ライフサイエンスコーパス: Vinca

1 e binding site on tubulin differing from the vinca alkaloid and dolastatin 10 binding sites, or that

2 The ability of a class of C-20' modified vinca alkaloid congeners to induce tubulin spiral format

3 e studies comparing the interaction of a new vinca alkaloid derivative, vinorelbine (Navelbine), with

4 ategy has allowed fast access to a family of vinca alkaloid derivatives with an enlarged and function

5 tafolide), a conjugate of folic acid and the vinca alkaloid desacetylvinblastine hydrazide (DAVLBH),

6 or the response of breast cancer patients to Vinca alkaloid drug treatment.

7 Because RALBP1 transports anthracycline and Vinca alkaloid drugs, as well as GS-E, and because it co

8 e role of single-agent vinblastine and other vinca alkaloid in the management of pediatric LGGs deser

9 Vinflunine is a novel Vinca alkaloid presently in Phase I clinical trials.

10 ults indicate that cryptophycin disrupts the Vinca alkaloid site of tubulin; however, the molecular d

11 Since chemical modifications of the vinca alkaloid structure are known to modulate the overa

12 lls created by continuous selection with the vinca alkaloid vincristine (HL60 RV+) or by retroviral i

13 ubulin that is distinct from the colchicine, vinca alkaloid, and paclitaxel binding sites and some, i

14 ne (Navelbine), an amphiphilic semisynthetic Vinca alkaloid, has displayed superior activity and decr

15 Vinflunine, a novel vinca alkaloid, showed some activity and was recently ap

16 ffer significantly from those of the classic Vinca alkaloid, vinblastine.

17 itors sodium azide/2-deoxyglucose and by the vinca alkaloid, vincristine, but not by the chemotherape

18 ntered by cancer patients receiving taxane-, vinca alkaloid- or platin-based chemotherapy.

19 nucleotides are allosteric effectors of the vinca alkaloid-induced self-association of tubulin.

20 ed by the observation that the energetics of vinca alkaloid-induced tubulin spiral polymers, or spira

21 erently from vinblastine, a first generation Vinca alkaloid.

22 kg, intravenous methylprednisolone 30 mg/kg, Vinca alkaloids (VCR 0.03 mg/kg), and/or intravenous ant

23 o other groups of anticancer drugs including vinca alkaloids (vinblastine and vincristine) and anthra

24 the massive stable structures observed with vinca alkaloids and antimitotic peptides.

25 with Dx5, with decreased cross-resistance to Vinca alkaloids and no resistance to dactinomycin.

26 ive inhibition of the tubulin binding of the Vinca alkaloids and other antimitotic agents, (2) proxim

27 Hybrids of vinca alkaloids and phomopsin A have been elaborated wit

28 ent antimitotic cancer chemotherapy based on vinca alkaloids and taxanes target tubulin, a protein re

29 Some of the drugs, such as Vinca alkaloids and taxol, are routinely used for cancer

30 Vinca alkaloids appear to inhibit cell proliferation by

31 Taxanes and Vinca alkaloids are among the most active classes of dru

32 Vinca alkaloids are antimitotic drugs that inhibit micro

33 Vinca alkaloids are antineoplastic agents that halt cell

34 Taxanes and vinca alkaloids are in widespread use and have demonstra

35 residues that are crucial to the binding of vinca alkaloids are shown to be strongly involved in lon

36 of the initial interaction between P-gp and Vinca alkaloids occurs in the cytoplasm.

37 Drugs such as taxanes and vinca alkaloids specifically target microtubules and cau

38 hmin expression on the action of taxanes and Vinca alkaloids using a panel of human breast cancer cel

39 ty (many-fold greater than paclitaxel or the vinca alkaloids) raises important questions about its me

40 otherapeutic drugs (e.g., anthracyclines and vinca alkaloids) should concentrate in acidic organelles

41 775), KSP (ispinesib), and tubulin (taxanes, vinca alkaloids), are presented.

42 nclude liposomal anthracyclines, paclitaxel, vinca alkaloids, and bleomycin.

43 ance to anthracyclines, epipodophyllotoxins, vinca alkaloids, and some alkylating agents.

44 e to killing by MDR-sensitive drugs, such as vinca alkaloids, anthracyclines, podophyllins, and pacli

45 geting agents (MTA), such as the taxanes and vinca alkaloids, are used to treat a variety of cancers

46 AB-5, like taxanes and vinca alkaloids, blocks cell division during mitosis.

47 often used in combination with bleomycin and vinca alkaloids, can lead to vascular events including a

48 agents in clinical use, the taxanes and the vinca alkaloids, come from terrestrial sources, the sea

49 ide was accompanied by cell sensitization to Vinca alkaloids, gramicidin D, and Taxol with no effect

50 active route to the tetracyclic core of some vinca alkaloids, including the tetrahydroisoquinocarbazo

51 Cross-resistance was observed to Vinca alkaloids, including vincristine, vinorelbine, and

52 superior antitumor activity to that of other Vinca alkaloids, including vinorelbine from which it was

53 Whereas many drugs, including the vinca alkaloids, often become less effective when p53 is

54 y developed a new group of folate-conjugated Vinca alkaloids, one of which, EC145, emerged as a candi

55 xic agents such as liposomal anthracyclines, vinca alkaloids, or paclitaxel.

56 ored cellular sensitivity to anthracyclines, Vinca alkaloids, taxanes, and other anticancer drugs.

57 The two second-generation Vinca alkaloids, vinorelbine and vinflunine, affect micr

58 eases microtubule binding and sensitivity to Vinca alkaloids, which promotes microtubule depolymeriza

59 grafted tumors as effectively as taxanes and vinca alkaloids.

60 rarely has been applied to studies involving vinca alkaloids.

61 e efficacy of paclitaxel, docetaxel, and the vinca alkaloids.

62 umor activities of the two second-generation Vinca alkaloids.

63 , including platinum compounds, taxanes, and vinca alkaloids.

64 nding of paclitaxel and increased binding of Vinca alkaloids.

65 y to paclitaxel and decreased sensitivity to vinca alkaloids.

66 s using anthracyclines, glucocorticoids, and Vinca alkaloids.

67 r 6 mutants were cross-resistant only to the Vinca alkaloids.

68 ivative, vinorelbine (Navelbine), with other vinca alkaloids.

69 f the energetics of spiral formation for two vinca alkaloids: a novel difluorinated vinorelbine deriv

70 e zoospores of P. nicotianae infected annual vinca and P. sojae race 25 successfully attacked a non-h

71 he total synthesis of several members of the vinca and tacaman classes of indole alkaloids has been a

72 s resistant to other antimicrotubule agents, vincas and taxanes, were screened.

73 The ADC prepared had a vinca-antibody ratio of 20:1.

74 e dilantin binding site is distinct from the Vinca binding site, and these independent binding modes

75 gion of the tubulin heterodimer close to the vinca binding site.

76 ielded a distance between the colchicine and vinca binding sites on tubulin of approximately 40 A.

77 The first example of vinca derivatives 16-18 able to modulate P-glycoprotein

78 ing studies, carried out with two of the new vinca derivatives, provide useful hints about how a give

79 te on beta-tubulin that is distinct from the vinca domain and that blocks the formation of longitudin

80 e "vinca site" and the "peptide site" of the vinca domain in tubulin.

81 tion of alpha beta-tubulin dimers with three vinca domain-binding peptides--cryptophycin 1, hemiaster

82 Using trastuzumab and a vinca drug derivative to demonstrate the utility of this

83 gs in clinic today, particularly taxanes and Vincas, face challenges including frequent visits to the

84 We demonstrate here that vinca-induced tubulin-spiraling potential is significant

85 bioinformatic screen of transcriptomes from Vinca minor, Rauvolfia serpentina, and C. roseus to iden

86 diverse peptide-like molecules, binds to the Vinca-peptide site in tubulin, disrupts normal microtubu

87 Four previously unidentified, Vinca-related mutations, involving three amino acids, ha

88 orated with the aim of interfering with the "vinca site" and the "peptide site" of the vinca domain i

89 taxel.1 Instead, they inhibit the binding of vincas to tubulin.