ライフサイエンスコーパス: N-methyl-N-nitrosourea

1 lls by treatment with the methylating agent, N-methyl-N-nitrosourea.

2 ation with other agents to rats treated with N-methyl-N-nitrosourea.

3 ere sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitroso

4 Of 30 rats injected with N-methyl-N-nitrosourea, 17 developed mammary tumors.

5 N-methyl-N-nitrosourea accelerated tumor formation, and

6 prostate of a Lobund/Wistar rat treated with N-methyl-N-nitrosourea and testosterone propionate.

7 f age from mice that were and were not given N-methyl-N-nitrosourea, and analyzed by histopathologic

8 ere resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sens

9 e in sensitivity to methyl methanesulfonate, N-methyl-N-nitrosourea, and the chemotherapeutic drugs t

10 given drinking water with or without 240 ppm N-methyl-N-nitrosourea at 5 weeks of age and thereafter

11 Rats were injected with N-methyl-N-nitrosourea at 7 weeks of age; 2 weeks later,

12 Herein we report that DNA methylation by N-methyl-N-nitrosourea at N7-guanine is regioselectively

13 Glial cells were exposed to 1 mM N-methyl-N-nitrosourea for 1 h and allowed 8 or 24 h for

14 wn also to prevent mammary cancer induced by N-methyl-N-nitrosourea in rats.

15 C57BL/6J mice were given N-methyl-N-nitrosourea in their drinking water and sacri

16 hat 1 is very effective in the prevention of N-methyl-N-nitrosourea induced mammary cancers in rats w

17 and treatment of breast cancer using the rat N-methyl-N'-nitrosourea-induced and spontaneous HER-2/ne

18 mmary glands (IC50 = 3.2 microM) and reduced N-methyl-N-nitrosourea-induced mammary tumorigenesis whe

19 quine significantly reduced the incidence of N-methyl-N-nitrosourea-induced mammary tumors in our ani

20 e effect of p.o. administered resveratrol on N-methyl-N-nitrosourea-induced mammary tumors was studie

21 increased incidence and decreased latency of N-methyl-N-nitrosourea-induced thymic lymphoma compared

22 nate, followed by a single i.v. injection of N-methyl-N-nitrosourea (MNU) and chronic androgen stimul

23 rentiated adenocarcinoma with invasion after N-methyl-N-nitrosourea (MNU) and testosterone treatments

24 To determine whether N-methyl-N-nitrosourea (MNU) can induce malignant transf

25 ere used: (a) a single i.v. dose of 50 mg of N-methyl-N-nitrosourea (MNU) per kg body weight, followe

26 The other is postnatal day (P)0 N-methyl-N-nitrosourea (MNU) treatment.

27 imes more resistant to the alkylating agent, N-methyl-N-nitrosourea (MNU), than control cultures.

28 In addition, after exposure to N-methyl-N-nitrosourea (MNU), the latency of mammary tum

29 are the predominant sites of methylation by N-methyl-N-nitrosourea (MNU), which is used to produce a

30 ts such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU), while expression of R137Q

31 N-methyl-N-nitrosourea (MNU)-dependent gastric cancer wa

32 l, an active component of Cassia seed, in an N-methyl-N-nitrosourea (MNU)-induced mouse model of RP.

33 is an effective chemopreventive agent in the N-methyl-N-nitrosourea (MNU)-induced rat mammary tumor m

34 F-1-deficient mice are highly susceptible to N-methyl-N-nitrosourea (MNU)-induced T lymphomas.

35 of H202 and cytokines on the enhancement of N-methyl-N-nitrosourea (MNU)-initiated transformation of

36 uanine (m6G)-containing oligonucleotides and N-methyl-N-nitrosourea (MNU)-treated DNA templates by th

37 were treated at 5 weeks of age with 50 mg/kg N-methyl-N-nitrosourea (MNU).

38 t to 6-thioguanine and the methylating agent N-methyl-N-nitrosourea (MNU).

39 40 rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU; 30 mg/kg body weight).

40 Using N-methyl-N-nitrosourea- (MNU-) modified DNA templates in

41 the toxic effects of the methylating agents, N-methyl-N-nitrosourea, N-methyl-N'nitro-N-nitrosoguanid

42 oxic agents (Cisplatin, Nitrogen Mustard and N-methyl-N-nitrosourea (NMNU/MNU)) within mice either si

43 tly within the bladder lumen of rats bearing N-methyl-N-nitrosourea (NMU)-induced bladder cancer and

44 ents, MMS, DMS, and MeI but not by SN1 agent N-methyl-N-nitrosourea or by gamma irradiation.

45 f human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-N-nitrosogua

46 ning 1 week prior to administration of 35 mg N-methyl-N-nitrosourea per kg body weight, groups of 20

47 rinary bladders initiated with a low dose of N-methyl-N-nitrosourea resulted in a significant increas

48 Previously, we showed that N-methyl-N-nitrosourea-transformed MCF12F breast epithel

49 guous cadmium-transformed MECs (Cd-MECs) and N-methyl-N-nitrosourea-transformed MECs (MNU-MECs) on NS

50 ivation induced by the DNA methylating agent N-methyl-N-nitrosourea was also shown to be hMSH2-depend

51 Chemical mutagenesis with N-methyl-N-nitrosourea was employed to study the pattern