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1 usly the crosslinking of formal C-C pairs by mechlorethamine).
2 Q sensitizes E. coli to the nitrogen mustard mechlorethamine.
3 ks by nitrogen mustards, e.g., melphalan and mechlorethamine.
4  formal mismatch pairs can be crosslinked by mechlorethamine.
5 l comparing mechlorethamine, 0.02%, gel with mechlorethamine, 0.02%, compounded ointment.
6                           The use of a novel mechlorethamine, 0.02%, gel in the treatment of patients
7 bserver-blinded, multicenter trial comparing mechlorethamine, 0.02%, gel with mechlorethamine, 0.02%,
8 ma effects of romidepsin in combination with mechlorethamine, an alkylating agent, in cutaneous T-cel
9 vity yeast pso2Delta mutants display towards mechlorethamine, an ICL-inducing compound.
10  the C-C cross-link is pH dependent for both mechlorethamine and chlorambucil.
11                                              Mechlorethamine and melphalan are used as model systems
12    A detailed analysis of energy profiles of mechlorethamine and melphalan binding to guanine and ade
13 cross-linking by two nitrogen mustard drugs, mechlorethamine and melphalan.
14  the monofunctionally bound intermediates of mechlorethamine and phosphoramide mustard assumed thermo
15                                              Mechlorethamine and phosphoramide mustard induced intras
16 thylenemelamine, and short-lived response to mechlorethamine and prednisone.
17 thecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasm
18  involved in the repair of nitrogen mustard (mechlorethamine)- and cisplatin-induced DNA ICLs, but th
19 zine, and prednisone (MOPP) or procarbazine, mechlorethamine, and vinblastine (PAVe) in S studies; MO
20 ealed that curcumin inhibited camptothecin-, mechlorethamine-, and doxorubicin-induced apoptosis of M
21 he face of treatment with alkylating agents (mechlorethamine), anthracylines (doxorubicin), and micro
22                             For the mustards mechlorethamine, chlorambucil, and melphalan, both sites
23       Here, we report the formation of a new mechlorethamine cross-link with the d[GXC].d[GYC] fragme
24                                              Mechlorethamine cross-links this fragment preferentially
25 (10)-C(29) and C(13)-C(26), we show that two mechlorethamine crosslinks form between C(13) and C(29)
26 rgic contact dermatitis to topically applied mechlorethamine decreased with advancing stage of diseas
27                                Cisplatin and mechlorethamine, DNA crosslinking agents, caused dose- a
28 uced dose of bleomycin compared with VBM) or mechlorethamine, doxorubicin, vinblastine, vincristine,
29 in, vinblastine, and dacarbazine (ABVD) with mechlorethamine, doxorubicin, vincristine, bleomycin, vi
30 itor, SD-282, suppressed MKP-1 activation by mechlorethamine, enhanced active JNK levels, and increas
31 esponse analyses demonstrated superiority of mechlorethamine gel to ointment (P< .01).
32                           Response rates for mechlorethamine gel vs ointment were 58.5% vs 47.7% by t
33   Combination treatment with doxorubicin and mechlorethamine had similar effects, and the enhanced ef
34                    Nitrogen mustards such as mechlorethamine have previously been shown to covalently
35 ethyl-N'-nitro-N-nitrosoguanidine (MNNG) and mechlorethamine HCl (HN2), oxidizing agents, such as hyd
36 ically used nitrogen mustard antitumour drug mechlorethamine (HN2), were quantitated at the level of
37 e results support a role for romidepsin plus mechlorethamine in combination in the treatment of cutan
38 est that the C-C mismatch is cross-linked by mechlorethamine in the minor groove.
39 ated with triplet repeat expansion diseases, mechlorethamine may serve as a useful probe for these st
40              Compared to a nitrogen mustard (mechlorethamine, MCE) MEBAC produces higher DPC yields a
41  chemotherapeutic nitrogen mustards (namely, mechlorethamine, melphalan, and chlorambucil), at least
42 ed responses in 52% of patients treated with mechlorethamine (nitrogen mustard), vincristine, and pro
43 in the aprt gene was treated with melphalan, mechlorethamine or phosphoramide mustard.
44 on of a reactive intermediate in the case of mechlorethamine, our model predicts a significant prefer
45             Consistently, the combination of mechlorethamine plus romidepsin resulted in downregulati
46 sity of pretransplantation chemotherapy with mechlorethamine (relative risks [RRs] = 2.0 and 4.3 for
47 doxorubicin, cyclophosphamide, and etoposide/mechlorethamine, vincristine, procarbazine, and predniso
48 curs after frontline chemotherapy with MOPP (mechlorethamine, vincristine, procarbazine, and predniso
49       A randomized trial designed to compare mechlorethamine, vincristine, procarbazine, and predniso
50                     Primary chemotherapy was mechlorethamine, vincristine, procarbazine, and predniso
51 cin, vinblastine, and dacarbazine (ABVD) and mechlorethamine, vincristine, procarbazine, prednisone,
52                                              Mechlorethamine was applied once daily for up to 12 mont
53 rmation of corresponding aziridinium ion for mechlorethamine, while the formation of the aziridinium
54 A mycosis fungoides who had not used topical mechlorethamine within 2 years and were naive to prior u