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1 was observed after treatment with N-ethyl-N-nitrosourea.
2 mouse mutation that was induced by N-ethyl-N-nitrosourea.
3 n the mouse Nell1 gene, induced by N-ethyl-N-nitrosourea.
4 fonate, N-propyl-N-nitrosourea and N-butyl-N-nitrosourea.
5 gs temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea.
6 tment with the methylating agent, N-methyl-N-nitrosourea.
7 eous spectrum or that derived from N-ethyl,N-nitrosourea.
8 g agents such as cisplatin and bichloroethyl nitrosourea.
9 mbination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
10 mbination of BG and 1,3-bis(2-chloroethyl)-1-nitrosourea.
11 ea-type drugs, e.g. 1,3-bis(2-chloroethyl)-1-nitrosourea.
12 ation with 13 mg/m2 1,3-bis(2-chloroethyl)-1-nitrosourea.
13 r 2 x LD10 doses of 1,3-bis(2-chloroethyl)-1-nitrosourea.
14 reatment with the powerful mutagen N-ethyl-N-nitrosourea.
15 th the alkylator agent 1,3-bis-chloroethyl-1-nitrosourea.
16 had been treated with the mutagen N-ethyl-N-nitrosourea.
17 esirable toxicophores contained in antitumor nitrosoureas.
18 e or recurrent malignant glioma resistant to nitrosoureas.
19 astoma multiforme, and 11 had received prior nitrosoureas.
20 with the resistance of glioma cell lines to nitrosoureas.
21 lopment of drug resistance for the antitumor nitrosoureas.
22 and in the absence and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosour
23 onstrating a wider margin of safety than the nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)
25 h a strong DNA-alkylating mutagen, N-ethyl-N-nitrosourea, 55% of transgenic mice developed AML and th
26 hanced following administration of N-ethyl-N-nitrosourea, a carcinogen that induces DNA mutations.
27 the antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea, a chemotherapeutic used to combat various b
29 the GR inhibitor, 1,3 bis-(2 chloroethyl)-1-nitrosourea, abolished the inhibitory effect of flow.
31 motherapy [25 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea administered with a single i.p. injection] o
34 ious GR inhibitors, N,N-bis(2-chloroethyl)-N-nitrosourea, an anticancer drug with IC(50) = 647 microm
35 y rats were given an injection of 1-methyl-1-nitrosourea and fed purified diets ad libitum or at 60%
37 HeLa cells against 1,3-bis(2-chloroethyl)-1-nitrosourea and methyl methanesulfonate cytotoxicity eit
38 stogenic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C (MMC), as measured by cell k
40 tant to DN, were mutagenized using N-ethyl-N-nitrosourea and screened for mutants that developed exce
42 mice that were and were not given N-methyl-N-nitrosourea, and analyzed by histopathologic and molecul
43 nt to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to th
44 eated with the chemical carcinogen N-ethyl-N-nitrosourea, and continuously passaged to yield cell pop
45 ivity to methyl methanesulfonate, N-methyl-N-nitrosourea, and the chemotherapeutic drugs temozolomide
47 ing water with or without 240 ppm N-methyl-N-nitrosourea at 5 weeks of age and thereafter on alternat
49 primary end point was successfully met using nitrosourea-based (pre-TMZ) chemotherapy era historic co
53 onse to exposure to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) alone; however, 70-80% of cells were
54 1omega) of low-dose 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and a second group receiving two cycl
55 chemotherapy agents 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cis-diamminedichloroplatinum (cis
57 on of radiation and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) chemotherapy in three primary human g
58 ons of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU) increased intracellular GSSG and decr
59 titumor efficacy of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is being tested in clinical trials.
60 ional DNA alkylator 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is cytotoxic primarily by inducing DN
61 ens were used: vincristine, bis-chloro-ethyl nitrosourea (BCNU) melphalan, cyclophosphamide, and pred
62 exposure to either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or glutathione reductase-specific siR
64 chemotherapy using 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) resulted in similar increases in gene
65 to cell killing by 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) than overexpression of nucl-MGMT.
66 B/c model followed by N,N-bis(2-chloroethyl)-nitrosourea (BCNU) treatment to enhance donor-cell engra
67 -linking reaction of N,N'-bis(2-chloroethyl)-nitrosourea (BCNU) were investigated using synthetic oli
68 nSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) would lead to an increased level of i
69 of temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and no further sensitization occurs
70 oreductase enzymes (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), arsenite, and phenylarsine oxide) su
71 mise its integrity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) and UV rays) enh
72 In combination with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the prodrugs were not effective adju
73 e of 35 mg/m(2) of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), which was otherwise ineffective as a
74 , a time interval in which bis(2-chloroethyl)nitrosourea (BCNU)-induced chloroethyl adducts are fully
79 an, and carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)] weakly induced luciferase activity i
80 of antitumor agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine) into biodegradable polyme
81 such as carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], lomustine [1-(2-chloroethyl)-3-cyclo
83 mulation of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), an effective agent used in the treat
84 lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU], and streptozotocin, to yield consist
88 ized the tumors to N,N'-bis(2-chloroethyl)-N-nitrosourea chemotherapy, as measured by reduced biolumi
89 ng chemotherapeutic drugs as 2-chloroethyl-N-nitrosourea (CNU) derivatives is countered by the repair
91 e development of CDH comes from an N-ethyl-N-nitrosourea -derived mouse strain, eyes2, which has a ho
92 MT inhibitor O(6)-benzylguanine (O(6)BG) and nitrosourea drugs such as carmustine and methylating age
95 ing a forward genomics approach by N-ethyl-N-nitrosourea (ENU) germline mutagenesis in mice, we ident
96 e mutations with the point mutagen N-ethyl-N-nitrosourea (ENU) is a key strategy for analysing the hu
97 ntional germ-cell mutagenesis with N-ethyl-N-nitrosourea (ENU) is compromised by an inability to moni
98 generated by the chemical mutagen n-ethyl-n-nitrosourea (ENU) mapped a new mutant locus (5772SB) ter
100 Cdh23(nmf308/nmf308) mice produced by the N-nitrosourea (ENU) mutagenesis program were used as an an
101 de, phenotype-driven, large-scale N-ethyl-N--nitrosourea (ENU) mutagenesis screen for dominant mutati
103 humans and mice, we established an N-ethyl-N-nitrosourea (ENU) mutagenesis screen to identify modifie
108 vention, we carried out a dominant N-ethyl-N-nitrosourea (ENU) mutagenesis suppressor screen in Mecp2
110 phthalmoscopy identified a line of N-ethyl-N-nitrosourea (ENU) mutagenized mice demonstrating retinal
111 or the production of mice carrying N-ethyl-N-nitrosourea (ENU) mutations and their screening for audi
112 Point mutations induced by N -ethyl- N -nitrosourea (ENU) provide a unique mutant resource becau
113 arrow with the chemical carcinogen N-ethyl-N-nitrosourea (ENU) resulted in significantly accelerated
114 by five, independent mutations in N-ethyl-N-nitrosourea (ENU) saturation mutagenesis experiments wit
115 a second-generation (G2) dominant N-ethyl-N-nitrosourea (ENU) screen especially designed to detect s
116 ance has been used to sensitize an N-ethyl-N-nitrosourea (ENU) screen to identify novel mutations res
117 nctional IkappaBNS derived from an N-ethyl-N-nitrosourea (ENU) screen, named bumble, to investigate t
118 le to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes that regulate t-AML
120 pase-9, caspase-3, and bax mutants) to ethyl-nitrosourea (ENU), a known DNA mutagen and neural carcin
121 tagen of choice for mouse has been N-ethyl-N-nitrosourea (ENU), an alkylating agent that mainly cause
122 mice to benzo[a]pyrene (B[a]P) or N-ethyl-N-nitrosourea (ENU), daily for 28 consecutive days, and qu
123 to sublethal gamma-irradiation or N-ethyl-N-nitrosourea (ENU), MLL-CBP mice developed myelomonocytic
124 e mutations induced by the mutagen N-ethyl-N-nitrosourea (ENU), numerous animals died under specific
125 of mice with the alkylating agent, N-ethyl-N-nitrosourea (ENU), regardless of the levels of expressio
126 with a potent DNA alkylating agent, N-ethyl-nitrosourea (ENU), to induce secondary cooperating mutat
127 agenized with the germline mutagen N-ethyl-N-nitrosourea (ENU), we identified a recessive mutation co
128 nse b (pob), was isolated using an N-ethyl N-nitrosourea (ENU)-based screening strategy designed to i
131 flatoxin B1 (AFB1)-induced, 14% of N-ethyl-N-nitrosourea (ENU)-induced and 12% of spontaneous lung ad
133 e developed protocols for creating N-ethyl-N-nitrosourea (ENU)-induced germline mutations in several
135 describe the effects of seven new N-ethyl-N-nitrosourea (ENU)-induced Kitl(Sl) mutations and two pre
137 he identification of a hyperactive N-ethyl-N-nitrosourea (ENU)-induced mouse mutant with abnormalitie
147 ains and used the panel to map two N-ethyl-N-nitrosourea (ENU)-induced mutations responsible for visi
150 s and is mutationally activated in N-ethyl-N-nitrosourea (ENU)-induced rodent tumors of the Schwann c
151 resonance imaging (MRI)-localized N-ethyl-N-nitrosourea (ENU)-induced tumors in rat brains with thos
159 chain alkylating agents including N-ethyl-N-nitrosourea, ethyl methanesulfonate, N-propyl-N-nitrosou
160 wide allelotyping of early passage N-ethyl-N-nitrosourea-exposed cell populations revealed aberration
161 is end, we identified two separate N-ethyl-N-nitrosourea-generated mouse lines that harbor either a p
162 e procarbazine, nitrogen mustard, melphalan, nitrosoureas (> or = 2 cycles of any of these drugs) or
163 mers containing 10% 1,3-bis(2-chloroethyl)-1-nitrosourea had significantly improved survival compared
164 the random germ line mutagen ENU (N-ethyl-N-nitrosourea), have disclosed key molecules in the TLR si
165 factors do not predict benefit from adjuvant nitrosourea in malignant gliomas, and long-term survival
169 nsferase (AGT), that enhances sensitivity to nitrosoureas in tumor-cell lines and tumor-bearing anima
170 tathione reductase (1,3-bis(2-chloroethyl)-1-nitrosourea) in the presence or absence of FBP (3.5 mM).
171 ry effective in the prevention of N-methyl-N-nitrosourea induced mammary cancers in rats without sign
174 n timing in vivo, we exploited the N-ethyl-N-nitrosourea-induced afterhours mutant Fbxl3(Afh) to stab
176 ele of the insulin receptor and an N-ethyl-N-nitrosourea-induced alternative splice mutation in the r
177 t of breast cancer using the rat N-methyl-N'-nitrosourea-induced and spontaneous HER-2/neu transgenic
179 As a consequence of a recessive N-ethyl-N-nitrosourea-induced germline mutation in the P-loop of G
181 ions in Herc2 in three independent N-ethyl-N-nitrosourea-induced jdf2 mutant alleles, each leading to
183 x(+/-) mice develop significantly more ethyl nitrosourea-induced lung tumors and lymphomas in compari
185 eriments were conducted using the 1-methyl-1-nitrosourea-induced mammary cancer model in which rats w
186 s (IC50 = 3.2 microM) and reduced N-methyl-N-nitrosourea-induced mammary tumorigenesis when administe
187 ficantly reduced the incidence of N-methyl-N-nitrosourea-induced mammary tumors in our animal model s
188 p.o. administered resveratrol on N-methyl-N-nitrosourea-induced mammary tumors was studied in female
190 ive phenotype that results from an N-ethyl-N-nitrosourea-induced missense mutation in the Tlr9 gene (
191 he cleft secondary palate 1 (csp1) N-ethyl-N-nitrosourea-induced mouse model of non-syndromic cleft p
192 s, Dnah11 and Mks1, in independent N-ethyl-N-nitrosourea-induced mouse mutant lines with heritable re
193 ants, we identified ostes, a novel N-ethyl N-nitrosourea-induced mouse mutant with muscle atrophy.
195 ficiency anemia, as revealed by an N-ethyl-N-nitrosourea-induced mouse phenotype called sublytic.
196 o22 is a mutant mouse produced via N-ethyl-N-nitrosourea-induced mutagenesis that shows sterility wit
202 ified 'triple D' (3d), a recessive N-ethyl-N-nitrosourea-induced mutation and phenotype in which no s
204 ection was revealed by a recessive N-ethyl-N-nitrosourea-induced mutation called warmflash (wmfl).
205 d p27(-/-) mice displayed a higher N-ethyl-N-nitrosourea-induced mutation frequency in the colon than
209 ) resulting from three independent N-ethyl-N-nitrosourea-induced mutations in host cell factor C2 (Hc
211 od for real-time identification of N-ethyl-N-nitrosourea-induced mutations that cause phenotypes in m
212 out a genome-wide screen for novel N-ethyl-N-nitrosourea-induced mutations that give rise to eye and
213 Eleven independent, recessive, N-ethyl-N-nitrosourea-induced mutations that map to a approximatel
218 vel zebrafish gata1 mutant with an N-ethyl-N-nitrosourea-induced point mutation in the C-finger (gata
221 ncidence and decreased latency of N-methyl-N-nitrosourea-induced thymic lymphoma compared to wild-typ
223 Primary mouse hepatocytes harboring an ethyl-nitrosourea-induced, ER-retained mutant LDLR secreted co
224 Failure of pancreatic tumors to respond to nitrosoureas is related to high levels of MGMT expressio
225 malignant gliomas within the brain, and that nitrosoureas may have therapeutic benefits in addition t
226 wed by a single i.v. injection of N-methyl-N-nitrosourea (MNU) and chronic androgen stimulation.
228 ed either by exposure to carcinogens (methyl-nitrosourea (MNU) and urethane) or by genetic activation
230 a) a single i.v. dose of 50 mg of N-methyl-N-nitrosourea (MNU) per kg body weight, followed by chroni
232 In addition, after exposure to N-methyl-N-nitrosourea (MNU), the latency of mammary tumor developm
233 edominant sites of methylation by N-methyl-N-nitrosourea (MNU), which is used to produce a variety of
234 methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU), while expression of R137Q in pol beta
239 )-containing oligonucleotides and N-methyl-N-nitrosourea (MNU)-treated DNA templates by the 3' --> 5'
247 lved in hematopoiesis, we performed an ethyl-nitrosourea mutagenesis screen in zebrafish (Danio rerio
249 rward genetic screen in mice using N-ethyl-N-nitrosourea mutagenesis to identify genetic mutations th
251 ant mouse line 20884, generated by N-ethyl-N-nitrosourea mutagenesis, which is characterized by adult
253 Forward genetic screens with ENU (N-ethyl-N-nitrosourea) mutagenesis can facilitate gene discovery,
254 nother coronin 1A mutant during an N-ethyl-N-nitrosourea-mutagenesis screen for T cell-lymphopenic mi
255 mice obtained from the breeding of N-ethyl-N-nitrosourea mutagenized mice were formalin-fixed and sta
257 igh frequency ultrasound to screen N-ethyl-N-nitrosourea mutagenized mouse fetuses for congenital car
260 germline mutant mice derived from N-ethyl-N-nitrosourea-mutagenized grandsires for intestinal homeos
262 Here we identify, from a screen of N-ethyl-N-nitrosourea-mutagenized mice, a mutation causing both pr
266 ) was detected in third-generation N-ethyl-N-nitrosourea-mutated mice that showed defective responses
268 ffects of the methylating agents, N-methyl-N-nitrosourea, N-methyl-N'nitro-N-nitrosoguanidine and met
269 (Cisplatin, Nitrogen Mustard and N-methyl-N-nitrosourea (NMNU/MNU)) within mice either singly or dou
271 n, and invasion and determine the effects of nitrosoureas on these cell movement-related processes.
273 ls with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-N-nitrosoguanidine resu
274 reductase (GR) with 1,3-bis[2-chloroethyl]-1-nitrosourea or transfection of macrophages with small in
278 ltransferase (AGT), has been shown to reduce nitrosourea resistance and, thus, enhance the efficacy o
279 producing tumor regression in patients with nitrosourea-resistant malignant glioma, although stable
281 Treatment of the DNA template with N-ethyl-N-nitrosourea resulted in a dose-dependent inhibition of D
282 /scid mice with gamma radiation or N-ethyl-N-nitrosourea resulted in approximately 86% incidence of T
284 se excision from DNA exposed to [3H]methyl-N-nitrosourea showed that the purified Nth1 enzyme did not
285 eased cellular resistance to 2-chloroethyl-N-nitrosourea suggests a therapeutic significance for PKC-
286 mutagenesis in C57BL/6J mice using N-ethyl-N-nitrosourea to identify mutations causing high blood glu
290 ing in first-generation progeny of N-ethyl-N-nitrosourea-treated mice, involving 23 essential immune
291 ATP:Pi ratios after 1,3-bis(2-chloroethyl)-1-nitrosourea treatment indicate improved bioenergetic sta
292 uanine induced by chemotherapeutic N-alkyl N-nitrosourea-type drugs, e.g. 1,3-bis(2-chloroethyl)-1-ni
296 cell resistance to 1,3-bis(2-chloroethyl)-1-nitrosourea, we performed a novel dose escalation clinic
297 is more potent than N,N-bis(2-chloroethyl)-N-nitrosourea, which is currently the most commonly employ
299 otoxic effects of alkylating agents, such as nitrosoureas, which play a central role in the treatment
300 cells to killing by 1,3-bis(2-chloroethyl)-1-nitrosourea, with O6-benzyl-3'-O-(gamma-folyl)-2'-deoxyg
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