ライフサイエンスコーパス: MMR

1 MMR defects in EECs are associated with a number of well

2 MMR deficiency was most commonly due to alterations in M

3 MMR induces similar antibody responses in 12-month-old c

4 MMR must be able to recognize non-Watson-Crick base pair

5 MMR vaccine receipt (0, 1, 2 doses) between birth and 5

6 (DC-SIGN) and macrophage mannose receptor 1 (MMR-1).

7 ver, during a measles epidemic in 2013-2014, MMR vaccination was also offered to 6-14-month-olds in m

8 e immunoglobulin G (IgG) antibodies to all 3 MMR antigens were measured with enzyme-linked immunosorb

9 If these countries had the 25th and 75th MMR and NMR percentiles (MMR, IQR 36-190; NMR, 9-24) obs

10 r response (pre-MMR, BCR-ABL1 >0.1%, n = 8), MMR (BCR-ABL1 </=0.1%, n = 20), molecular response(4.5)

11 6-14-month-olds in municipalities with <90% MMR vaccination coverage.

12 e POLD1-R689W expression was combined with a MMR defect, indicating that the mutator effect of POLD1-

13 of the 19 detected variants fully abrogated MMR activity and that five of the detected variants atte

14 dings represent a novel mechanism to acquire MMR deficiency/microsatellite alterations.

15 In addition, MMR decreases the alignment file sizes by more than 50%,

16 essed in these extracts and failed to affect MMR directionality, but extracts supplemented with exoge

17 Among MMR-D tumors, the median number of mutations was 50 (ran

18 NA, and Pol epsilon was found to catalyze an MMR reaction that required Mlh1-Pms1.

19 Age and MMR status were marginally significant.

20 ic alterations initiated by inflammation and MMR proteins lead to gene silencing during tumorigenesis

21 ite instability (MSI), MLH1 methylation, and MMR protein expression.

22 A total of 254 patients had MSI and MMR results available.

23 Both POLE mutation and MMR-D were associated with significantly reduced risk of

24 human DCs by LPS via binding to DC-SIGN and MMR-1, leading to attenuated TLR signaling.

25 d G-C mutations, which suggests that UNG and MMR can operate within the same time frame during SHM.

26 Anti-MMR 3.49 was denoted as the lead cross-reactive MMR-targ

27 Cross-reactive anti-MMR sdAbs were generated after immunization of an alpaca

28 hat five of the detected variants attenuated MMR activity.

29 use of the conserved nature of the bacterial MMR system, pORTMAGE simultaneously allows genome editin

30 alternative to the canonical MutS-MutL-based MMR.

31 PPI inhibitor, 26 PPIs in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specificall

32 exploratory analysis of interaction between MMR status and adjuvant therapy showed a trend toward im

33 systems to investigate interactions between MMR and CAF-1- and ASF1A-H3-H4-dependent histone (H3-H4)

34 ttle is known about the interactions between MMR and the chromatin environment.

35 The relationships between MMR classes and clinicopathologic variables were assesse

36 y used genetic markers such as combined BRAF-MMR status have also been found to be prognostic.

37 The NLR, PLR, and combined BRAF-MMR status were not independently significant.

38 ghter strand from unnecessary degradation by MMR machinery.

39 ti-recombination, hallmarks of the canonical MMR.

40 We undertook tumor typing to classify MMR defects to determine if MMR status is prognostic or

41 atches precluded binding of purified E. coli MMR protein MutS.

42 (MMR) where K-H depletion led to concomitant MMR deficiency and compromised global microsatellite sta

43 tivation of MSH2 expression and consequently MMR-dependent apoptosis in these cells.

44 consequence of reduced stability of the core MMR proteins (MLH1 and PMS2) caused by elevated basal ca

45 with DNA mismatch repair protein deficiency (MMR-D) on the basis of increased mutational load.

46 y exclusive with mismatch repair deficiency (MMR-D) in the 6277 cases for whom both markers were dete

47 urrence of stage III colon cancer, deficient MMR was significantly associated with better SAR, and th

48 SAR was observed for patients with deficient MMR tumors of the proximal vs distal colon (AHR, 0.57; 9

49 the reconstitution of Pol epsilon-dependent MMR using S. cerevisiae proteins.

50 delta)- and DNA polymerase (Pol )-dependent MMR reactions is suppressed by CAF-1- and ASF1A-H3-H4-de

51 dly drives extinction of haploid and diploid MMR-proficient cells.

52 short-patch and long-patch 5' nick-directed MMR of a substrate containing a +1 (+T) mispair.

53 Inherited inactivating mutations in DNA MMR genes are causative for the cancer predisposition Ly

54 ed to post-transcriptionally repress the DNA MMR gene mutS in stationary phase, possibly limiting MMR

55 Improving 2-dose MMR coverage among HCWs would have likely reduced the si

56 hs in municipalities with routine first-dose MMR vaccine coverage of <90%.

57 0.01) after the introduction of the two-dose MMR vaccine.

58 Early MMR vaccination is well tolerated, with the lowest AE fr

59 For infants who received an early MMR vaccine dose (n = 962), we asked for information abo

60 ion between the risk of AEs and age at early MMR vaccination.

61 Parents of all infants targeted for early MMR vaccination were asked to participate.

62 ) and 350 infants (36.4%) who received early MMR vaccination reported local and systemic AEs, respect

63 We studied the effectiveness of the early MMR vaccination schedule.

64 s accumulated over five generations in eight MMR-deficient mutation accumulation (MA) lines of the mo

65 ut not germline) mutations in genes encoding MMR proteins (double somatic).

66 worse for women whose tumors had epigenetic MMR defects compared with the MMR normal group (hazard r

67 trate that Pol epsilon can act in eukaryotic MMR in vitro.

68 mercially available ssODN design that evades MMR and enables subtle gene modification in MMR-proficie

69 Thirteen percent (n = 28) exhibited MMR-D by immunohistochemistry.

70 age 18 months, compared with risk following MMR vaccine and vaccine uptake for 2-dose MCV and single

71 tational load cutoff of >/= 20 and < 150 for MMR-D detection, sensitivity and specificity were both 1

72 om 224 patients with unique CRC analyzed for MMR status also underwent MSK-IMPACT.

73 eveloping measles) x 100] was calculated for MMR, IG, and any PEP (MMR or IG) for nonimmune contacts

74 ultation at GTEN sites, 16% met criteria for MMR vaccination according to the provider's assessment,

75 ers considered 6612 (16%) to be eligible for MMR vaccine at the time of pretravel consultation.

76 Significant interactions were found for MMR (P = .03) and KRAS (P = .02) by primary tumor site f

77 Also, genomics for MMR are warranted.

78 findings indicate that distinct pathways for MMR have evolved at least twice in nature.

79 des a highly accurate means of screening for MMR-D in the same assay that is used for tumor genotypin

80 Subsequent selection for MMR-deficient cells using the guanine analog 6-thioguani

81 ncy, cellular mechanism, and selectivity for MMR-deficient cells.

82 Each tumor was assigned to one of four MMR classes: normal, epigenetic defect, probable mutatio

83 asker, detection thresholds improve further (MMR+).

84 other Lynch-associated mismatch repair gene (MMR) mutations.

85 The global MMR fell from 385 deaths per 100,000 livebirths (80% UI

86 Four hundred two patients (89.3%) had MMR-proficient tumors, and 32 patients (8%) had at least

87 Forty-eight patients (10.7%) had MMR-deficient tumors, and 40 patients (83.3%) had at lea

88 Women with tumors that had MMR defects were likely to have higher-grade cancers and

89 Of 528 patients who had MMR mutations, 63 (11.9%) had breast cancer only and 144

90 Human MMR occurs in the chromatin environment, but little is k

91 ping to classify MMR defects to determine if MMR status is prognostic or predictive.

92 ar in extent to that observed in immunogenic MMR-D cancers.

93 New-generation TKIs improve MMR but not the overall survival at 1 year in patients w

94 to 90) compared with six (range, 0 to 17) in MMR-proficient/POLE wild-type tumors (P < .001).

95 Additionally, in MMR-proficient Escherichia coli, LNA modification of the

96 se embryonic stem cells as effectively as in MMR-deficient cells.

97 A 5% decline in MMR vaccine coverage in the United States would result i

98 An increase in MMR vaccination of eligible U.S. adult travelers could r

99 MMR and enables subtle gene modification in MMR-proficient cells.

100 Although overtly deleterious mutations in MMR genes can clearly be ascribed as the cause of LS, th

101 more somatic (but not germline) mutations in MMR proteins also have mutations in PIK3CA; mutations in

102 Epigenetic and probable mutations in MMR were significantly associated with higher grade and

103 ting the restored immune control observed in MMR and MR(4.5) is not an entirely TKI-mediated effect.

104 ymerase delta is similar to that observed in MMR-deficient cancers.

105 seen less frequently and typically occur in MMR-deficient tumors.

106 Patients in MMR and MR(4.5) had a more mature, cytolytic CD57(+)CD62

107 lesion induced by Rh-PPO is not repaired in MMR-deficient cells, resulting in selective cytotoxicity

108 psilon (Pol epsilon) may also play a role in MMR.

109 es, allowed 1-, 2-, or 3-bp substitutions in MMR-proficient mouse embryonic stem cells as effectively

110 sence of other prognostic factors, including MMR deficiency.

111 These data indicate MMR deficiency in colorectal cancer can give rise to ini

112 uclease with no structural homology to known MMR factors, is required for mutation avoidance and anti

113 In strains lacking MMR, the mismatches persist.

114 revention were used to simulate county-level MMR vaccination coverage in children (age 2-11 years) in

115 mutS in stationary phase, possibly limiting MMR to allow increased mutagenesis.

116 Cancers that have lost MMR function are common and comprise an important clinic

117 ysis was the proportion of patients who lost MMR on de-escalation and regained MMR on TKI resumption.

118 ng TKI was predictive of failure to maintain MMR later on.

119 Mechanistically, MMR deficiency in K-H-depleted cells was a consequence o

120 Most MMR-eligible travelers who were not vaccinated were eval

121 xtracellular domains of both human and mouse MMR.

122 :ABL1 ratio consistently <0.1%) but not MR4 (MMR cohort) for 12 months or longer.

123 MSI/MMR testing reliably identifies LS probands, although 7.

124 available LS CRCs demonstrated abnormal MSI/MMR results.

125 t diagnosis, personal/family history, or MSI/MMR results.

126 plored by stratifying the results by mutated MMR gene, sex, and a history of CRTs.

127 Stratification by mutated MMR gene, sex, and CRT history did not show significantl

128 ormal, epigenetic defect, probable mutation (MMR defect not attributable to MLH1 methylation), or MSI

129 bias characteristic of organisms with normal MMR function.

130 Febrile seizures occurred after dose 1 of MMR vaccine at a known low increased risk (RI, 2.71; 95%

131 tolerability of this early administration of MMR vaccine.

132 ) met the inclusion criteria for analysis of MMR, IG, and any PEP effectiveness, respectively.

133 Blocking of MMR-1 or DC-SIGN with neutralizing Abs partially inhibit

134 studies suggest that Mbd4 is a component of MMR-directed DNA end processing.

135 nalog 6-thioguanine allowed the detection of MMR-abrogating VUS.

136 However, the directionality of MMR with respect to the chromosome, which comprises pare

137 recombination, examine the directionality of MMR, and quantify the nucleotide-dependence, sequence co

138 Students who had received a second dose of MMR vaccine 13 years or more before the outbreak had an

139 Students who had received a third dose of MMR vaccine had a lower risk of mumps than did those who

140 t the campaign to administer a third dose of MMR vaccine improved mumps outbreak control and that wan

141 ling data to support a routine third dose of MMR vaccine.

142 students had received at least two doses of MMR vaccine.

143 Here, we examined the effectiveness of MMR and IG PEP among children exposed to measles during

144 Effectiveness of MMR PEP was 83.4% (95% confidence interval [CI], 34.4%,

145 ere, we determine the genome-wide effects of MMR on mutation.

146 ists, and obstetricians and the logarithm of MMR, and we explored the correlation for an upper and a

147 Molecular recurrence was defined as loss of MMR (BCR-ABL1:ABL1 ratio >0.1%) on two consecutive sampl

148 ed to oxidative stress suggests that loss of MMR-dependent apoptosis could be a potential mechanism f

149 y applicable for investigating mechanisms of MMR in vivo.

150 New-generation TKIs increased the rate of MMR at 1 year compared with imatinib (overall OR, 2.22;

151 these mice underscores the critical role of MMR in maintaining general genomic stability.

152 dicate that measuring the combined status of MMR, HR, NER, and MGMT provided a more robust prediction

153 Altered immune surveillance of MMR-deficient tumors, and other host/tumor interactions,

154 Based on MMR estimates for 2015, we constructed projections to sh

155 conductive hearing loss (CHL) in gerbils on MMR characteristics, as a test for putative CNS mechanis

156 ting DNA polymerase proofreading activity or MMR function cause mutator phenotypes and consequently i

157 backgrounds where DNA polymerase function or MMR activity is partially compromised.

158 00] was calculated for MMR, IG, and any PEP (MMR or IG) for nonimmune contacts aged <19 years.

159 Effectiveness of receiving any PEP (MMR or IG) was 92.9% (95% CI, 56.2%, 99.8%).

160 d the 25th and 75th MMR and NMR percentiles (MMR, IQR 36-190; NMR, 9-24) observed in countries (N=48)

161 al threshold of 20% would identify potential MMR in an additional 14% of cases with peak tryptase (Tp

162 ntified up to 120 further cases of potential MMR in the absence of tryptase increments.

163 D-1(+)CD4(+)/CD8(+) T cells persisted in pre-MMR CML patients on TKI.

164 fore achieving major molecular response (pre-MMR, BCR-ABL1 >0.1%, n = 8), MMR (BCR-ABL1 </=0.1%, n =

165 men whose tumors were classified as probable MMR mutation (P = .001).

166 roved progression-free survival for probable MMR mutation cases.

167 nts whose tumors had deficient vs proficient MMR had significantly better SAR (adjusted hazard ratio

168 Compared with mismatch repair proficient (MMR-P) POLE wild-type tumours, POLE-mutant colorectal ca

169 % reduction in the maternal mortality ratio (MMR) between 1990 and 2015.

170 3.49 was denoted as the lead cross-reactive MMR-targeting sdAb.

171 in historical cohorts recommended to receive MMR vaccine before school entry, and on-time vaccination

172 Of the contacts included, 44 received MMR PEP and 77 received IG PEP.

173 A total of 278 children (71.1%) had received MMR followed by MMRV vaccine, 97 (24.8%) had received MM

174 wed by MMRV vaccine, 97 (24.8%) had received MMR vaccine only, and 16 (4.1%) had received neither vac

175 s who lost MMR on de-escalation and regained MMR on TKI resumption.

176 ccurred, and all relapsing patients regained MMR and MR4.5 after restarting therapy.

177 d molecular recurrence, all of whom regained MMR within 4 months of full-dose TKI resumption (median

178 enefit is called modulation masking release (MMR).

179 opathologic significance of mismatch repair (MMR) defects in endometrioid endometrial cancer (EEC) ha

180 Mismatch repair (MMR) deficiency (MMRD) and microsatellite instability (M

181 ncluding: tumor testing for mismatch repair (MMR) deficiency in Lynch syndrome establishing a new par

182 Mismatch repair (MMR) deficiency was determined by microsatellite instabi

183 tic variables that included mismatch repair (MMR) deficiency, ColDx high-risk patients exhibited sign

184 Decreased expression of mismatch repair (MMR) gene MSH2 in cells exposed to oxidative stress sugg

185 y missense mutations in DNA mismatch repair (MMR) genes.

186 ne mutation in one of their mismatch repair (MMR) genes.

187 germline mutation in three mismatch repair (MMR) genes: MLH1, MSH2, and MSH6.

188 Mismatch repair (MMR) is a conserved mechanism exploited by cells to corr

189 Mismatch repair (MMR) is a near ubiquitous pathway, essential for the mai

190 thylation, methyl-dependent mismatch repair (MMR) is deleterious and, fueled by the drug-induced erro

191 Mismatch repair (MMR) is one of the main systems maintaining fidelity of

192 DNA mismatch repair (MMR) is required for the maintenance of genome stability

193 mple, by the well-known DNA mismatch repair (MMR) mechanism.

194 describe a large cohort of mismatch repair (MMR) mutation carriers ascertained through multigene pan

195 In Escherichia coli, a DNA mismatch repair (MMR) pathway corrects errors that occur during DNA repli

196 The DNA mismatch repair (MMR) pathway recognizes and repairs errors in base pairi

197 l-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to generate mutations at G-C and A-T base

198 of MutS homolog 2 (MSH2), a mismatch repair (MMR) protein, abrogated early inflammation-induced epige

199 nd Saccharomyces cerevisiae mismatch repair (MMR) proteins catalyze two MMR reactions in vitro.

200 mutations in genes encoding mismatch repair (MMR) proteins.

201 mine the association of DNA mismatch repair (MMR) status and somatic mutation in the B-Raf proto-onco

202 nation of MGMT activity and mismatch repair (MMR) status of the tumor are important parameters that d

203 e (mGPS), and combined BRAF-mismatch repair (MMR) status.

204 However, DNA mismatch repair (MMR) suppresses the efficiency of gene modification by >

205 The DNA mismatch repair (MMR) system corrects DNA mismatches in the genome.

206 matches are repaired by the mismatch repair (MMR) system, producing a gene conversion event.

207 tein of the methyl-directed mismatch repair (MMR) system, we achieved a transient suppression of DNA

208 on repair and MSH2-mediated mismatch repair (MMR) to yield mutations and DNA strand lesions.

209 d involvement of K-H in DNA mismatch repair (MMR) where K-H depletion led to concomitant MMR deficien

210 tide excision repair (NER), mismatch repair (MMR), non-homologous end joining (NHEJ), homologous reco

211 activity, small changes in mismatch repair (MMR), nucleotide excision repair (NER), and homologous r

212 , a key protein involved in mismatch repair (MMR), suppresses telomeric sequence insertion (TSI) at i

213 Mismatch repair (MMR)-deficient colorectal cancer cells formed heterozygo

214 quently in hypermutated DNA mismatch repair (MMR)-proficient tumors and appear to be responsible for

215 e excision repair (BER) and mismatch repair (MMR).

216 ofreading activity, and DNA mismatch repair (MMR).

217 atellite instability [MSI], mismatch repair [MMR] deficiency) is unknown.

218 We present the multi-mapper resolution (MMR) tool that infers optimal mapping locations from the

219 ing was quantified by the mismatch response (MMR) measured with a traditional oddball paradigm using

220 tients with stable major molecular response (MMR), but not MR4, have not been studied, nor has the ef

221 d as the loss of a major molecular response (MMR).

222 rall survival, and major molecular response (MMR).

223 Pan-caspase inhibitor treatment restored MMR protein loss.

224 case example of measles, mumps, and rubella (MMR) vaccination and measles.

225 Two doses of measles, mumps, and rubella (MMR) vaccine are 97% effective against measles, but wani

226 nely, the first measles, mumps, and rubella (MMR) vaccine dose is given at 14 months of age in the Ne

227 wo doses of the measles, mumps, and rubella (MMR) vaccine; and proportions with medical or personal-b

228 ible to receive the measles, mumps, rubella (MMR) vaccine.

229 ddlers given MMRV and measles-mumps-rubella (MMR) and a national cohort study of vaccine coverage rat

230 pediatric schedule of measles-mumps-rubella (MMR) or measles-mumps-rubella-varicella (MMRV) vaccine w

231 Measles-mumps-rubella (MMR) vaccination coverage with at least a single dose wa

232 rotect young infants, measles-mumps-rubella (MMR) vaccination was offered to those aged 6-14 months i

233 on of PCR testing and measles-mumps-rubella (MMR) vaccination.

234 Measles-mumps-rubella (MMR) vaccinations have been offered to Finnish children

235 g introduction of the measles-mumps-rubella (MMR) vaccine in 1988.

236 f a third dose of the measles-mumps-rubella (MMR) vaccine in stemming a mumps outbreak is unknown.

237 isk of mumps if they had received the second MMR dose 13 years or more before the outbreak.

238 status and years since receipt of the second MMR vaccine dose.

239 riant; 9 patients (18.8%) had double somatic MMR mutations (including 2 with germline biallelic MUTYH

240 :ABL1 ratio <0.01%; MR4 cohort) or in stable MMR (BCR-ABL1:ABL1 ratio consistently <0.1%) but not MR4

241 MMRV induced higher GMCs than MMR (P < .001).

242 hes are repaired by the MMR system; and that MMR repairs about three times more mismatches produced i

243 cidate a crucial mechanism that ensures that MMR is initiated only after detection of a DNA mismatch.

244 Our results provide direct evidence that MMR and BER, operating together, form a novel hybrid pat

245 This finding supports the idea that MMR occurs before the DNA mismatch is packaged into the

246 This latter observation indicates that MMR preferentially protects genes from mutation and has

247 For SNVs, we show that MMR deficiency both increases their frequency and change

248 Our final genome-wide analyses show that MMR deficiency disproportionately increases the numbers

249 cies, Arabidopsis thaliana We then show that MMR deficiency greatly increases the frequency of both s

250 Previous research has suggested that MMR coincides with replication-coupled assembly of the n

251 ents with MMR normal tumors, suggesting that MMR defects may counteract the effects of negative progn

252 The MMR and ITPC data from the children with autism showed e

253 able O(6)-mG-T mispair-containing DNA by the MMR system and CAF-1-dependent packaging of the newly re

254 ucleosomes suppresses its degradation by the MMR system, thereby defending the cell against killing b

255 ucleosomes suppresses its degradation by the MMR system.

256 most of these mismatches are repaired by the MMR system; and that MMR repairs about three times more

257 easily identified as being distinct from the MMR-D tumors with > 150 mutations each.

258 -4.8] of 121 evaluable patients) than in the MMR cohort (nine [19%; 90% CI 9.5-28.0] of 48 evaluable

259 implications of germline alterations in the MMR genes in rectal cancer.

260 ent a global mapping of hetDNA formed in the MMR-defective mlh1 strain.

261 o had multigene panel testing, including the MMR and EPCAM genes, between March 2012 and June 2015 (N

262 10, 2015, we enrolled 174 patients into the MMR cohort (n=49) or the MR4 cohort (n=125).

263 Our efficient implementation of the MMR algorithm is easily applicable as a post-processing

264 rious mutations that disrupt function of the MMR gene product: 31 in MLH1 (61%), 11 in MSH2 (21%), 3

265 sections were assessed for expression of the MMR proteins mutL homologue 1, mutS homologue 2, mutS ho

266 Specifically, an activity of the MMR system causes degradation of irreparable O(6)-mG-T m

267 nd that CAF-1 suppresses the activity of the MMR system in the cytotoxic response of yeast mgt1Delta

268 whether CAF-1 modulates the activity of the MMR system in the cytotoxic response to Sn1-type methyla

269 ears, and probably reflect the impact of the MMR vaccine programme and the use of more sensitive diag

270 sceptible persons, and administration of the MMR vaccine to more than 10,000 persons.

271 l, 97% had received at least one dose of the MMR vaccine, with 2.5% having personal-belief exemptions

272 Of the MMR-eligible, 3477 (53%) were not vaccinated at the visi

273 Paradoxically, the MMR-nicking complex Pms2/Mlh1 is apparently dispensable

274 Regional progress in reducing the MMR since 1990 ranged from an annual rate of reduction o

275 main protein 4 (MBD4) has been linked to the MMR pathway through its interaction with MutL homologue

276 had epigenetic MMR defects compared with the MMR normal group (hazard ratio, 1.37; P < .05; 95% CI, 1

277 We administered a third MMR dose (MMR3) to young adults and assessed immunogenic

278 A total of 1,024 tumors were assigned to MMR classes.

279 cificity and are preferentially cytotoxic to MMR-deficient cells.

280 spectra of spontaneous mutations similar to MMR-bearing species, suggesting the existence of an alte

281 ), Polio, Measles, Rubella, Mumps, trivalent MMR vaccine and Haemophilus influenza type B (HiB) vacci

282 mismatch repair (MMR) proteins catalyze two MMR reactions in vitro.

283 Measles, mumps, and rubella vaccine (MMR) or immune globulin (IG) are routinely used for meas

284 tumors with >/= 20 mutations, 28 (90%) were MMR-D.

285 % of the 193 tumors with < 20 mutations were MMR-proficient.

286 cultured in low doses of Nutlin-3a, whereas MMR-corrected counterparts did not.

287 a, health officials implemented a widespread MMR vaccine campaign.

288 Filtering alignments with MMR can significantly improve the performance of downstr

289 s determined for each case and compared with MMR status as determined by routine immunohistochemistry

290 tly reduced risk of recurrence compared with MMR-P colorectal cancers in multivariable analysis (HR 0

291 istone (H3-H4)2 tetramers is compatible with MMR and protects the discontinuous daughter strand from

292 model proposed that UNG could cooperate with MMR by excising a second uracil in the vicinity of the U

293 e (H3-H4)2 tetramers does not interfere with MMR reactions.

294 ar-old Finnish children vaccinated once with MMR vaccine at 11-19 months of age.

295 vestigation of cancer risks in patients with MMR mutations.

296 these patients were similar to patients with MMR normal tumors, suggesting that MMR defects may count

297 kely to determine outcomes for patients with MMR-deficient tumors.

298 Patients with MMR-proficient tumors and BRAF or KRAS mutations had sta

299 with MR4 or greater, but also in those with MMR but not MR4.

300 with the original masker, thresholds worsen (MMR-).