ライフサイエンスコーパス: MMR

1 MMR deficiency was defined by complete loss of nuclear e

2 MMR proteins were also down-regulated in patient-derived

3 MMR-3 receipt increased antibody levels that may protect

4 MMR-deficient gliomas were characterized by a lack of pr

5 MMR-IHC with targeted MLH1-methylation testing was more

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

7 .5% (468/484) specificity; 64% MSI-H and 73% MMR deficient tumours unexplained by LS or MLH1-hypermet

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

9 6-14-month-olds in municipalities with <90% MMR vaccination coverage.

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

11 scrambling the IDRs in both subunits ablates MMR in vivo.

12 y, some parents are still hesitant to accept MMR vaccination of their children.

13 responses to anti-PD-1 immunotherapy across MMR-deficient human cancers.

14 imilarly, no increased risk for autism after MMR vaccination was consistently observed in subgroups o

15 e not observed in infants vaccinated against MMR (measles, mumps, and rubella), but were confirmed in

16 MRP cohort with normal IHC expression of all MMR proteins.

17 After an MMR vaccine booster dose, we noted a seroconversion of 7

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

19 wo percent of 4,902 screened patients had an MMR-deficient cancer by IHC.

20 Experiments were performed in an MMR-proficient strain, a strain with compromised mismatc

21 the state-level synthetic control analysis, MMR coverage in California increased by 3.3% relative to

22 nts with tumours harbouring NTRK fusions and MMR deficiencies, respectively, regardless of primary tu

23 f the POLE allele, its expression level, and MMR status.

24 mulation on DNA interferes with both MMR and MMR-independent process(es).

25 Hazard ratios for MMRV and MMR + V versus MMR estimated in the per-protocol cohort

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

27 tions and immunohistochemistry-based p53 and MMR protein expression.

28 s are corrected by Poldelta proofreading and MMR.

29 ella vaccine and collectively referred to as MMR vaccine) uptake was monitored with the use of the Ci

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 tudies have not found an association between MMR vaccination and autism, including a study that found

33 The aIRR for the association between MMR-2 and admissions for infection of any duration was 0

34 There was no association between MMR-2 and antibiotic prescriptions (aIRR, 1.01; 95% conf

35 ver-accumulation on DNA interferes with both MMR and MMR-independent process(es).

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 ssociated with acquired resistance driven by MMR defects in chemotherapy-sensitive gliomas that recur

39 Severe illness by MMR vaccines can be caused by inborn errors of type I an

40 ion of phenotypes underlies the catastrophic MMR defect seen with the mutant MutLalpha in vivo.

41 Comparing MMR-vaccinated with MMR-unvaccinated children yielded a

42 pital admissions for any infection comparing MMR-2 as most recent vaccine with not having MMR-2 as th

43 mitation of the study was failure to conduct MMR germline sequencing for the whole study population,

44 es and identify patients with constitutional MMR-deficiency syndrome.

45 Tumors with mismatch repair deficiency (MMR-d) are characterized by sequence alterations in micr

46 ity (MSI) and/or mismatch repair deficiency (MMR-D) testing has traditionally been performed in patie

47 can identify DNA mismatch repair deficient (MMR-D) and/or tumor mutational burden-high (TMB-H) endom

48 g of LS-positive MSI-H/I tumors demonstrated MMR-D in 98.2% (56 of 57) of available cases.

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

50 ms1 complexes with shorter IDRs that disrupt MMR retain wild-type DNA binding affinity but are impair

51 diomic-clinical classification distinguished MMR-D from copy number (CN)-low-like and CN-high-like EC

52 ntify previously unappreciated roles for DNA MMR as a central modulator of cellular fate and a contri

53 riants in MLH1 and MSH2 cause defects in DNA MMR.

54 re treatment through the upregulation of DNA MMR.

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

56 virally induced oxidative damage by the DNA MMR pathway not only allowed cell survival of infection,

57 Enhanced viral suppression of the DNA MMR pathway prevented club cell survival and increased t

58 Young adults with two documented MMR doses were administered MMR3.

59 Dominant MMR models posit that after mismatch recognition, ATP co

60 0.01) after the introduction of the two-dose MMR vaccine.

61 ne measles-mumps-rubella vaccine (MMR) dose (MMR + V), versus two MMR doses (control vaccine) for the

62 studies concluded that Escherichia coli (Ec) MMR employed EcMutS, EcMutL, EcMutH, EcUvrD, EcSSB and o

63 y the Elg1 complex is critical for efficient MMR: PCNA needs to be on DNA long enough to enable MMR,

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

65 mumps-rubella (MMR) vaccine (given as either MMR or measles-mumps-rubella-varicella vaccine and colle

66 CNA needs to be on DNA long enough to enable MMR, but if it is retained too long it interferes with d

67 omotes DNA configurations that could enhance MMR efficiency by facilitating MutLalpha nicking the DNA

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

69 We designed a decision tree to evaluate MMR vaccination at a pretravel health encounter (PHE), c

70 Four weeks following MMR-3 receipt, levels of IgG, anti-vaccine strain, and a

71 7.9-99.6) for MMRV and 89.5% (86.1-92.1) for MMR + V.

72 4.0-96.4) for MMRV and 67.2% (62.3-71.5) for MMR + V; vaccine efficacy against moderate or severe var

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 egies for risk stratifying women with EC for MMR germline sequencing.

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

77 Also, genomics for MMR are warranted.

78 IHC for MMR assessment is a useful tool for patient selection.

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

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

81 H/I tumors, immunohistochemical staining for MMR-D was assessed.

82 re mutagenesis in the presence of functional MMR.

83 Fusions were present in 5% of MSI-H/MMR-D colorectal carcinoma compared with 0.4% of MSS/MMR

84 ectal carcinoma (P < 0.001) and 15% of MSI-H/MMR-D colorectal carcinoma with wild-type RAS/BRAF.

85 MSI-H/MMR-D is predictive of LS across a much broader tumor sp

86 ogrammed death-ligand 1 expression and MSI-H/MMR-D status were not associated with objective response

87 assessment for LS for patients with an MSI-H/MMR-D tumor, regardless of cancer type or family cancer

88 Two of six patients with MSI-H/MMR-D tumors responded.

89 MSI-H/MMR-D tumors, for which pembrolizumab is a standard ther

90 high and/or mismatch repair deficient (MSI-H/MMR-D) status, and somatic and germline genomic correlat

91 ) of colorectal carcinoma fusions were MSI-H/MMR-D.

92 1.8% to 5.1%) had LS, and 11 more (2.2%) had MMR variants of uncertain significance.

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

94 ractory cancers (2.0% of those screened) had MMR deficiency as defined in NCI-MATCH.

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

96 MMR-2 as most recent vaccine with not having MMR-2 as the most recent vaccine.

97 return to US communities with heterogeneous MMR coverage.

98 turning to US communities with heterogeneous MMR coverage.

99 turning to US communities with heterogeneous MMR coverage.

100 1), but thereafter mortality was not higher (MMR = 0.94; 95% CI, 0.47-1.86).

101 is achieved moderate accuracy in identifying MMR-D and TMB-H ECs directly from CE-CT.

102 PHEs that improve MMR vaccination among US international travelers could r

103 Nivolumab has promising activity in MMR-deficient noncolorectal cancers of a wide variety of

104 e response to PD-1 blockade immunotherapy in MMR-d human and mouse tumors.

105 did not detect microsatellite instability in MMR-deficient gliomas, single-cell whole-genome sequenci

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

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

108 lexes found in mammals and a minor player in MMR.

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

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

111 etween Lynch syndrome-associated variants in MMR genes and risks of adenoma and CRC and somatic mutat

112 ntries, we associated pathogenic variants in MMR genes with risk of adenoma and CRC, and somatic muta

113 ng agent can determine the effects of VUS in MMR genes and identify patients with constitutional MMR-

114 e consistent with an exonuclease-independent MMR strand excision mechanism that relies on EcMutL-EcUv

115 oteins MutSalpha and MutLalpha that initiate MMR cause Lynch syndrome, the most common hereditary can

116 In strains lacking MMR, the mismatches persist.

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

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

119 letely for a further 2 years, without losing MMR.

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

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

122 ch is the recommended age of the second MMR [MMR-2]) until age 60 months.

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

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

125 e loss of nuclear expression of MLH1 or MSH2 MMR gene products by immunohistochemistry (IHC).

126 available LS CRCs demonstrated abnormal MSI/MMR results.

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

128 lorectal carcinoma compared with 0.4% of MSS/MMR-P colorectal carcinoma (P < 0.001) and 15% of MSI-H/

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

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

131 ould increase the probability that MutS-MutL MMR initiation complexes localize near the mismatch.

132 pairs) by MSH2 and MLH1 (likely noncanonical MMR).

133 bias characteristic of organisms with normal MMR function.

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

135 Decreasing acceptance of MMR vaccination has led to outbreaks or resurgence of me

136 cting peptide motif, causing accumulation of MMR intermediates.

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

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

139 1) to receive two doses of MMRV, one dose of MMR and one dose of varicella vaccine, or two doses of M

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

141 lliamsburg who received at least one dose of MMR vaccine increased from 79.5% to 91.1% among children

142 persons who might have received two doses of MMR but lack documentation.

143 e dose of varicella vaccine, or two doses of MMR, 42 days apart.

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

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

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

147 No evidence of MMR infections was found, but 8 (0.7%) SOT recipients de

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

149 endence is not attributable to acute loss of MMR gene function but might arise during sustained MMR-d

150 bservations contrast with dominant models of MMR initiation that envision diffusive MutS-MutL complex

151 However, the significance of MMR mutations in lung cancer has not been well character

152 Patients who tested nonimmune were offered MMR vaccination or intravenous immunoglobulin depending

153 llance guidelines might be adjusted based on MMR gene variants.

154 remaining 8 VUS had intermediate effects on MMR capacity and could not be classified.

155 registries were used to link information on MMR vaccination, autism diagnoses, other childhood vacci

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

157 therapy in high-frequency MSI (MSI-H) and/or MMR-D tumors now supports testing for MSI in all advance

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

159 00] was calculated for MMR, IG, and any PEP (MMR or IG) for nonimmune contacts aged <19 years.

160 ormal (p53abn), POLE-ultramutated (POLEmut), MMR-deficient (MMRd), or no specific molecular profile (

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

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

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

164 o examine the trends of the overall CS rate, MMR, and PMR across different stages.

165 outcomes included maternal mortality ratio (MMR) and perinatal mortality rate (PMR), all obtained fr

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

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

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

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

170 EGFRvIII-specific knockdown reduced MMR protein expression thereby increasing TMZ resistance

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

172 All recurrences regained MMR within 5 months of treatment resumption.

173 n EGFRvIII expressing cells, which regulates MMR protein expression downstream of EGFRvIII.

174 A shared paradigm of mismatch repair (MMR) across biology depicts extensive exonuclease-driven

175 F inhibition down-regulates mismatch repair (MMR) and homologous recombination DNA-repair genes and c

176 n using yeast defective for mismatch repair (MMR) and/or leading strand (Polepsilon) or lagging stran

177 a central co-ordinator for mismatch repair (MMR) as well as DNA replication.

178 yeast MutLalpha (Mlh1-Pms1) mismatch repair (MMR) complex.

179 DNA mismatch repair (MMR) corrects errors that occur during DNA replication.

180 Mismatch repair (MMR) deficiencies are a hallmark of various cancers caus

181 notably BRCA1/2 mutations, mismatch repair (MMR) deficiencies or NTRK1-3 fusions, have shown conside

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

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

184 is dependent on functional mismatch repair (MMR) factors, including MutLgamma, a heterodimer of MLH1

185 s caused by variants in DNA mismatch repair (MMR) genes and associated with an increased risk of colo

186 fects in DNA polymerase and mismatch repair (MMR) genes, and a more common post-treatment pathway, as

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

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

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

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

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

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

193 we discovered that the DNA mismatch repair (MMR) pathway is essential for club cell survival of IAV

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

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

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

197 enotype requires functional mismatch repair (MMR) proteins and p53.

198 f expression of one or more mismatch repair (MMR) proteins and/or documented mutation in the exonucle

199 a higher expression of DNA mismatch repair (MMR) proteins in EGFRvIII+ cells and patient tumor sampl

200 ohistochemistry for p53 and mismatch repair (MMR) proteins, and DNA sequencing for POLE exonuclease d

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 The post-replicative mismatch repair (MMR) system has anti-recombination activity that limits

205 more, TC-NER interacts with mismatch repair (MMR) under physiological conditions to produce strand bi

206 repair pathways, including mismatch repair (MMR), have been linked to higher tumor mutation burden a

207 Mismatch repair (MMR), IHC, and promoter hypermethylation status of MLH1

208 MSI, caused by defective mismatch repair (MMR), occurs frequently in colorectal, endometrial and g

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

210 DNA mismatch repair (MMR), the guardian of the genome, commences when MutS id

211 eviously showed activity in mismatch repair (MMR)-deficient colon cancer.

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

213 variants, with and without mismatch repair (MMR).

214 genes are required for DNA mismatch repair (MMR).

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

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

217 ng Poldelta proofreading or mismatch repair (MMR).

218 thogenic variants affecting mismatch-repair (MMR) genes.

219 demonstrate that signature mismatch-repair (MMR) mutations activate enhancers using a xenograft tumo

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

221 o) less than 0.1% (major molecular response [MMR]) in the 12 months before entry.

222 ination against measles, mumps, and rubella (MMR) and yellow fever (YF) with live attenuated viruses

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

224 on coverage of measles, mumps, and rubella (MMR) vaccination, nonmedical exemption, and medical exem

225 suggested that measles, mumps, and rubella (MMR) vaccine causes autism.

226 ecommended 2 doses of mumps-measles-rubella (MMR) vaccine.

227 ed link between the measles, mumps, rubella (MMR) vaccine and autism continues to cause concern and c

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

229 Increasing measles-mumps-rubella (MMR) vaccination among departing US travelers could redu

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

231 Measles-mumps-rubella (MMR) vaccine (given as either MMR or measles-mumps-rubel

232 ction of the two-dose measles-mumps-rubella (MMR) vaccine in 1996, and the implementation of the Newb

233 immunized (2 doses of measles-mumps-rubella [MMR] vaccine) students and residents were tested; 305 of

234 , which is the recommended age of the second MMR [MMR-2]) until age 60 months.

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

236 the participants (80%) received their second MMR vaccine >=10 years prior to study participation.

237 Somatic MMR sequencing was performed when indicative molecular f

238 eliably identified both germline and somatic MMR mutations.

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

240 d by LS or MLH1-hypermethylation had somatic MMR mutations.

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

242 merits further study in patients with stable MMR.

243 ne function but might arise during sustained MMR-deficiency.

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

245 nd autism, including a study that found that MMR vaccine was not associated with an increased risk of

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

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

248 Our results suggest that MMR signature mutations activate enhancers in CRC tumor

249 The study strongly supports that MMR vaccination does not increase the risk for autism, d

250 The MMR (Z = -4.368, p < 0.001) and PMR (Z = -13.142, p < 0.

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

252 The MMR process causes death of cells with methylation-damag

253 children from the MMRV group, 2266 from the MMR + V group, and 744 from the MMR group.

254 266 from the MMR + V group, and 744 from the MMR group.

255 children in the MMRV group, 469 (21%) in the MMR + V group, and 352 (47%) in the MMR group had varice

256 in the MMRV group, 317 (16%) of 1978 in the MMR + V group, and 93 (15%) of 641 in the MMR group.

257 -4.8] of 121 evaluable patients) than in the MMR cohort (nine [19%; 90% CI 9.5-28.0] of 48 evaluable

258 Using tumor models defective in the MMR gene Mlh1 (dMLH1), we show that dMLH1 tumor cells ac

259 ) in the MMR + V group, and 352 (47%) in the MMR group had varicella.

260 In the MMR group, 16 (33%) entrants completed the study and rec

261 he MMR + V group, and 93 (15%) of 641 in the MMR group.

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

263 ay 6, 2015, we enrolled 49 patients into the MMR group and 125 into the MR4 group.

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

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

266 between 0.1% and 0.01% were allocated to the MMR group.

267 harges for rubella is most likely due to the MMR vaccine.

268 nomas (GOAs) show better outcomes than their MMR-proficient counterparts and high immunotherapy sensi

269 stimate hazard ratios of autism according to MMR vaccination status, with adjustment for age, birth y

270 utL complex that is the major contributor to MMR, is either not required for expansion or plays a lim

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

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

273 ing Rh-PPO as a chemotherapeutic targeted to MMR-deficient cancers.

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

275 in 1053 (27.1%) fewer cases requiring tumor MMR IHC.

276 d in 668 (17.2%) fewer cases requiring tumor MMR IHC.

277 lla vaccine (MMR) dose (MMR + V), versus two MMR doses (control vaccine) for the prevention of confir

278 icative tumour molecular features, underwent MMR germline sequencing.

279 Tumours underwent MMR immunohistochemistry (IHC), microsatellite instabili

280 this study, we discovered a hitherto unknown MMR mechanism that modulates genome stability and has im

281 ven after one measles-mumps-rubella vaccine (MMR) dose (MMR + V), versus two MMR doses (control vacci

282 A third measles-mumps-rubella vaccine (MMR) dose (MMR3) is recommended in the United States for

283 he live measles, mumps, and rubella vaccine (MMR) is associated with a lower rate of off-target infec

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

285 third dose of measles-mumps-rubella vaccine (MMR-3) in 150 young adults.

286 Hazard ratios for MMRV and MMR + V versus MMR estimated in the per-protocol cohort using a Cox pro

287 The prespecified primary study outcome was MMR vaccination in the state analysis and overall vaccin

288 In total 132/500 tumours were MMR deficient by IHC of which 83/132 (63%) had MLH1-hype

289 nt with genesis before one year of age, when MMR vaccine is typically administered.

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

291 f the remaining patients had LS (16/132 with MMR deficiency, 12%).

292 common symptoms potentially associated with MMR.

293 by temozolomide-induced damage in cells with MMR deficiency.

294 vestigation of cancer risks in patients with MMR mutations.

295 Patients with MMR-deficient colorectal cancer were excluded.

296 te their tumor immunogenicity, patients with MMR-deficient tumors experience highly variable response

297 volumab would have activity in patients with MMR-deficient, noncolorectal tumors.

298 In this study, revaccination with MMR appeared safe in relation to off-target infections a

299 Comparing MMR-vaccinated with MMR-unvaccinated children yielded a fully adjusted autis

300 s and selectively induce cytotoxicity within MMR-deficient cells.