ライフサイエンスコーパス: MMS

1 MMS is an autosomal recessive condition described thus f

2 MMS is known to inhibit replication though activation of

3 MMS plus low glucose (2 mm) or pyruvate (5 mm) gave 11-

4 MMS sensitivity of these mutants was contingent on the s

5 MMS-induced DNA lesions include base damages such as 3-m

6 r show that PRR pathway preference in 0.001% MMS depends on timing and context; cells preferentially

7 nts in their exquisite sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive

8 28 (16 MMS, 12 USS) of 58 (48.3%; 95% CI 35.0-61.8) of the inva

9 42 (MMS) and 45 (USS) primary ovarian and tubal cancers were

10 S), and participant changing their mind (483 MMS, 1490 USS).

11 ended on Dec 31, 2011, and included 345,570 MMS and 327,775 USS annual screening episodes.

12 attend three appointments for the screen (72 MMS, 757 USS), and participant changing their mind (483

13 Among 20 821 MMS procedures, 149 adverse events (0.72%), including 4

14 e subunits Rnr1 and Rnr3, thereby abrogating MMS-induced mutagenesis and enhancing cell lethality.

15 agents such as methylmethanesulphonic acid (MMS) and mitomycin C (MMC) as the wild-type cells.

16 e mutable than the beta-pol null cells after MMS exposure.

17 A similar result was obtained after MMS treatment of these cells.

18 Mean (SD) time to recurrence after MMS was 3.91 (4.4) years, and after WLE, 4.45 (2.7) year

19 ng and translation influence viability after MMS damage.

20 ncreased sensitivity to the alkylating agent MMS and hyper-recombination in an oligonucleotide-mediat

21 ive to treatment with the DNA damaging agent MMS.

22 These analyses generated an MMS factor that was loaded by BMI, waist-to-hip ratio, s

23 es, as measured by SE (r=0.642, P<.0001) and MMS (r=0.443, P<.04), and with post-OLT changes (for SE:

24 by NAD(P)H depletion, from both H(2)O(2) and MMS exposures.

25 Spontaneously arising and MMS-induced insertion/deletion mutations and large rearr

26 ue to their role in regulating the basal and MMS-induced expression of DNA glycosylase Mag1.

27 emale sterility, cell cycle checkpoints, and MMS resistance).

28 ay between initial physician examination and MMS predicted defect size (p = 0.0004), with greater tha

29 lele exhibited significant filamentation and MMS sensitivity in this background whereas mutations tha

30 ing of tRNA modifications caused by H2O2 and MMS.

31 ic increase in sensitivity to chronic HU and MMS treatment; however, these double mutants were not ch

32 ogue, but when added together KIC (2 mm) and MMS stimulated insulin release 7-fold (versus 12-fold fo

33 tag recBCD) were more sensitive to MNNG and MMS than the single mutants suggesting that homologous r

34 ts to DSBs induced by exposure to X rays and MMS.

35 h in turn regulates ergosterol synthesis and MMS resistance.

36 cells against cell killing by BCNU, TMZ, and MMS, which is consistent with the possibility that mitoc

37 e RAD6 epistasis group in response to UV and MMS exposure.

38 ltaddc1 dpb11-1 double mutant is more UV and MMS sensitive than the Deltaddc1 or the dpb11-1 single m

39 nner, preventing mutations induced by UV and MMS, respectively.

40 is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protect

41 intermediates via a route that is likely At-MMS and UV sensitive81 dependent.

42 can be readily conjugated to magnetic beads, MMS-based SELEX provides a general platform for rapid ge

43 logs of yeast Rad5, can discriminate between MMS-induced versus UV-induced DNA damage.

44 n the mean number for all physicians billing MMS.

45 ly sensitive to replicative stress caused by MMS and not to more direct DNA breaks.

46 scriptional regulation of the RTP801 gene by MMS.

47 or accurate repair of DNA lesions induced by MMS.

48 an additional pathway that is stimulated by MMS-induced damage.

49 to ovarian cancer by Dec 31, 2014, comparing MMS and USS separately with no screening, ascertained by

50 t analysis identified seven highly connected MMS-toxicity modulating proteins associated with transla

51 In contrast, MMS promotes the degradation of HLTF and the interaction

52 Correspondingly, MMS treatment was capable of stimulating a 2.5 kb RTP801

53 A-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, trans

54 te sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive opportunity to stud

55 We show that upon exposure to low-dose MMS, a PRR-defective rad18Delta mutant stalls into a len

56 During MMS, unlike WLE, the entire cutaneous surgical margin is

57 cs and antibiotics and sterile gloves during MMS were associated with modest reduction of risk for ad

58 , which is nonetheless managed safely during MMS.

59 cted, including 28 borderline tumours (eight MMS, 20 USS).

60 REV3 cooperates with the endonuclease MMS and UV-sensitive protein81 in response to interstran

61 show that, upon incubation in egg extracts, MMS-treated DNA activates a diffusible inhibitor that bl

62 A further 13 (five MMS, eight USS) women developed primary ovarian cancer d

63 (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to

64 st-OLT changes (for SE: r=-0.583, P<.01; for MMS: r=-0.536, P<.01).

65 tive values were 89.5%, 99.8%, and 35.1% for MMS, and 75.0%, 98.2%, and 2.8% for USS, respectively.

66 bal cancers were 89.4%, 99.8%, and 43.3% for MMS, and 84.9%, 98.2%, and 5.3% for USS, respectively.

67 exists in the number of stages per case for MMS for head and neck, genitalia, hands, and feet skin c

68 itutional US ambulatory referral centers for MMS.

69 hysicians who received Medicare payments for MMS from any practice performing MMS on the head and nec

70 A screen for MMS-sensitive mutants identified a novel truncation alle

71 ned as those whose mean number of stages for MMS was 2 standard deviations greater than the mean numb

72 Five-year overall survival for MMS was 92% and for WLE was 94% (P = .28).

73 (FLAG)betabeta' isolated from MMS-treated MHY343 cells or cells containing a deletion

74 s resume the cell cycle during recovery from MMS-induced DNA damage in S-phase.

75 utively and in the presence of the genotoxin MMS.

76 determining cellular morphology following HU/MMS treatment.

77 ng a causative role for DONSON disruption in MMS.

78 ete replication fork arrest and lethality in MMS, demonstrating that Rad53 deactivation is a key mech

79 Replication intermediates persisted in MMS-treated cells, suggesting that replication fork move

80 ment contribute to the slowing of S phase in MMS-treated fission yeast cells.

81 in pph3Delta cells slows fork progression in MMS, whereas deactivation of Rad53, through expression o

82 increased and prolonged gamma-H2AX signal in MMS-treated BRCA1/2 cells suggested an aberrant processi

83 In HaCaT human keratinocytes, MMS was able to induce a rapid increase in the mRNA leve

84 ydroxyurea (HU) and methyl methanesulfonate (MMS) activates DNA integrity checkpoints; in checkpoint-

85 ersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deoxyuridine, agents that in

86 g reagents, such as methyl methanesulfonate (MMS) and H2O2.

87 DNA-damaging agents methyl methanesulfonate (MMS) and hydroxyurea by a mechanism(s) that requires the

88 of cells exposed to methyl methanesulfonate (MMS) and in the absence of Mag1, Rad30 and Rev3, human p

89 ng reagents such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU), while expression

90 hypersensitivity to methyl methanesulfonate (MMS) and nitrogen mustard (HN2).

91 el of resistance to methyl methanesulfonate (MMS) and temozolomide (TMZ) but simultaneous overexpress

92 ause sensitivity to methyl methanesulfonate (MMS) and/or ionizing radiation, along with follow-up cha

93 he alkylating agent methyl methanesulfonate (MMS) compared to the parent strain.

94 DNA damaging agent methyl methanesulfonate (MMS) in comparison to responses to acute heat shock, loo

95 mined the repair of methyl methanesulfonate (MMS) induced DNA damage in haploid G1 yeast cells, so th

96 he alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (damage resistance pro

97 ptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-deficient mre11-3 and sae2D

98 otic checkpoint and methyl methanesulfonate (MMS) sensitivity.

99 ng with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a function of a particular

100 he alkylating agent methyl methanesulfonate (MMS) was also observed for siRNA-mediated ATR silencing.

101 this question using methyl methanesulfonate (MMS), a base-damaging agent.

102 s were sensitive to methyl methanesulfonate (MMS), and rev1 rad30 or rev3 rad30 double mutant cells w

103 spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces more base substit

104 ydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferating cell nuclear a

105 DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fitness profiling of

106 mitomycin C (MC) or methyl methanesulfonate (MMS), as well as homologous recombination in Hfr mating

107 the genotoxic agent methyl methanesulfonate (MMS), but the molecular basis of genotoxic stress is unc

108 ing agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint.

109 V)-C radiation, and methyl methanesulfonate (MMS), indicating the broad relevance of HRR to genotoxic

110 DNA damaging agent, methyl methanesulfonate (MMS), induces RTP801 transcription.

111 ing UV irradiation, methyl methanesulfonate (MMS), mitomycin C, phleomycin, hydrogen peroxide, and hy

112 eroxide (H(2)O(2)), methyl methanesulfonate (MMS), or camptothecin by monitoring NAD(P)H.

113 1-oxide (4-NQO) and methyl methanesulfonate (MMS), or when an HO endonuclease-induced DSB was introdu

114 DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell survival required a functional

115 DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimensional gel analyses of rep

116 irs the response to methyl methanesulfonate (MMS)-induced DNA lesions and disrupts telomeric silencin

117 3 (E2) and promotes methyl methanesulfonate (MMS)-induced PCNA polyubiquitination.

118 he alkylating agent methyl methanesulfonate (MMS).

119 with the genotoxin methyl methanesulfonate (MMS).

120 he alkylating agent methyl methanesulfonate (MMS).

121 t (UV) light and to methyl methanesulfonate (MMS).

122 ting agents such as methyl methanesulfonate (MMS).

123 s in sensitivity to methyl methanesulfonate (MMS).

124 ing agents, such as methyl methanesulfonate (MMS).

125 nsitivity to 0.001% methyl methanesulfonate (MMS).

126 A damage induced by methyl methanesulfonate (MMS).

127 thout DNA damage by methyl methanesulfonate (MMS).

128 he alkylating agent methyl methanesulfonate (MMS).

129 eplication forks in methyl-methanesulfonate (MMS)-damaged cells, under different conditions of Rad53

130 xposure of yeast to methyl-methanesulfonate (MMS).

131 chemicals such as methyl methanesulphonate (MMS) and N-ethyl-N-nitrosurea.

132 radiation (UV) or Methyl methanesulphonate (MMS) is independent of p53 status.

133 ing agents such as methyl methanesulphonate (MMS), absence of the full-length form of Translation Ini

134 hypersensitive to methyl methanesulphonate (MMS), suggesting that PARP activity and DNA repair respo

135 e alkylating agent methyl methanesulphonate (MMS).

136 oped microscale molecular mass sensor (micro-MMS) is presented.

137 rates the molecular mass range of the micro-MMS can be, in principle, tuned from less than 10(2) g/m

138 The micro-MMS employs a widely applicable technique of measuring t

139 The ratio data from the micro-MMS is also demonstrated to readily provide a "universal

140 ameters are important to interpret the micro-MMS output: the radius of the interrogating light probe

141 The micro-MMS samples the RIG with probe beams at two positions al

142 EMS; point mutations required 1.25 microg/mL MMS and 1.40 microg/mL EMS before a mutagenic effect was

143 f chromosomal aberrations was 0.85 microg/mL MMS and 1.40 microg/mL EMS; point mutations required 1.2

144 Also Crt1, the repressor of model MMS-inducible ribonucleotide reductase genes, was found

145 esolution, NASA's Magnetospheric Multiscale (MMS) mission has found direct evidence for electron dema

146 ields with NASA's Magnetospheric Multiscale (MMS) mission, we utilize Earth's magnetosphere as a plas

147 y observed by the Magnetospheric Multiscale (MMS) spacecraft.

148 In INS-1 cells, neither MMS nor KIC (10 mm) was an insulin secretagogue, but whe

149 ), non-ovarian cancer or other disease (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), rel

150 ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to attend three appointments for t

151 (MRS), whose function is required for normal MMS.

152 of restoring MMS-resistance to the normally MMS-sensitive strain.

153 base excision repair (BER) activity but not MMS sensitivity.

154 were measured in the presence and absence of MMS.

155 mstances in which the additional benefits of MMS outweigh its higher cost are needed, still lacking,

156 Shu complex promotes high-fidelity bypass of MMS-induced alkylation damage, such as N3-methyladenine,

157 ied analysis of death from ovarian cancer of MMS versus no screening with exclusion of prevalent case

158 n does not appear to be the primary cause of MMS sensitivity of the double tailless mutants.

159 nt a determinant of outcome as the choice of MMS or excision.

160 opic locus contributing to the clustering of MMS-related phenotypes.

161 ng fibroblasts treated with a combination of MMS and 4-AN, a complete inhibition of DNA synthesis is

162 Much of the data regarding complications of MMS are anecdotal or report findings from single centers

163 e able to abrogate the stimulatory effect of MMS, indicating that Elk-1 and C/EBP are both involved i

164 are as sensitive to the cytotoxic effects of MMS and MNNG as the most base excision repair (BER)-defi

165 ighly sensitized to the cytotoxic effects of MMS by 4-amino-1,8-naphthalimide (4-AN), an inhibitor of

166 nd 28% (-3 to 49) in years 7-14 in favour of MMS.

167 of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising duri

168 Based on the heat-lability of MMS-induced base damage, an assay was developed that mon

169 tant when cells replicate in the presence of MMS, and that double deletions lead to a greater reducti

170 H3 N-tails are important for the removal of MMS-induced DNA lesions due to their role in regulating

171 find that REV3 is required for the repair of MMS-induced lesions when recombinational repair is compr

172 The sensitivity and specificity of MMS for detection of iEOCs were 85.8% (95% CI, 79.3% to

173 s Snail and vimentin, and a subpopulation of MMS-treated cells displayed an elongated fibroblast-like

174 e that RTP801 is a transcriptional target of MMS in human keratinocytes and that C/EBP is implicated

175 ind, randomized, placebo-controlled trial of MMS in 17- to 45-y-old Gambian women who were menstruati

176 In 20 years, use of MMS has grown approximately 10-fold and its cost now exc

177 mission, as measured by either SE (P<.01) or MMS (P<.04).

178 roup after OLT, as measured by SE (P<.03) or MMS (P<.02).

179 60 mg of iron and 400 mug of folic acid, or MMS containing a daily allowance of 15 micronutrients, i

180 in response to changing levels of copper or MMS.

181 eletion renders the yeast sensitive to UV or MMS treatment.

182 yeast genes involved in the repair of UV- or MMS-induced DNA damage.

183 We have also mapped our MMS-toxicity modulating proteins onto an E. coli protein

184 The mean number of stages per MMS case for all physicians practicing from January 2012

185 305 individual billing physicians performing MMS.

186 ayments for MMS from any practice performing MMS on the head and neck, genitalia, hands, and feet reg

187 nsulin release in fresh islets, and KIC plus MMS gave synergistic insulin release in cultured human i

188 r RNR3 were hypersensitive to rapamycin plus MMS, providing the first demonstration that Rnr3 contrib

189 These agents also potentiated MMS-induced insulin release in fresh islets, and KIC plu

190 ins of Sgs1 directly required for processing MMS-induced DNA damage, most notably the helicase domain

191 efined by ATP-dependent DNA Helicase RECQ4A, MMS and UV-sensitive protein81, REV3, and the ATPase Rad

192 Reduced MMS was largely independent of adult pigmentation patter

193 ound that 4 hypomorphs significantly reduced MMS to varying degrees.

194 d that Mag1 is the major enzyme that removes MMS-damaged bases.

195 d51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase.

196 f these proteins function together to resist MMS-induced DNA damage and promote gene conversion at bl

197 is only recently enabled by high-resolution MMS observations.

198 liminated filamentation and largely restored MMS resistance.

199 eta, iota and kappa are capable of restoring MMS-resistance to the normally MMS-sensitive strain.

200 ndom numbers to annual multimodal screening (MMS) with serum CA125 interpreted with use of the risk o

201 as a second-line test (multimodal screening [MMS]; n=50 640); or annual screening with transvaginal u

202 The micromagnetic separation (MMS) chip integrates microfabricated ferromagnetic struc

203 A FACS-based shRNA screen identified several MMS genes as essential for the epithelial-mesenchymal tr

204 We document a mid-millennium shift (MMS) in ocean-atmosphere circulation around 1500-1650 CE

205 nnon entropy (SE) and median mobility shift (MMS) values derived from the heteroduplex mobility assay

206 nated the "mesenchymal metabolic signature" (MMS).

207 or the Shu complex in the repair of specific MMS-induced DNA lesions and elucidate the interplay betw

208 screening by using the multimodal strategy (MMS) in which annual serum cancer antigen 125 (CA-125) w

209 havior, we measured the male mating success (MMS) of 12 hypomorphic y mutants and matched-outbred-bac

210 Monomethyl succinate (MMS) combined with a barely stimulatory concentration of

211 DNA alkylation by methyl methane sulfonate (MMS) induces Cdc6 degradation independently of p53.

212 anidine (MNNG) and methyl methane sulfonate (MMS) produce a wide variety of N- and O-methylated bases

213 cells treated with methyl methane sulfonate (MMS), hydroxyurea (HU) or camptothecin (CPT), we show th

214 e alkylating agent methyl-methane sulfonate (MMS), we obtained approximately 2 x 10(5) active mutants

215 droxyurea (HU) and methyl-methane sulfonate (MMS).

216 tion-blocking agent methylmethane sulfonate (MMS) in smc6 mutants, with double deletions conferring s

217 on and DNA targets: methylmethane sulfonate (MMS), methylnitrosourea (MNU), ethylmethane sulfonate (E

218 ce to DNA damage by methylmethane sulfonate (MMS).

219 O2) and alkylation (methylmethane sulfonate, MMS) stresses induced nearly identical patterns of up- a

220 onal multiple-micronutrient supplementation (MMS) affects placental function.

221 cian practices in Mohs micrographic surgery (MMS) and the associated factors.

222 rrence rates with Mohs micrographic surgery (MMS) are modestly better than those for excision surgery

223 s associated with Mohs micrographic surgery (MMS) can guide clinical management.

224 However, Mohs micrographic surgery (MMS) is now used to treat a growing subset of individual

225 likely to receive Mohs micrographic surgery (MMS) over excision.

226 defect size after Mohs micrographic surgery (MMS).

227 involved in the multiple metabolic syndrome (MMS).

228 n disease, microcephaly-micromelia syndrome (MMS).

229 Our data also indicate that MMS-induced mutations at adenine nucleotides are signifi

230 re, a gel mobility shift assay revealed that MMS was able to initiate rapid formation of a protein co

231 thyl methanesulfonate (MMS), and showed that MMS also induces more base substitution mutations in BRC

232 Our data suggest that MMS-induced genes undergo transcription complex assembly

233 The MMS coincided with the deepest LIA cooling and was proba

234 The MMS sensitivity of a Pol4-deficient strain can be rescue

235 The MMS-induced increase in mutant frequency in beta-pol nul

236 ila ortholog of the yeast snm1 gene, and the MMS- and HN2-sensitive mus301 mutant defines the Drosoph

237 We found that both the MMS sensitivity and growth phenotypes of DCDC-deficient

238 bination, which is a phenotype shared by the MMS-hypersensitive DNA repair mutants rad2, rhp55 and NE

239 x 10(5) active mutants that complemented the MMS sensitivity of AP endonuclease-deficient E. coli.

240 ar of diagnosis was 2008 (1986-2013) for the MMS group vs 2003 (1978-2013) for the WLE group (P < .00

241 Melanoma-specific mortality for the MMS group was 2 vs 13 patients for the WLE group, with m

242 clease activity, and the main reason for the MMS sensitivity of nth1 cells appears to be their lack o

243 97 of 50 078 (0.2%) women from the MMS group and 845 of 48 230 (1.8%) from the USS group un

244 d a repeat test, and 167 (0.3%) women in the MMS group and 1894 (3.9%) women in the USS group require

245 verall recurrence rates were 5 (1.8%) in the MMS group and 22 (5.7%) in the WLE group (P = .07).

246 The 5-year recurrence rate was 1.1% in the MMS group and 4.1% in the WLE group (P = .07).

247 Overall, 4355 of 50 078 (8.7%) women in the MMS group and 5779 of 48 230 (12.0%) women in the USS gr

248 Of these women, 148 (0.29%) women in the MMS group, 154 (0.30%) in the USS group, and 347 (0.34%)

249 ncer in 1282 (0.6%) women: 338 (0.7%) in the MMS group, 314 (0.6%) in the USS group, and 630 (0.6%) i

250 e for analysis: 50,624 (>99.9%) women in the MMS group, 50,623 (>99.9%) in the USS group, and 101,299

251 flexible parametric model showed that in the MMS group, this mortality effect was made up of 8% (-20

252 Specificity was higher in the MMS than in the USS group, resulting in lower rates of r

253 4 results in a 6- to 14-fold increase in the MMS-induced mutation frequency and in a significant incr

254 The sensitivity of the MMS and USS screening strategies is encouraging.

255 Operation of the MMS device is facile and robust and demonstrates high re

256 age analysis (GENEHUNTER version 2.1) of the MMS factor was conducted in the combined marker set samp

257 atients on the GUG, 19.0% of patients on the MMS, 44.0% of patients on the GDS15, and 64.9% of patien

258 These deletion mutations also rescue the MMS sensitivity of esc2Delta cells.

259 eckpoint-defective mrc1 alleles suppress the MMS sensitivity and the checkpoint recovery defect of di

260 Women randomised to the MMS group had their blood tested for CA125 and those ran

261 y allocated 202,638 women: 50,640 (25.0%) to MMS, 50,639 (25.0%) to USS, and 101,359 (50.0%) to no sc

262 identify chromosomal regions contributing to MMS-related traits represented by composite factors deri

263 tored wild-type resistance of this mutant to MMS, H2O2, and SIN-1.

264 yeast, the response of the Rad53 pathway to MMS is compromised due to a loss of Sod1 activity, consi

265 s modest capacities to provide resistance to MMS and to resolve recombination-dependent X-shaped mole

266 mouse cells were slightly more resistant to MMS than wild-type cells, probably due to the production

267 expression in wild-type cells in response to MMS but was nonresponsive in cells lacking the TF.

268 n even after S phase, and normal response to MMS damage correlates with the maintenance of intact Dfp

269 d Rtt107 with Dpb11 (hTopBP1) in response to MMS-induced DNA alkylation, suggesting that Slx4 and Rtt

270 function separately from REV3 in response to MMS.

271 981 bp of the promoter that is responsive to MMS treatment.

272 -chromosome mutants were solely sensitive to MMS and define 8 new mutagen-sensitive genes (mus212-mus

273 r priA (primosome) genes are as sensitive to MMS and MNNG as alkA tag bacteria.

274 cells were synergistically more sensitive to MMS than the respective single mutant strains.

275 e short hairpin RNA increases sensitivity to MMS and enhances genomic instability.

276 of PARP activity results in sensitization to MMS through maintenance of an ATR and Chk1-dependent S-p

277 ant animals were significantly sensitized to MMS or X rays.

278 main reasons for withdrawal were death (two MMS, 28 USS), non-ovarian cancer or other disease (none

279 renders tel1-Delta cells (but not wild type) MMS-sensitive, demonstrating that, under certain conditi

280 lence screen, 50 078 (98.9%) women underwent MMS, and 48 230 (95.2%) underwent USS.

281 nd ENU showed linear dose-responses, whereas MMS and EMS had nonlinear curves containing a range of n

282 s 0-14 of 15% (95% CI -3 to 30; p=0.10) with MMS and 11% (-7 to 27; p=0.21) with USS.

283 stone H4; this event is also associated with MMS- or phleomycin-induced DSBs but not with UV-induced

284 e kinetic simulation and its comparison with MMS observations, we show for the first time that ion-sc

285 in in these cells positively correlates with MMS in a subset of mutants.

286 The early invitation with MMS group had an infant mortality rate of 16.8 per 1000

287 Early invitation with MMS group had an under 5-year mortality rate of 18 per 1

288 Usual invitation with MMS group had the highest incidence of spontaneous abort

289 andom sample of patients treated for KC with MMS were selected for telephone interview.

290 nsecutive sample of patients presenting with MMS for 35 weeks at each center, with staggered start ti

291 noted a significant mortality reduction with MMS when prevalent cases were excluded.

292 functional categories over-represented with MMS-toxicity modulating proteins and demonstrate that, i

293 There were 277 patients treated with MMS (mean [SD] age, 64.0 [13.1] years; 62.1% male) and 3

294 e outcomes of patients with MIS treated with MMS compared with those treated with WLE.

295 c survival of patients with MIS treated with MMS compared with WLE.

296 The same strains either treated with MMS or containing a crt1Delta gave ratios between 0.49 a

297 sisted of 662 patients with MIS treated with MMS or WLE per standard of care in dermatology and surge

298 UV-irradiated cells or in cells treated with MMS requires Huwe1 and is associated with release of Cdc

299 s an activation of Chk1 after treatment with MMS and 4-AN, which can be suppressed by caffeine.

300 In yng2, MMS treatment causes a persistent Mec1-dependent intra-S