with ALL common type, which developed 14 months after the diagnosis of severe AA, successfully treated with corticosteroids. ALL was treated with standard induction chemotherapy but remission has not been achieved. The patient died 6 weeks after the diagnosis of ALL because of central nervous system bleeding. The pattern of IgH gene rearrangement analyzed with PCR method in bone marrow from the period of AA diagnosis and in peripheral blood mononuclear cells from ALL diagnosis showed two different monoclonal IgH configurations as the results of biallelic monoclonal rearrangement of IgH genes. The observed bands in both specimens were identical and indicated that leukemic cells originated from B-cell progenitor were also present in the bone marrow when AA was diagnosed. We suggest that molecular analysis of monoclonality in patients with AA may be important for proper selection of the rare cases of ALL first presenting as marrow aplasia.

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