ライフサイエンスコーパス: mitomycin

1 s 1, 8, 15, and 22, followed by 1 week rest; mitomycin 10 mg/m2 intravenous bolus infusion every 6 we

2 acil (1000 mg/m2 on days 1-4 and 29-32) plus mitomycin (10 mg/m2 on days 1 and 29) and radiotherapy (

3 ned to one of four groups, to receive either mitomycin (12 mg/m(2) on day 1) or cisplatin (60 mg/m(2)

4 py [n=136]); to ASC plus MVP (four cycles of mitomycin 6 mg/m2, vinblastine 6 mg/m2, and cisplatin 50

5 of DHS5373 revealed continued production of mitomycin A and mitomycin C in addition to the accumulat

6 Likewise, MitN was also shown to convert mitomycin A to mitomycin F under the same reaction condi

7 of the 7-OMe group that is characteristic of mitomycins A and B and demonstrates the prerequisite of

8 esis of the quinone methoxy group present in mitomycins A and B.

9 Production of mitomycins A and C or mitomycin B was selectively restor

10 not involved directly in the biosynthesis of mitomycins A and C.

11 had been deleted failed to produce the three mitomycins (A, B, and C) that are typically isolated fro

12 n C in addition to the accumulation of a new mitomycin analog, 9-epi-mitomycin C.

13 Mitomycin and platinum-based chemotherapeutic agents wer

14 e survival rate from concurrent fluorouracil/mitomycin and radiation is only approximately 65%.

15 l comparing treatment with fluorouracil plus mitomycin and radiotherapy vs treatment with fluorouraci

16 I Randomized Study of 5-Fluorouracil (5-FU), Mitomycin, and Radiotherapy Versus 5-Fluorouracil, Cispl

17 Mitomycins are bioreductively activated DNA-alkylating a

18 bined with intraperitoneal chemotherapy with mitomycin at 42 degrees C.

19 Production of mitomycins A and C or mitomycin B was selectively restored upon supplementing

20 igned to 1 of 2 intervention groups: (1) the mitomycin-based group (n = 341), who received fluorourac

21 5% confidence interval [CI], 53%-67%) in the mitomycin-based group and 54% (95% CI, 46%-60%) in the c

22 rvival rate was 75% (95% CI, 67%-81%) in the mitomycin-based group and 70% (95% CI, 63%-76%) in the c

23 te of colostomy was significantly better for mitomycin-based than cisplatin-based treatment (10% vs 1

24 improve disease-free-survival compared with mitomycin-based therapy, but cisplatin-based therapy res

25 higher rate of colostomy (P = .03) than was mitomycin-based therapy.

26 antly higher rate of colostomy compared with mitomycin-based therapy.

27 Severe hematologic toxicity was worse with mitomycin-based treatment (P < .001).

28 and 15% (95% CI, 10%-20%), respectively, for mitomycin-based treatment and 33% (95% CI, 27%-40%) and

29 to methyltransferases, is located within the mitomycin biosynthetic gene cluster.

30 An inframe deletion in mitN of the mitomycin biosynthetic pathway was generated in Streptom

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 Although both mitomycin C and ionizing radiation induced FANCD2 monoub

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

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

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

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

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

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

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

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

105 c conjunctival resection followed by topical mitomycin C application.

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

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

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

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

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

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

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

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

114 Mitomycin C enhanced transport of Cx43 from the endoplas

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

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

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

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

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

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

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

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

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

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

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

126 3 nm solid-state laser (SSL) with adjunctive Mitomycin C in eyes previously treated with laser assist

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

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

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

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

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

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

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

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

135 Subconjunctival mitomycin C injection may cause limbal stem cell deficie

136 Mitomycin C is a natural product with potent alkylating

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 553 mutant strain was much more sensitive to mitomycin C than the WT strain, indicating that HP1553 i

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

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

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

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

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

159 Mitomycin C treatment also protected GJIC from disruptio

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

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

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

163 erating cell nuclear antigen irrespective of mitomycin C treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 3B, and Mahlavu)-to ultraviolet irradiation, mitomycin C, doxorubicin, cisplatin, sorafenib, and lapa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 Mitomycin C-sensitive clones from a transposon mutagenes

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

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

224 HDAC10 resulted in increased sensitivity to mitomycin C.

225 no influence on sensitivity to cisplatin or mitomycin C.

226 titutively during growth and were induced by mitomycin C.

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

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

229 following treatment with the genotoxic drug mitomycin C.

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

231 and chemicals such as hydrogen peroxide and mitomycin C.

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

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

234 kinase substrate required for resistance to mitomycin C.

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

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

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

238 susceptibility, and cellular sensitivity to mitomycin C.

239 ed PRDX3 expression increases sensitivity to mitomycin C.

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

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

242 age after treatment with the genotoxic agent mitomycin C.

243 action against noncancer prostate cells over mitomycin C.

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

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

246 and cellular sensitivity to the crosslinker mitomycin C.

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

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

249 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]).

250 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 more sensitive to cytotoxic drugs including Mitomycin, Camptothecin and Cisplatin.

270 , and endophthalmitis, as they relate to the mitomycin concentration administered during the operatio

271 the Kaplan-Meier method, and the relation to mitomycin concentration applied during trabeculectomy.

272 the rate of trabeculectomy complications and mitomycin dose used was P = .77.

273 the presence of S-adenosylmethionine yielded mitomycin E showing that the enzyme functions as an azir

274 itN was also shown to convert mitomycin A to mitomycin F under the same reaction conditions.

275 esis of a 3-oxo-leucomitosane related to the mitomycin family of alkaloids.

276 391 of 432 (90.5%) patients in the mitomycin group versus 386 of 431 (89.6%) in the cisplat

277 The use of antimetabolite agents, such as mitomycin, has increased the rate of complications after

278 ion of fluorouracil (FU) in combination with mitomycin improves the survival of patients with pancrea

279 not support the use of cisplatin in place of mitomycin in combination with fluorouracil and radiother

280 The cytotoxicity displayed by mitomycins is dependent on their electrochemical potenti

281 more stable N-trityl hemiaminal resemble the mitomycin K substitution pattern.

282 ith ICL agents (cisplatin, camptothecin, and mitomycin), lamin A/C-deficient cells displayed normal g

283 veldt implant (tube) and trabeculectomy with mitomycin may be similarly effective in lowering intraoc

284 d efficacy of KLH were compared with that of mitomycin (MM).

285 oradiation (CCR) with fluorouracil (FU) plus mitomycin (MMC) decreased colostomy failure (CF) when co

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

287 three treatment groups: RT/fluorouracil (FU)/mitomycin (n = 472), RT/FU/cisplatin (n = 320), and RT/F

288 re substitution occurred at C(10) and C(9a) (mitomycin numbering) providing a CD(3) ether and a CD(3)

289 enrolled 940 patients: 472 were assigned to mitomycin, of whom 246 were assigned to no maintenance,

290 minimisation) to receive either intravenous mitomycin (one dose of 12 mg/m(2) on day 1) or intraveno

291 ty-eight patients received fluorouracil (FU)/mitomycin, one received FU/cisplatin, and four received

292 osteochondral defect of the right femur and mitomycin-pretreated apoptotic ADSCs in an osteochondral

293 ehavior of typical aziridinomitosenes in the mitomycin series.

294 ations does not appear to be associated with mitomycin use during a mean follow-up of 7.7 years.

295 ere similar in each group (334/472 [71%] for mitomycin vs 337/468 [72%] for cisplatin).

296 he cost-effectiveness of trabeculectomy with mitomycin vs tube insertion.

297 l cancer to date--show that fluorouracil and mitomycin with 50.4 Gy radiotherapy in 28 daily fraction

298 We investigated whether replacing mitomycin with cisplatin in chemoradiation improves resp

299 synthetic pathway leading to the subclass of mitomycins with 9alpha-stereochemistry but is not involv

300 have been found to be similar in efficacy to mitomycin, with interferon being extremely well tolerate