ライフサイエンスコーパス: mitomycin C

1 le ethanol), and an uncompetitive inhibitor (Mitomycin C).

2 d a well-known cell proliferation inhibitor (mitomycin-C).

3 rase inhibition, but not DNA crosslinking by mitomycin C.

4 HDAC10 resulted in increased sensitivity to mitomycin C.

5 no influence on sensitivity to cisplatin or mitomycin C.

6 titutively during growth and were induced by mitomycin C.

7 are hypersensitive to the DNA-damaging agent mitomycin C.

8 ypersensitive to the DNA cross-linking agent mitomycin C.

9 following treatment with the genotoxic drug mitomycin C.

10 ion for the production of the clinical agent mitomycin C.

11 and chemicals such as hydrogen peroxide and mitomycin C.

12 ed DPPIV- rats that had been pretreated with mitomycin C.

13 ce were exposed to five once weekly doses of mitomycin C.

14 ccumulation of a new mitomycin analog, 9-epi-mitomycin C.

15 kinase substrate required for resistance to mitomycin C.

16 levels of resistance to the DNA cross-linker mitomycin C.

17 and had an impaired ability to protect from mitomycin C.

18 ar resistance to the DNA cross-linking agent mitomycin C.

19 susceptibility, and cellular sensitivity to mitomycin C.

20 ed PRDX3 expression increases sensitivity to mitomycin C.

21 is synergistic with damage caused by UV and mitomycin C.

22 n challenge with the DNA cross-linking agent mitomycin C.

23 phages was induced with hydrogen peroxide or mitomycin C.

24 by the chemotherapeutic agents etoposide and mitomycin C.

25 treatment with doxorubicin or 5-fluorouracil/mitomycin C.

26 ity to cisplatin and oxaliplatin, but not to mitomycin C.

27 nsitivity to DNA crosslinking agents such as mitomycin C.

28 vity to platinum and oxaliplatin, but not to mitomycin C.

29 and Nbs1 in response to gamma-irradiation or mitomycin C.

30 to interstrand crosslinking agents, such as mitomycin C.

31 nticancer agents cisplatin, oxaliplatin, and mitomycin C.

32 umor necrosis factor alpha/cycloheximide and mitomycin C.

33 imetic chemicals methyl methanesulfonate and mitomycin C.

34 age after treatment with the genotoxic agent mitomycin C.

35 action against noncancer prostate cells over mitomycin C.

36 alternative host and could not be induced by mitomycin C.

37 tion, and dose and duration of treatment for mitomycin C.

38 and cellular sensitivity to the crosslinker mitomycin C.

39 highly sensitive to the cross-linking agent mitomycin C.

40 non-penetrating glaucoma surgery (NPGS) with mitomycin-C.

41 Mitomycin C 0.02% was used after the PRK to prevent haze

42 In order to lower IOP, trabeculectomy with mitomycin C (0.2 mg/cc) was performed under general anes

43 ldt glaucoma implant) or trabeculectomy with mitomycin C (0.4 mg/ml for 2 minutes).

44 ant) and 105 patients to trabeculectomy with mitomycin C (0.4 mg/mL for 4 minutes).

45 Hg [95% CI, -3.90 to -1.39]; TE and DS with mitomycin C: -0.83 mm Hg [95% CI, -2.40 to 0.74]).

46 The clinical success of mitomycin C (1) and its associated toxicities and resist

47 omparator-vinorelbine (30 mg/m(2) weekly) or mitomycin C (10 mg/m(2) day 1 and every 28 days) plus vi

48 ions 1 to 5 and 16 to 20 of radiotherapy and mitomycin C (12 mg per square meter) on day 1.

49 e in the reduction in IOP (TE and DS without mitomycin C: -2.65 mm Hg [95% CI, -3.90 to -1.39]; TE an

50 primary medical treatments for OSSN include mitomycin C, 5-fluorouracil, and interferon alpha2b.

51 nts who underwent trabeculectomy (Trab) with mitomycin-C (74 eyes of 64 patients) with >/=4 reliable

52 road range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topo

53 upon FtsZ depletion and exposure of cells to mitomycin C, a DNA damaging agent, which interferes with

54 y and chromosomal breakage when treated with mitomycin C, a DNA interstrand crosslinker.

55 ent of a wild-type P. aeruginosa strain with mitomycin C, a DNA-damaging agent, resulted in the inhib

56 ylation site mutations are hypersensitive to mitomycin C, a genotoxic agent that induces interstrand

57 sitivity and short incubation times (1 ng/mL mitomycin C after 90 min).

58 mycin C analogue which is twice as potent as mitomycin C against the prostate cancer cells.

59 red with conjunctival or limbal autograft or mitomycin C alone.

60 to be much more sensitive than its parent to mitomycin C, an agent predominantly causing DNA double-s

61 l synthesis and rapid discovery of MTSB-6, a mitomycin C analogue which is twice as potent as mitomyc

62 rently being investigated as alternatives to mitomycin C and 5-fluorouracil to reduce inflammation an

63 ckout cells display increased sensitivity to mitomycin C and a delay in FANCD2 foci formation compare

64 wering, stem fasciation, hypersensitivity to mitomycin C and amino acid analogs, hyposensitivity to t

65 onic exposure to genotoxic molecules such as mitomycin C and antibiotics of the fluoroquinolone famil

66 ponse to DNA damage caused by diepoxybutane, mitomycin C and bleomycin.

67 Depletion of SLX4 causes sensitivity to mitomycin C and camptothecin and reduces the efficiency

68 s induced by chemotherapeutic agents such as mitomycin C and cisplatin.

69 the presence of DNA-damaging agents, such as mitomycin C and cisplatin.

70 mong other adjuvants, there is evidence that mitomycin C and conjunctival or limbal autografts reduce

71 e levels induced by two DNA-damaging agents, mitomycin C and daunorubicin, and two apoptosis-inducing

72 )-guanines, similar to cross-links formed by mitomycin C and enals.

73 by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308

74 ned their characteristic hypersensitivity to mitomycin C and exhibited high levels of chromosomal ins

75 my groups were treated intraoperatively with mitomycin C and followed postoperatively for 2 years.

76 , cancer predisposition, hypersensitivity to mitomycin C and gamma-irradiation, shortened telomeres,

77 Although both mitomycin C and ionizing radiation induced FANCD2 monoub

78 ity upon exposure to the DNA-damaging agents mitomycin C and Irofulven, but not etoposide and camptot

79 but they are not sensitive to treatment with mitomycin C and methyl methanesulfonate.

80 ersensitivity to the DNA-cross-linking agent mitomycin C and moderately increased sensitivity to ioni

81 ients treated with concurrent 5-fluorouracil/mitomycin C and radiotherapy.

82 ere hypersensitive to the crosslinking agent mitomycin C and some to cis-platin, as measured by cell

83 y to the DNA interstrand cross-linking agent mitomycin C and the topoisomerase-1 inhibitor camptothec

84 t monoubiquitination of PCNA is required for Mitomycin C and Ultraviolet Light inducible SNM1A nuclea

85 tes exhibit RecA-dependent induction by both mitomycin C and UV radiation.

86 heir pretreatment with low concentrations of mitomycin C and vincristine, suggesting that these agent

87 cytotoxic effects of the DNA-damaging agents mitomycin C and Vp-16.

88 t, intraoperative mitomycin C, postoperative mitomycin C, and amniotic membrane transplantation for p

89 llowed by combined-modality therapy with FU, mitomycin C, and concurrent radiation results in long-te

90 persensitivity to the DNA crosslinking agent mitomycin C, and karyotypes feature genomic instability.

91 ticancer DNA crosslinking agents (cisplatin, mitomycin C, and melphalan).

92 We revealed that paclitaxel, doxorubicin, mitomycin C, and methotrexate up-regulated the ability o

93 d chemotherapeutic agents: cyclophosphamide, mitomycin C, and procarbazine.

94 he known DNA interstrand cross-linking agent mitomycin C, and the importance of the gene PSO2 known t

95 ficient tumors were shown to be sensitive to mitomycin C, and the mechanism was presumed to be a defe

96 sensitivity to the DNA cross-linking reagent mitomycin C, and this phenotype can be rescued by comple

97 y autologous serum, steroids, ascorbic acid, mitomycin-c, and NSAIDS.

98 Mitomycin C appears to improve the success rates of EN-D

99 rrence rates of pterygium after surgery with mitomycin C application between the CAU and CLAU groups,

100 c conjunctival resection followed by topical mitomycin C application.

101 dications, techniques, and current trends of mitomycin-C application in corneal refractive surgery.

102 n and its derivatives, nitrogen mustards and mitomycin C, are used widely in cancer chemotherapy.

103 affects tolerance to the DNA-damaging agent mitomycin C, argue that this prototypic eukaryotic membe

104 Electromotive intravesical mitomycin C as well as local microwave hyperthermia have

105 omy achieved comparable surgical outcomes to mitomycin C-augmented combined trabeculotomy-trabeculect

106 ommenced and he underwent a successful right Mitomycin C-augmented trabeculectomy.

107 ly 4-nitro-o-phenylenediamine, sodium azide, mitomycin C, benzo[a]pyrene, aflatoxin B1 and 2-aminoflu

108 cytotoxic antimetabolites, 5-flurouracil and mitomycin C both prolong success but with the increased

109 s have sensitivity to the ICL-inducing agent mitomycin C but do not exhibit chromosome breakage or ce

110 lular resistance to a DNA-crosslinking drug, mitomycin C, but not for the monoubiquitination of FANCD

111 ing the C-terminal bromodomain to X-rays and mitomycin C, but not to other forms of abiotic stress, e

112 These cells were hypersensitive to mitomycin C, but unlike cells defective in other core co

113 Smoothing agents and intraoperative mitomycin C can be helpful for certain disorders.

114 tivation of mitomycin C with implications in mitomycin C chemotherapy.

115 terial chemoperfusion was performed by using mitomycin C, cisplatin, and gemcitabine.

116 he exposure of cells to UV irradiation or to mitomycin C, cisplatin, camptothecin, or etoposide, with

117 nchronous chemotherapy with fluorouracil and mitomycin C combined with radiotherapy significantly imp

118 DNA cross-linking by mitomycin C delayed segregation, and the accumulation of

119 Inhibition of cell proliferation by mitomycin C did not affect the enhancing effect of IL-2

120 3B, and Mahlavu)-to ultraviolet irradiation, mitomycin C, doxorubicin, cisplatin, sorafenib, and lapa

121 ral other anticancer agents (5-fluorouracil, mitomycin C, doxorubicin, colchicine, vinorelbine, and p

122 common use of antineoplastic agents such as mitomycin C, doxorubicin, or oxaliplatin with hypertherm

123 Intraoperative adjunction of mitomycin C during fornix reconstruction with amniotic m

124 Use of conjunctival or limbal autografts or mitomycin C during or after pterygium excision reduced r

125 Mitomycin C enhanced transport of Cx43 from the endoplas

126 s in response to either gamma-irradiation or mitomycin C exposure, two DNA-damaging agents.

127 fected in pol kappa-depleted cells following mitomycin C exposure.

128 ibrovascular tissue and application of 0.02% mitomycin C for 3 minutes.

129 PRK enhancement with adjunctive use of Mitomycin C for the correction of residual error of refr

130 temperate phage, PhiHAP-1, was induced with mitomycin C from a Halomonas aquamarina strain isolated

131 ion of conjunctival or limbal autograft with mitomycin C further reduces the recurrence rate after pt

132 eater than additive fashion with doxorubicin/mitomycin C/gemcitabine/cisplatin/paclitaxel to cause ce

133 anesulfonate (generating alkylation damage), mitomycin C (generating interstrand cross-links), or pot

134 eculotomy with trabeculectomy augmented with mitomycin C (Group II).

135 Mitomycin C has been shown in studies to be highly effec

136 early experience with the adjunctive use of mitomycin C has demonstrated good results.

137 he constant evolution of refractive surgery, mitomycin-C has come to the forefront as a modulator of

138 the mutant strains to UV irradiation and to mitomycin C highlighted the importance of the targeted g

139 ty of stresses including the genotoxic agent mitomycin C, hydrogen peroxide and at least four differe

140 arious dose levels of three model toxicants, mitomycin C, hydrogen peroxide, and lead nitrate, the an

141 levels of methylnitrosourea, diepoxybutane, mitomycin C, hydroxyurea, doxorubicin, and UV light stim

142 PIP-box mutant protein fails to correct the mitomycin C hypersensitivity of FA-D2 patient cells.

143 mutant FANCE protein fails to complement the mitomycin C hypersensitivity of the transfected cells.

144 ants were capable of fully complementing the mitomycin-C hypersensitivity phenotype of FA-C cells but

145 aled continued production of mitomycin A and mitomycin C in addition to the accumulation of a new mit

146 3 nm solid-state laser (SSL) with adjunctive Mitomycin C in eyes previously treated with laser assist

147 ecreased cellular survival after exposure to mitomycin C in normal fibroblasts depleted for Tip60 ind

148 hough their cells showed mild sensitivity to mitomycin C in terms of cell survival and G(2) phase arr

149 were similar to outcomes for intraoperative mitomycin C in the few studies that directly compared th

150 e differences between the platinum drugs and mitomycin C in the spectrum of required translesional po

151 ifibrotic agents, namely, 5-fluorouracil and mitomycin C, in conjunction with glaucoma surgery has re

152 t of V. cholerae with the SOS-inducing agent mitomycin C increased the level of ctxA mRNA approximate

153 that RAD51 foci are induced by cisplatin or mitomycin C independently of ERCC1, but that mitomycin C

154 inhibitory concentration of ciprofloxacin or mitomycin C induced sbcDC transcription but repressed th

155 O1(-/-) mice showed a complete resistance to mitomycin C-induced bone marrow cytotoxicity and reducti

156 (+/-) mice also showed limited resistance to mitomycin C-induced bone marrow cytotoxicity.

157 ciated with protection against cisplatin and mitomycin C-induced chromosomal aberrations, and both ar

158 Furthermore, mitomycin C-induced DNA double-strand breaks (DSBs) are

159 amage, we analyzed gene expression following mitomycin C-induced genotoxic stress in human E6-express

160 mitomycin C independently of ERCC1, but that mitomycin C-induced HR measured in a reporter construct

161 Here, we report that mitomycin C-induced lesions inhibit replication fork elo

162 frequencies of spontaneous and radiation- or mitomycin C-induced micronucleated erythrocytes, indicat

163 Mitomycin C induces both MC-mono-dG and cross-linked dG-

164 , p21(-/-) cells exhibit increased levels of mitomycin C-inducible complex chromosomal aberrations an

165 VSH-1 is a mitomycin C-inducible prophage of the anaerobic spiroche

166 lysogeny proxy determined using DNA-damaging mitomycin C inductions.

167 Subconjunctival mitomycin C injection may cause limbal stem cell deficie

168 , smoother stromal beds, and introduction of mitomycin-C intraoperatively have all improved safety ou

169 inct but related to the double alkylation by mitomycin C, involving a novel electrophilic spiro-cyclo

170 (VO; 26 patients), and irinotecan/cisplatin/mitomycin C (IPM; 49 patients).

171 Mitomycin C is a natural product with potent alkylating

172 n and duration of exposure to intraoperative mitomycin C is associated with increased efficacy.

173 of trabeculectomy in this population suggest mitomycin C is associated with increased risk of late in

174 Mitomycin-C is an antimetabolite that has seen increased

175 with antifibrotic agents (5-fluorouracil or mitomycin C) is still the next step in intraocular press

176 One member of this family, mitomycin C, is in clinical use as part of combination t

177 The cancer chemotherapeutic agent mitomycin C (MC) alkylates and cross-links DNA monofunct

178 rdless of the oxygenation state of the cell, mitomycin C (MC) cytotoxicity was enhanced in cells with

179 sure on human liver microsomal metabolism of mitomycin C (MC) in the presence of glutathione (GSH) an

180 Survival after treatment with UV, mitomycin C (MC) or methyl methanesulfonate (MMS), as we

181 on the activity of the antineoplastic agent mitomycin C (MC) under aerobic and hypoxic conditions we

182 Activation of p53 by the DNA damaging agent mitomycin C (MC) was accompanied by a potent repression

183 ptrB is specifically repressed by PrtR, and mitomycin C-mediated suppression of the TTSS is also abo

184 null MEFs were also moderately sensitive to mitomycin C, methyl methanesulfonate, and UV and gamma-r

185 ted with either ethylmethanesulfonate (EMS), mitomycin C, mitoxantrone or doxorubicin, at therapeutic

186 isplatin, 50 mg of doxorubicin, and 10 mg of mitomycin C mixed 1:1 with iodized oil.

187 ldt glaucoma implant) or trabeculectomy with mitomycin C (MMC 0.4 mg/mL for 4 minutes).

188 , reduced engraftment potential of HSPC, and Mitomycin C (MMC) -sensitive hematopoiesis), were absent

189 ion stress, including the crosslinking agent mitomycin C (MMC) and the replication inhibitor hydroxyu

190 Ten eyes received mitomycin C (MMC) and triamcinolone.

191 or indirectly with the DNA-damaging reagents mitomycin C (MMC) and UV irradiation.

192 Experience with mitomycin C (MMC) application during corneal surface abl

193 han control cells to DNA cross-linking agent mitomycin C (MMC) but were not hypersensitive to UV irra

194 show that the FDA-approved anti-cancer drug mitomycin C (MMC) eradicates persister cells through a g

195 he FA-characteristic growth inhibition after mitomycin C (MMC) exposure.

196 al setting who underwent trabeculectomy with mitomycin C (MMC) for uncontrolled elevated intraocular

197 Antifibrotics were used in 400 cases (93%): mitomycin C (MMC) in 271 (63%), 5-fluorouracil (5-FU) in

198 of tube-shunt surgery to trabeculectomy with mitomycin C (MMC) in eyes with previous cataract and/or

199 Mitomycin C (MMC) is a commonly used and extensively stu

200 Trabeculectomy with mitomycin C (MMC) is a major treatment option, although

201 Mitomycin C (MMC) led to decreased BRCA2 protein levels

202 y camptothecin (CAMPT), etoposide (ETOP), or mitomycin C (MMC) led to the formation of nuclear foci c

203 in one eye followed by treatment with either mitomycin C (MMC) or vehicle.

204 omal breakage assays, all control cells were mitomycin C (MMC) resistant, but eight samples (five of

205 Only FANCD2-44 corrected the mitomycin C (MMC) sensitivity of the transfected cells.

206 ion of Blm in Rad54(-/-) cells rescued their mitomycin C (MMC) sensitivity, and decreased both the le

207 e in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of

208 reased sensitivity to the DNA damaging agent mitomycin C (MMC) that correlates with delayed repair of

209 es a rapid liver repopulation protocol using mitomycin C (MMC) to block proliferation of rat hepatocy

210 mologists rely on accurate concentrations of mitomycin C (MMC) to prevent scarring with trabeculectom

211 interno gelatin microstent implantation with mitomycin C (MMC) versus trabeculectomy with MMC.

212 that combining use of the chemotherapy agent mitomycin C (MMC) with G207 will selectively up-regulate

213 in greatly increased cellular sensitivity to mitomycin C (MMC), and in increased levels of spontaneou

214 exposure to a bifunctional alkylating agent, mitomycin C (MMC), and that the progeny of exposed cells

215 n human cells results in hypersensitivity to mitomycin C (MMC), but not to IR.

216 oxins including another cross-linking agent, mitomycin C (MMC), indicating a potential role for TREX2

217 tant, sensitizes cells to IFNgamma/TNFalpha, mitomycin C (MMC), or serum deprivation in association w

218 mosomes in response to the DNA cross-linker, mitomycin C (MMC), thus mimicking the chromosome instabi

219 uivocal sensitivity to crosslinkers, such as mitomycin C (MMC), we find that they are largely resista

220 hocytes displayed higher levels of basal and mitomycin C (MMC)-induced chromosomal abnormalities.

221 ed DNA damage, but is deficient in repair of mitomycin C (MMC)-induced DNA damage.

222 Moreover, repair of mitomycin C (MMC)-induced DSBs and sister chromatid exch

223 e DNA interstrand crosslinks (ICLs), such as mitomycin C (MMC).

224 s in response to the DNA cross-linking agent mitomycin C (MMC).

225 , or the DNA interstrand cross-linking agent mitomycin C (MMC).

226 DNA interstrand cross-linking agents such as mitomycin C (MMC).

227 sitivity to DNA cross-linking agents such as mitomycin C (MMC).

228 atectomy (PRK) procedure with application of mitomycin C (MMC).

229 e radial formation by the ICL-inducing agent mitomycin C (MMC).

230 ing salinity and the DNA cross-linking agent mitomycin C (MMC).

231 ssociated with European-derived race; use of mitomycin C (MMC); higher concentrations of MMC, when us

232 RECQL5, but not BLM, conferred resistance to mitomycin C (MMC, an interstrand crosslinker) and campto

233 Mitomycin-C (MMC) and balanced saline solution (BSS) tre

234 e allocated to receive either intraoperative mitomycin-C (MMC) at a concentration of 0.2 mg/mL or pos

235 gen implant (OLO) versus trabeculectomy plus mitomycin-C (MMC) show contradictory results.

236 s and outcomes of 7 cases of PVOD induced by mitomycin-C (MMC) therapy from the French Pulmonary Hype

237 phacoemulsification and trabeculectomy with mitomycin-C (MMC) vs. Collagen Matrix (CM).

238 (3) Exogenous CTGF was injected into mitomycin-C (MMC)-treated filtering blebs and the scarin

239 ldt glaucoma implant) or trabeculectomy with mitomycin C ([MMC]; 0.4 mg/mL for 4 minutes).

240 the re-evaluation of the action mechanism of Mitomycin C (MtoC), a widely used antitumor chemotherape

241 Unlike mitomycin-C, neither CCG-222740 nor CCG-203971 caused an

242 through replication run off, as we show that mitomycin C or cisplatin-induced DNA lesions are not inc

243 with RAD51 in foci following treatment with mitomycin C or hydroxyurea, and colocalized very tightly

244 Cultured bovine CE cells were exposed to mitomycin C or other DNA-damaging agents.

245 Exposure of cells to mitomycin C or UV irradiation, but not ionizing radiatio

246 minimal effect on survival after exposure to mitomycin C or UV irradiation.

247 sed abdomen technique employed cisplatin and mitomycin-C or cisplatin and doxorubicin.

248 t genes that responded to hydrogen peroxide, mitomycin C, or phage induction were also identified.

249 ms of DNA damage, like exposure to UV light, mitomycin C, or phleomycin, also stimulate Tn7 transposi

250 eatment with DNA-damaging anticancer agents (mitomycin C, oxaliplatin, cisplatin, carboplatin, and a

251 unctival or limbal autograft, intraoperative mitomycin C, postoperative mitomycin C, and amniotic mem

252 Neither doxorubicin nor mitomycin C potentiated the cytotoxic effects of ischemi

253 Following mitomycin C pretreatment, the stent was placed ab intern

254 tivity, and partially impairs restoration of mitomycin C resistance.

255 Treatment with the DNA cross-linker mitomycin C results in a diffusion of foci and increased

256 the management of various corneal disorders, mitomycin-C seems to be a viable tool in the management

257 Furthermore, we identify that mitomycin C selectively triggers apoptosis in NSCs with

258 Mitomycin C-sensitive clones from a transposon mutagenes

259 ough damage-induced RAD51 foci formation and mitomycin C sensitivity appeared normal in MRG15-binding

260 efects, proliferation capacity reduction and mitomycin C sensitivity equivalent to those produced by

261 Moreover, in human cells exposed to mitomycin C, short interfering RNA-mediated knock-down o

262 epair or prevention of double strand breaks, mitomycin C significantly induces the specific expressio

263 ination and the response of rad23b plants to mitomycin C suggest that RAD23b regulates cell division.

264 n FA-D2(-/-) cells exposed to NSC 617145 and mitomycin C, suggesting that WRN helicase inhibition int

265 derably more sensitive to both etoposide and mitomycin C than cells that express no DNA-PKcs at all.

266 erately more sensitive to UV irradiation and mitomycin C than the wild-type strain, the lack of RecA

267 553 mutant strain was much more sensitive to mitomycin C than the WT strain, indicating that HP1553 i

268 lls more sensitive to the crosslinking agent mitomycin C than to ultraviolet radiation, suggesting th

269 oma was higher following trabeculectomy with mitomycin C than tube shunt surgery in the TVT Study.

270 cks hypersensitivity to IFNgamma/TNFalpha or mitomycin C that results in enhanced apoptosis.

271 resulted in survival of E. coli at levels of mitomycin C that were lethal to noncomplemented hosts.

272 ergistically with very low concentrations of mitomycin C to inhibit proliferation in a WRN-dependent

273 oup antimetabolite analysis, the addition of mitomycin C to TE and DS decreased the difference in the

274 wn to act synergistically with cisplatin and mitomycin C; to increase UVC-mediated cytotoxicity; to m

275 ence in intraocular pressure control between mitomycin-C trabeculectomy and nonpenetrating glaucoma s

276 of its perceived superior safety profile to mitomycin-C trabeculectomy.

277 tion of IFN-gamma production was observed in mitomycin C-treated CD8(+) immune T cells, thus independ

278 D8 cells, and immunization with a mixture of mitomycin C-treated cells from M2-CD83 plus M2-1D8 preve

279 Immunization with live or mitomycin C-treated M2-CD83 cells prevented outgrowth of

280 Mitomycin C treatment also protected GJIC from disruptio

281 10-fold more sensitive to UV irradiation and mitomycin C treatment and are twofold less efficient in

282 igG mutant was found to be more resistant to mitomycin C treatment than the wild-type strain, indicat

283 s RecA following methyl methanesulphonate or mitomycin C treatment, but is largely RecA-independent f

284 lts after 6 h of camptothecin, etoposide, or mitomycin C treatment, with the p53 protein phosphorylat

285 istant to Triton X extraction in response to mitomycin C treatment.

286 erating cell nuclear antigen irrespective of mitomycin C treatment.

287 XPF are hypersensitive to UV irradiation and mitomycin C treatment.

288 nto chromatin following DNA damage caused by mitomycin C treatment.

289 n loading and focus formation in response to mitomycin C treatment.

290 Of the adjuvants studied, only mitomycin C was associated with vision-threatening compl

291 e single-surgeon comparative study, PRK with mitomycin C was performed to correct hyperopia using Bau

292 ity of cells to the interstrand cross-linker mitomycin C, we found that treatment of cells with HDAC

293 lowing glaucoma surgery (trabeculectomy with mitomycin C) were included in this institutional study.

294 re almost completely resistant to killing by mitomycin C, which forms DNA adducts.

295 acil (FU) plus cisplatin followed by FU plus mitomycin C with concurrent radiation in patients with p

296 tin followed by two 28-day cycles of FU plus mitomycin C with concurrent split-course radiation.

297 vivo role of NQO1 in metabolic activation of mitomycin C with implications in mitomycin C chemotherap

298 Reaction of 9-epi-mitomycin C with MitN in the presence of S-adenosylmethi

299 outcome compared to PRK; however, the use of mitomycin-C with PRK has improved results.

300 In response to gamma-irradiation or mitomycin C, WRN leaves the nucleoli and co-localizes wi