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 highly sensitive to the cross-linking agent mitomycin C.

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

5 HDAC10 resulted in increased sensitivity to mitomycin C.

6 no influence on sensitivity to cisplatin or mitomycin C.

7 titutively during growth and were induced by mitomycin C.

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

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

10 following treatment with the genotoxic drug mitomycin C.

11 a 27% increased survival in the presence of mitomycin C.

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

13 and chemicals such as hydrogen peroxide and mitomycin C.

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

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

16 kinase substrate required for resistance to mitomycin C.

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

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

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

20 susceptibility, and cellular sensitivity to mitomycin C.

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

22 ed PRDX3 expression increases sensitivity to mitomycin C.

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

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

25 phages was induced with hydrogen peroxide or mitomycin C.

26 by the chemotherapeutic agents etoposide and mitomycin C.

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

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

29 nsitivity to DNA crosslinking agents such as mitomycin C.

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

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

32 age after treatment with the genotoxic agent mitomycin C.

33 action against noncancer prostate cells over mitomycin C.

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

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

36 and cellular sensitivity to the crosslinker mitomycin C.

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

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

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

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

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

42 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]).

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

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

45 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

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

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

48 Trabeculectomy with mitomycin C (8 eyes) and trabeculotomy (8 eyes) had 25%

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Although both mitomycin C and ionizing radiation induced FANCD2 monoub

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

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

76 The most potent FDA-approved drugs (mitomycin C and mithramycin A) and a promising natural p

77 rsensitivity to the DNA crosslinking agents, mitomycin C and olaparib, as proxies for functional DNA

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

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

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

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

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

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

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

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

86 en proliferating IA6+ cells are ablated with Mitomycin C, and injection of a single IA6+ Candidate st

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

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

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

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

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

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

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

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

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

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

97 c conjunctival resection followed by topical mitomycin C application.

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

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

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

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

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

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

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

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

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

107 lts in sensitivity to the DNA damaging agent mitomycin C, but not to any other type of DNA damage tes

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

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

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

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

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

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

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

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

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

117 3B, and Mahlavu)-to ultraviolet irradiation, mitomycin C, doxorubicin, cisplatin, sorafenib, and lapa

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

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

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

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

122 Mitomycin C enhanced transport of Cx43 from the endoplas

123 llapse caused by methyl methanesulfonate and mitomycin C exposure, a delayed and reduced RAD51 respon

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

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

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

127 le option for 9/22 (41%) and cryotherapy and Mitomycin C for 6/22 (27%) respondents.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 3 nm solid-state laser (SSL) with adjunctive Mitomycin C in eyes previously treated with laser assist

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

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

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

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

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

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

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

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

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

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

156 -binding activity and its capacity to rescue mitomycin C-induced cytotoxicity, accounting for two inf

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

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

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

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

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

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

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

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

165 Subconjunctival mitomycin C injection may cause limbal stem cell deficie

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

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

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

169 B. subtilis is a soil dwelling organism and mitomycin C is a natural antibiotic produced by the soil

170 Mitomycin C is a natural product with potent alkylating

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

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

173 Mitomycin-C is an antimetabolite that has seen increased

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

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

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

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

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

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

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

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

182 The anticancer drugs, mitomycin C (MIC(50) = 0.25 mug/ml) and mithramycin A (M

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

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

185 ) Baerveldt implant) and trabeculectomy with mitomycin C (MMC) (0.4 mg/ml for 4 minutes) in patients

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

187 r subconjunctival injection of a solution of mitomycin C (MMC) and 1% preservative-free lidocaine (as

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

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

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

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

192 excimer lasers and standardized surgical and mitomycin C (MMC) application protocols.

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 A single application of Mitomycin C (MMC) is used clinically in ophthalmology to

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 nonpenetrating deep sclerectomy (NPDS) with mitomycin C (MMC) versus XEN(R) gel stent with MMC.

213 Intraoperative mitomycin C (MMC) was associated with reduced failure fo

214 hanesulphonate (MMS), camptothecin (CPT) and mitomycin C (MMC), agents that hinder the progression of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 concentration of the DNA cross-linking agent mitomycin C (MMC).

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

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

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

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

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

237 y aimed to assess the role of intraoperative mitomycin-C (MMC) application during hyperopic LASIK cor

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

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

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

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

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

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

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

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

246 tero, microphtalmia, cellular sensitivity to mitomycin C, occasional limb abnormalities and hematolog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 Mitomycin C-sensitive clones from a transposon mutagenes

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

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

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

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

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

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

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

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

270 553 mutant strain was much more sensitive to mitomycin C than the WT strain, indicating that HP1553 i

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

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

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

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

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

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

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

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

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

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

281 Mitomycin C treatment also protected GJIC from disruptio

282 10-fold more sensitive to UV irradiation and mitomycin C treatment and are twofold less efficient in

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

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

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

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

287 erating cell nuclear antigen irrespective of 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 n experimental trabeculectomy surgeries with mitomycin C used as an adjuvant, there were no differenc

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

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

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

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

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

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

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

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

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

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