ライフサイエンスコーパス: teniposide

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1 a) resistant to paclitaxel, vinblastine, and teniposide.

2 ncreased with the resistance of the cells to teniposide.

3 a human cell line selected for resistance to teniposide.

4 ely 50 to 100 times better with than without teniposide, a compound that is also used as chemotherapy

5 x-stabilizing topo II inhibitors, etoposide, teniposide, amsacrine, and doxorubicin, but not to other

6 drug resistance ratios between etoposide and teniposide and between merbarone and SN-38.

7 ncluded the DNA topoisomerase II inhibitors, teniposide and doxorubicin.

8 found that the group 1 epipodophyllotoxins (teniposide and etoposide) consistently produced the grea

9 e to the non-intercalating agents etoposide, teniposide and merbarone, an effect that was maximal in

10 In the present study, we report that teniposide and various other chemotherapeutic agents ind

11 The pharmacokinetics of methotrexate, teniposide, and cytarabine, as well as the thiopurine me

12 lizing Topo II inhibitors such as etoposide, teniposide, and doxorubicin, which cause DNA damage, str

13 a regimen of cyclophosphamide, doxorubicin, teniposide, and prednisone (CHVP) versus CHVP plus IFN i

14 ved in FasL expression induced by etoposide, teniposide, and UV irradiation.

15 Consistent with our in vitro results, teniposide coadministration greatly enhanced fragmented

16 e, dexamethasone, 6-thioguanine, cytarabine, teniposide, daunorubicin or methotrexate.

17 natural product agents, including etoposide, teniposide, doxorubicin, and daunorubicin.

18 her, the systemic clearance of methotrexate, teniposide, etoposide, and cytarabine did not differ wit

19 nd its semi-synthetic anticancer derivatives teniposide, etoposide, and Etopophos.

20 h topoisomerase II inhibitors (most commonly teniposide, etoposide, or doxorubicin) have distinct cli

21 that, consistent with our in vitro results, teniposide exhibited the greatest level of transduction

22 l viability than Bcl-2 against etoposide and teniposide-induced cell death.

23 The teniposide-induced increase of cytochrome c was inhibite

24 in response to agents such as etoposide and teniposide might serve as an early signal to induce FasL

25 ystemic exposure to methotrexate, but not to teniposide or cytarabine, was significantly related to t

26 l lines, mutant p53 induction in response to teniposide or ionizing radiation and induction of the p5

27 ces in the pharmacokinetics of methotrexate, teniposide, or cytarabine or in erythrocyte thiopurine m

28 Faster clearance of teniposide (p=0.0001) and methotrexate (p=0.051), but no

29 ens that included high-dose methotrexate and teniposide plus cytarabine.

30 Our teniposide-resistant human lymphoblastic leukemia CEM ce

31 arresting mitosis, and induces apoptosis in teniposide-resistant lymphoblastoid T cells both in vitr

32 es in a human leukemic CEM cell line and two teniposide-resistant sublines, CEM/VM-1 and CEM/VM-1-5 (

33 ance-associated protein (MRP)-overexpressing teniposide-resistant T-cell lymphoma xenografts and prol

34 cted, teniposide treatment failed to regress teniposide-resistant xenografts, rather, treated mice su

35 ( approximately 40 and 400-fold resistant to teniposide, respectively).

36 e cells with equitoxic doses of merbarone or teniposide results in a G(2)/M arrest.

37 Finally, we explored the capability of teniposide to enhance transduction of fragment vectors i

38 As expected, teniposide treatment failed to regress teniposide-resist

39 The cytotoxic activities of etoposide, teniposide, vincristine, doxorubicin, daunorubicin, and

40 adiation and the topoisomerase II inhibitor, teniposide (VM-26) both increase levels of the cyclin de

41 oisomerase II-mediated DNA damage induced by teniposide (VM-26) results in the formation of high mole

42 ld more resistant to the epipodophyllotoxin, teniposide (VM-26), than the parental CEM cells.

43 dexrazoxane (ICRF187) and mechanistic poison teniposide (VM26), can interfere with DNA gate dynamics

44 uces GRP78 mRNA (8.5-fold) and resistance to teniposide (VM26).

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