ライフサイエンスコーパス: alkylator

1 ine (MNNG) is a direct-acting monofunctional alkylator.

2 lanoma, although this compound is a weak DNA alkylator.

3 t treated less than 2 months after high-dose alkylators.

4 inogenicity of N-nitroso compounds and other alkylators.

5 The bifunctional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is

6 The restricted-access alkylator, 2-[(trimethylammonium)ethyl]methanethiosulfon

7 The affinity alkylator, 5,10-secoestr-4-yne-3,10, 17-trione (secoster

8 combination regimens than single-agent oral alkylators (59% vs 20%, respectively; P = .003).

9 of proteasome inhibitors, dexamethasone, and alkylators achieve high response rates, although control

10 lar glutathione levels prior to intracarotid alkylator administration.

11 lls, transplanted mice were treated with the alkylator agent 1,3-bis-chloroethyl-1-nitrosourea.

12 nucleoside analogs, nucleoside analogs plus alkylator agents, or combination chemotherapies, such as

13 Current therapeutic modalities include alkylator agents, purine nucleoside analogues, and ritux

14 : therapy with either nucleoside analogs and alkylator agents, rituximab in combination with nucleosi

15 The data suggest high-dose alkylator and anthracycline chemotherapy increase the ri

16 Alkylators and anthracyclines were associated with an in

17 ide have been combined with corticosteroids, alkylators, and anthracyclines in front-line MM treatmen

18 e protein with acid, chaotropic denaturants, alkylators, and detergents failed to unmask N-terminal N

19 s who were previously exposed to bortezomib, alkylators, and other immunomodulatory drugs.

20 With this regimen, cumulative doses of alkylators, anthracyclines, and epipodophyllotoxins are

21 The classes of drugs reviewed include alkylators, antimetabolites, anthracyclines, taxanes, ca

22 Purine analogs and alkylators are important agents for treating chronic lym

23 Purine analogs and alkylators are important agents in the treatment of chro

24 romosomal aberrations after treatment with N-alkylators arise when replication forks collide with SSB

25 e model recapitulates many features of human alkylator-associated cancer and supports the hypothesis

26 The risk of developing an alkylator-associated malignancy is influenced by genetic

27 s could be a key step in the pathogenesis of alkylator-associated secondary malignancies.

28 icantly over the last decades from primarily alkylator-based chemotherapeutic agents with minimal eff

29 All patients received alkylator-based chemotherapy as a component of adjuvant

30 Conventional or high-dose alkylator-based chemotherapy is effective in almost two-

31 an adverse outcome in children treated with alkylator-based chemotherapy, independently of a variety

32 rnal-beam radiotherapy followed by a year of alkylator-based chemotherapy.

33 Treatment consisted of intensive alkylator-based induction chemotherapy with or without a

34 els of FLC at baseline and after 2 months of alkylator-based therapy.

35 andomized study suggesting it is superior to alkylator-based therapy.

36 Et743 appears to be unusual among other alkylators, because its adducts strongly inhibit intrace

37 e rituximab alone or rituximab combined with alkylators (bendamustine and cyclophosphamide), proteaso

38 oxia-activated prodrug that releases the DNA alkylator bromo-isophosphoramide mustard in hypoxic sett

39 Topoisomerase II inhibitors and alkylators can induce t-ML; additional risk factors for

40 d chemotherapy regimens containing high-dose alkylators can place women at risk for acute ovarian fai

41 ormalities associated with prior exposure to alkylator chemotherapy.

42 ormalities associated with prior exposure to alkylator chemotherapy.

43 -AML) is an important late adverse effect of alkylator chemotherapy.

44 nancies are a serious adverse consequence of alkylator chemotherapy.

45 The oligonucleotide-alkylator conjugates inhibited transcription elongation

46 n these data, we synthesized oligonucleotide-alkylator conjugates that would react with a specific gu

47 plication of triplex-forming oligonucleotide-alkylator conjugates to inhibit transcription elongation

48 n conclusion, in the overall population, the alkylator-containing triplets MPR and CPR were not super

49 P < .01) is significantly increased when the alkylator cyclophosphamide (CTX) is added to TLI/ATS con

50 ibitor DM1 (a maytansinoid), or with the DNA alkylator DC1 (a CC1065 analogue), have been evaluated f

51 c solid tumors with chemotherapy lacking the alkylator dose-intensity and prominence of etoposide tha

52 T expression provides cellular resistance to alkylator drugs, which can be administered to kill resid

53 No alkylators, epipodophylotoxins, anthracyclines, or radia

54 stant or susceptible to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes th

55 gents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV li

56 ng with the CNS cytotoxicity of intracarotid alkylators, even after BSO depletion of CNS glutathione.

57 In matched analyses, radiation and alkylator exposure are associated with secondary CRC.

58 n Casp9-deficient bone marrow chimeras after alkylator exposure.

59 y of 2-CdA and mitoxantrone in patients with alkylator-failed indolent lymphoma to determine the maxi

60 ation regimen are warranted in untreated and alkylator-failed indolent lymphoma.

61 ified use of topoisomerase-II inhibitors and alkylators first gained wide acceptance and produced bet

62 riplets MPR and CPR were not superior to the alkylator-free doublet Rd, which was associated with low

63 However, new alkylator-free schemes, such as lenalidomide plus low-do

64 were designed to react as polyfunctional DNA alkylators, generating novel types of DNA damage.

65 gs with high-dose methotrexate, most notably alkylators, high-dose cytarabine, and rituximab; and the

66 tumor cells to treatment with monofunctional alkylators, implicating inhibition of APE1 as a valid st

67 ospermin is a topoisomerase II-dependent DNA alkylator in advanced preclinical development.

68 e dexamethasone, are challenging the role of alkylators in myeloma treatment of elderly patients.

69 milar entry of Ca2+ induced by cell permeant alkylators indicated that this Ca2+ entry process was ac

70 a link between mismatch repair processing of alkylator-induced DNA damage and cell death.

71 ity factors, we established a mouse model of alkylator-induced malignancy.

72 e studies establish a novel in vivo model of alkylator-induced myeloid malignancy that will facilitat

73 trates that Nfkb1(-/-) cells accumulate more alkylator-induced, but not ionizing radiation (IR)-induc

74 or 7 were found in 10 cases, which suggests alkylator involvement.

75 reduce the mutagenic effects of specific DNA alkylators is unknown.

76 t autophagy and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (pacli

77 e, and resistance to the cytotoxicity of the alkylator MNNG.

78 revented by pretreatment with the sulfhydryl alkylator N-ethylmaleimide.

79 Casp9-deficient cells after exposure to the alkylator, N-ethyl-nitrosourea (ENU).

80 ichlorophenyl)1,2,3,4-oxatriazolium), or the alkylator, N-ethylmaleimide, was observed to be strongly

81 he currently recommended use of single-agent alkylator, nucleoside analog, or standard-dose rituximab

82 nalogs than with DNA-damaging agents such as alkylators or topoisomerase II inhibitors.

83 Our findings raise the possibility that alkylator-purine analog combination therapy may increase

84 de preclinical support for trials of TLI/ATG/alkylator regimens for MHC-mismatched BMT for hemoglobin

85 s occurred, with only 1 from ESRD but 4 from alkylator-related leukemia or myelodysplastic syndrome.

86 tients with multiple myeloma (MM), including alkylators, steroids, immunomodulatory agents (IMiDs), p

87 f 2,7-DAM with DNA; other known major groove alkylators such as aflatoxin, possessing aromatic struct

88 able, options include minimizing exposure to alkylators, such as single-agent low-dose targeted busul

89 tivation is effected by N-ethylmaleimide, an alkylator that slowly penetrates lipid bilayers.

90 al and cytogenetic findings implicated prior alkylator therapy in three cases and prior treatment wit

91 omib and lenalidomide and had adequate prior alkylator therapy were eligible.

92 tumors overexpress MGMT and are resistant to alkylator therapy.

93 Comparative studies involving related DNA alkylators, tomamycin and saframycin A, revealed inhibit

94 umor induction studies reveal that following alkylator treatment, but not IR, Nfkb1(-/-) mice develop

95 Ca2+ entry activated by either NO donors or alkylators was highly stimulated by Ca2+ pool depletion,

96 sensitivity to MeOSO2(CH2)2-lexitropsin, an alkylator which exclusively induces 3-meA lesions.

97 ich has been generally limited to lipophilic alkylators, which may not have efficacy against the tumo

98 Pluramycin is an intercalative guanine alkylator whose reactivity is increased by unwinding and

99 Laromustine is a sulfonylhdrazine alkylator with significant antileukemia activity.

100 ncluding one named PK11007, to be mild thiol alkylators with anticancer activity in several cell line

101 gents (r = -0.44) but not with resistance to alkylators with different mechanisms of action (r = -0.0