ライフサイエンスコーパス: MPM

1 MPM images corresponding to dysplastic nevi and melanoma

2 MPM imaging identified in vivo and noninvasively the mai

3 MPM is a rare but aggressive disease with poor treatment

4 MPM is largely unresponsive to conventional chemotherapy

5 MPM with moxifloxacin was demonstrated in various cell l

6 MPM, a noninvasive imaging modality that facilitates con

7 MPM-1-TIFSIX is thermally stable to 568 K and retains po

8 MPM-2 and Lsm11 foci are present in embryos lacking the

9 MPMs harvested from glabridin-treated E0 mice (20 microg

10 MPMs project population dynamics based on the reproducti

11 genome sequencing of tumor specimens from 10 MPM patients and matched control samples to identify pot

12 g nCounter system for miRNA profiling on 105 MPM samples and 10 healthy pleura.

13 A training set of 32 samples (16 MPM and 16 ADCA) was used to identify pairs of genes wit

14 phorylation of mitotic protein monoclonal-2 (MPM-2) mitotic proteins.

15 arcomatoid (H2373), and biphasic (MSTO-211H) MPM.

16 formed whole-exome sequencing on DNA from 22 MPMs and matched blood samples, and identified 517 somat

17 PM and lung cancer in 181 tissue samples (31 MPM and 150 ADCA).

18 ually to fold like potassium channels in a 4-MPM motif, instead of like conventional substrate porter

19 e topology of KdpA are consistent with the 4-MPM model, the one deviation can be explained by a plaus

20 Of the 43 MPM tissues and 7 cell lines, we have identified mutatio

21 ignaling components were characterized in 46 MPM patient tissue samples by RT-PCR and immunohistochem

22 we used an integrated genomic analysis of 53 MPM tumor samples to guide a focused sequencing effort t

23 These serines lie close to the Y(632)MPM motif that is implicated in the binding of p85alpha/

24 al twist, while an S configuration induced a MPM helical twist.

25 CD1c accommodated MPM's methylated alkyl chain exclusively in the A' pocke

26 etent and competent spermatocytes accumulate MPM-2 phosphoepitopes and phosphorylated histone H3 in r

27 paradigm for patients with locally advanced MPM.

28 39 is as effective or more effective against MPM cell lines as it is against the NSCLC cell line A549

29 d be an important target for therapy against MPM.

30 ly, ectopic expression of EPCR in aggressive MPM cells attenuated their growth potential, whereas EPC

31 ions that will improve the prognosis for all MPM patients.

32 ular signal-regulated kinases 1 and 2 in all MPM cell lines.

33 Although MPM is an extremely difficult disease to treat, with the

34 comes phosphorylated during maturation at an MPM-2 epitope and that this persists until the fertiliza

35 -phase kinase, which phosphorylates it at an MPM-2 epitope.

36 teric heat of adsorption yet reported for an MPM.

37 n = 4), normal pleura specimens (n = 5), and MPM and SV40-immortalized mesothelial cell lines (n = 5)

38 mal constituents gamma-tubulin, centrin, and MPM-2 (which detects phosphorylated epitopes) are traced

39 and the persistence of phosphohistone H3 and MPM-2 antibody staining.

40 Customization of SAPS II and MPM II0 to the Project IMPACT database resulted in well-

41 Customized versions of SAPS II and MPM II0 were obtained by fitting new logistic regression

42 nt in embryos lacking the histone locus, and MPM-2 foci are present in U7 mutants, which cannot corre

43 or the specific interaction between Pin1 and MPM-2 antigens.

44 Both Pin1 and MPM-2 selected similar phosphorylated serine-proline-con

45 ute, U7 small nuclear ribonucleoprotein, and MPM-2 phosphoepitope, we demonstrated sequential recruit

46 nce in outcome between patients with SPM and MPM related to factors other than closer surveillance an

47 Although overall fatalities due to SPM and MPM were similar, relative fatality for thicker SPM was

48 Current anti-MPM chemotherapy-based treatments are only marginally ef

49 The mitotic phosphoprotein antibody MPM-2 recognizes a significant subset of mitotically pho

50 mitotic SPB by the phospho-specific antibody MPM-2.

51 serine-proline-directed monoclonal antibody (MPM-2), and by changes in Cdc25 enzymatic activity.

52 ized by the mitotic phosphoprotein antibody, MPM-2.

53 he mitotic phosphoepitope-specific antibody, MPM-2, and co-localized with MPM-2 immunoreactivity in A

54 o-based diagnosis in differentiating between MPM and lung cancer in 181 tissue samples (31 MPM and 15

55 cal applicability for distinguishing between MPM and lung cancer.

56 found little difference in fatality between MPM and SPM (HR for MPM relative to SPM, 1.24 [95% CI, 0

57 ng three with either sarcomatoid or biphasic MPM.

58 s in serum samples from patients affected by MPM that specifically react with two different SV40 mimo

59 ) block production of angiogenic activity by MPMs and RAW cells.

60 The lipid portion of C32-MPM contains a C32-mycoketide, consisting of a saturated

61 beta-D-mannosyl phosphomycoketide (C32-MPM), a naturally occurring glycolipid found in the cell

62 ighly stereocontrolled method to prepare C32-MPM molecule with >96% stereopurity from a single >99% e

63 vations were made possible by using clearing MPM, demonstrating the utility of this technique for stu

64 ptember 2012 and April 2014, with a clinical MPM-based tomograph.

65 Conclusion MPM is an aggressive and rapidly fatal disease.

66 eded to validate the technique and correlate MPM performance with histopathologic examination.

67 ns are postulated to have four corresponding MPM motifs within a single sequence.

68 ated to gender and histology appear to drive MPM.

69 Notably, each MPM had a different mutation profile, and no mutated gen

70 verall survival in patients with epithelioid MPM undergoing EPP and suggests that those with simultan

71 11, a total of 529 patients with epithelioid MPM underwent complete resection by EPP as part of a mul

72 ion of Ad.EPCR into mice with an established MPM originating from MPM cells lacking EPCR reduced the

73 tudy, nine chemotherapy-naive patients (five MPM, four NSCLC) received weekly ADI-PEG 20 doses of 18

74 smer-Lemeshow statistic was 12.3 ( >.14) for MPM II0, and 8.17 (p >.42) for SAPS II, after customizat

75 operating characteristic curve was 0.83 for MPM II0 and 0.872 for SAPS II following model customizat

76 ved antibiotic, as a cell-labeling agent for MPM.

77 or NSCLC and by modified RECIST criteria for MPM.

78 uestioned the safety and efficacy of EPP for MPM.

79 ence in fatality between MPM and SPM (HR for MPM relative to SPM, 1.24 [95% CI, 0.91-1.69; P = .18]).

80 of this pathway could have implications for MPM resistance to chemotherapy.

81 obviate unnecessary invasive procedures for MPM.

82 athway is a potential therapeutic target for MPM.

83 B is found in all cells after its formation, MPM-2 labels the HLB only in cells with active Cyclin E/

84 ition in MPM cell lines in vitro, using four MPM cell lines derived from previously untreated patient

85 Mb of cDNA were sequenced from each of four MPMs, from a control pulmonary adenocarcinoma (ADCA), an

86 In the four MPMs, 15 nonsynonymous mutations were discovered: 7 were

87 FR), and a subset of cell lines derived from MPM patients express both EGFR and transforming growth f

88 nfirm microstructural measurements made from MPM images.

89 ice with an established MPM originating from MPM cells lacking EPCR reduced the progression of tumor

90 Our data indicate that in serum samples from MPM-affected patients (n = 97), the prevalence of antibo

91 The outputs from MPMs have direct biological interpretations, facilitatin

92 Glabridin inhibited superoxide release from MPMs in response to phorbol 12-myristate 13-acetate, or

93 We show that H2373 MPM cells, which show 89% growth inhibition at 10 microM

94 ligand hepatocyte growth factor (HGF) in H28 MPM cells, with robust expression of c-Met.

95 ignant pleural diseases (MPDs); 57 of 67 had MPM.

96 reas those with greater loss of function had MPMs and/or positive family history.

97 years; 75 men, 25 women) suspected of having MPM pleural abnormalities underwent positron emission to

98 However, MPM application to human tissues is limited by weak endo

99 ogical pathways in MPM using discarded human MPM tumor specimens (n = 40), normal lung specimens (n =

100 nant pleural mesothelioma (MPM), using human MPM cells that lack or express tissue factor, EPCR or PA

101 Three immortalized MPM cell lines (H2959, H2373 and H2591) were exposed to

102 immunohistochemistry was increased (82%) in MPM in general compared with normal.

103 ne resulted in moderate clinical activity in MPM.

104 f miRNAs expression is highly deregulated in MPM and that a 2-miRNA signature can be a new useful too

105 Previously observed differences in MPM RNA expression levels were confirmed.

106 Single-agent erlotinib was not effective in MPM, despite high expression of EGFR.

107 ha, suggesting an autocrine role for EGFR in MPM.

108 ndothelial cell protein C receptor (EPCR) in MPM cells suppresses tumorigenicity.

109 sk (3.3 [1.43-7.43]; P < .01), especially in MPM (4.5 [1.83-11.01]; P < .01) and high nevi count (>20

110 mmary, our data show that EPCR expression in MPM cells promotes tumor cell apoptosis, and intrapleura

111 Expression in MPM tissues by immunohistochemistry was increased (82%)

112 irmed as an independent prognostic factor in MPM (HR 2.07, 95% CI 1.23-3.46; P = 0.01).

113 ies have failed to reveal SV40 footprints in MPM and its association with this neoplasm.

114 d CD36 expression and foam cell formation in MPM.

115 no mutated gene was previously implicated in MPM.

116 determined the effects of EGFR inhibition in MPM cell lines in vitro, using four MPM cell lines deriv

117 influnine, a novel microtubule inhibitor, in MPM.

118 o-factor, and we show that BAP1 knockdown in MPM cell lines affects E2F and Polycomb target genes.

119 hyper-methylation caused very low levels in MPM cell lines and specimens.

120 with a focus on the expanding role of MMT in MPM.

121 tified important common somatic mutations in MPM, these studies have focused on small sets of genes a

122 dies showed that by day 4, most organisms in MPM were not viable.

123 al molecular and pathobiological pathways in MPM using discarded human MPM tumor specimens (n = 40),

124 re can be a new useful tool for prognosis in MPM.

125 ary, Gli activation plays a critical role in MPM.

126 l resection increase survival selectively in MPM patients with normal pretreatment serum CRP levels.

127 mcitabine has not previously been studied in MPM to our knowledge.

128 ic model was reported to predict survival in MPM.

129 cted, although at a lower prevalence than in MPM, in blood specimens from healthy donors.

130 of EGFR tyrosine kinase inhibitors (TKIs) in MPM.

131 ination is both active and well tolerated in MPM and deserves further exploration.

132 e significantly mutated (q-score >/= 0.8) in MPMs.

133 , RNA helicase and p53 signaling pathways in MPMs.

134 h BKM120 was highly synergetic in inhibiting MPM tumor growth.

135 transfecting miRNA mimics or inhibitors into MPM cell lines, and performing Matrigel invasion, cell p

136 graphic metrics that can be derived from its MPMs.

137 emic brain and mouse peritoneal macrophages (MPM).

138 studies, using mouse peritoneal macrophages (MPMs) and the J-774 A.1 macrophage-like cell line.

139 The main MPM feature associated with the BCC lesions involved nes

140 and risk for multiple primary malignancies (MPMs).

141 t MPM-1-TIFSIX, a molecular porous material (MPM) based upon the neutral metal complex [Cu2(adenine)4

142 als with incident multiple primary melanoma (MPM) and 2424 with incident single primary melanoma unse

143 271 patients with multiple primary melanoma (MPM) without mutations affecting p16INK4A (wild-type p16

144 nomas (SPMs) and multiple primary melanomas (MPMs) of any stage.

145 dified perforated bovine collagen membranes (MPM test group, 10 sites).

146 Malignant pleural mesothelioma (MPM) carries a poor prognosis due to chemoresistance.

147 tissues and malignant pleural mesothelioma (MPM) cell lines as compared to benign tissues (pleura, p

148 Malignant pleural mesothelioma (MPM) expresses high levels of epidermal growth factor re

149 Malignant pleural mesothelioma (MPM) is a deadly disease that occurs in 2,000 to 3,000 p

150 Malignant pleural mesothelioma (MPM) is a disease of increasing incidence for which trea

151 Malignant pleural mesothelioma (MPM) is a highly aggressive and generally incurable canc

152 Malignant pleural mesothelioma (MPM) is a highly aggressive tumor with poor prognosis.

153 Malignant pleural mesothelioma (MPM) is a highly lethal, poorly understood neoplasm that

154 Malignant pleural mesothelioma (MPM) is a rare malignancy with no known curative modalit

155 Malignant pleural mesothelioma (MPM) is an aggressive cancer that is commonly associated

156 Malignant pleural mesothelioma (MPM) is an aggressive cancer that occurs more frequently

157 Malignant pleural mesothelioma (MPM) is an aggressive human cancer and miRNAs can play a

158 Malignant pleural mesothelioma (MPM) is an aggressive neoplasm associated with asbestos

159 Malignant pleural mesothelioma (MPM) is an aggressive thoracic cancer with a high mortal

160 Human malignant pleural mesothelioma (MPM) is considered a rare tumor, but recent estimations

161 IMPRINT for malignant pleural mesothelioma (MPM) is safe and has an acceptable rate of RP.

162 S1-deficient malignant pleural mesothelioma (MPM) or non-small-cell lung cancer (NSCLC).

163 03) from 216 malignant pleural mesothelioma (MPM) tumors.

164 Treatment of malignant pleural mesothelioma (MPM) with Ranpirnase (Onconase) results in disruption of

165 he growth of malignant pleural mesothelioma (MPM), using human MPM cells that lack or express tissue

166 treatment of malignant pleural mesothelioma (MPM).

167 activity in malignant pleural mesothelioma (MPM).

168 y studied in malignant pleural mesothelioma (MPM).

169 atients with malignant pleural mesothelioma (MPM).

170 epithelioid malignant pleural mesothelioma (MPM).

171 surgery for malignant pleural mesothelioma (MPM); however, it is unclear if these results are genera

172 tion between malignant pleural mesothelioma (MPM)and adenocarcinoma (ADCA) of the lung can be cumbers

173 xpressed in malignant pleural mesotheliomas (MPM), was detected in serum using an electrochemical sur

174 LC), and 71 malignant pleural mesotheliomas (MPM).

175 s unique to malignant pleural mesotheliomas (MPMs) and not present in control tissues.

176 Malignant pleural mesotheliomas (MPMs) often show CDKN2A and NF2 inactivation, but other

177 detected in malignant pleural mesotheliomas (MPMs), their role in the pathogenesis and clinical behav

178 on method used is the material point method (MPM), and the particular variation used here takes advan

179 tiphoton excitation fluorescence microscopy (MPM) can image certain molecular processes in vivo.

180 Multiphoton microscopy (MPM) has found a niche in the world of biological imagin

181 Multiphoton microscopy (MPM) holds promise as a noninvasive imaging technique fo

182 We analyzed multiphoton microscopy (MPM) images corresponding to 15 lesions (five in each gr

183 Multiphoton microscopy (MPM) is a nonlinear fluorescence microscopic technique w

184 evelopment of serial multiphoton microscopy (MPM) of the same glomeruli over several days to visualiz

185 ecent translation of multiphoton microscopy (MPM) to clinical practice raises the possibility of noni

186 resolution live-cell multiphoton microscopy (MPM) to directly observe cellular interactions and dynam

187 g approach that uses multiphoton microscopy (MPM) to directly visualize podocyte [Ca(2)(+)]i dynamics

188 the new technique of multiphoton microscopy (MPM) with clearing to a new mouse model of cisplatin-ind

189 onics, particularly multi-photon microscopy (MPM) and new molecular and genetic tools are empowering

190 enopus Cdc25C and characterizing the mitotic MPM-2 epitope kinases in Xenopus oocytes and egg extract

191 By mapping the mitotic MPM-2 epitopes in Xenopus Cdc25C and characterizing the

192 cently developed multistate parabolic model (MPM).

193 urvival by using Mortality Prediction Model (MPM-0) scores, age, gender, and number of units of packe

194 (SAPS) II, and Mortality Probability Models (MPM) II were evaluated for discrimination and calibratio

195 Matrix population models (MPMs) are among the most widely used demographic tools b

196 r to contain four sequential M1-P-M2 motifs (MPM), which are likely to have arisen from gene duplicat

197 We evaluated the new MPM medium for the growth of Borrelia burgdorferi.

198 ial, whereas EPCR silencing in nonaggressive MPM cells engineered to overexpress tissue factor increa

199 issue factor overexpression in nonaggressive MPM cells that expressed EPCR and PAR1 with minimal leve

200 e patients with unresectable, nonsarcomatoid MPM (Eastern Cooperative Oncology Group performance stat

201 enhanced clinical outcomes when using novel MPMs compared to OMs in guided tissue regeneration proce

202 Intrapleural administration of MPM cells expressing tissue factor and PAR1 but lacking

203 first unbiased view of the genomic basis of MPM.

204 The M phase-associated burst of MPM-2 reactivity can be induced in Xenopus oocytes and e

205 ndicate that the M phase-associated burst of MPM-2 reactivity represents a novel type of protein phos

206 dominant role in M phase-associated burst of MPM-2 reactivity.

207 nciples and evolving concepts in the care of MPM patients with a focus on the expanding role of MMT i

208 ssessed by comparing frequencies in cases of MPM versus cases with a single first primary melanoma, a

209 we found that the differential diagnoses of MPM and lung ADCA were 95% and 99% accurate, respectivel

210 seful in the early and accurate diagnosis of MPM and lung cancer.

211 with a histologically confirmed diagnosis of MPM were eligible for enrollment onto this multicenter p

212 ts with histologic or cytologic diagnosis of MPM were included.

213 The homology of MPM motifs is supported by a statistical comparison of t

214 beled anti-HER1 antibodies in the imaging of MPM in preclinical models.

215 ld be further evaluated in the management of MPM.

216 PAR1, and an orthotopic nude mouse model of MPM.

217 s the progression of MPM in a mouse model of MPM.

218 iptional deregulation in the pathogenesis of MPM.

219 ates the versatility and predictive power of MPM, an important new tool for the design and synthesis

220 ne therapy could suppress the progression of MPM in a mouse model of MPM.

221 modulated some protumorigenic properties of MPM cells, such as clonogenicity, cell migration and res

222 tations and has implications for revision of MPM staging criteria.

223 ession was investigated in a large series of MPM to discover new pathways helpful in diagnosis, progn

224 est that SV40 is associated with a subset of MPM and circulates in humans.

225 trated synergistic effects in suppression of MPM proliferation in vitro.

226 mir-145-OCT4 interaction for the survival of MPM cells.

227 Treatment of MPM cell lines with mir-145 agonists negatively modulate

228 Treatment of MPM cells with these inhibitors also significantly decre

229 was to evaluate survival after treatment of MPM with cancer-directed surgery and to explore the effe

230 the latest developments in the treatment of MPM.

231 s may advance the molecular understanding of MPM and identify therapeutic interventions that will imp

232 We recommend users of MPM make MPM0-III their primary model.

233 tic inactivating mutations in BAP1 in 23% of MPMs.

234 Approximately 70% of MPMs have high levels of expression of the epidermal gro

235 mal demographic records exist in the form of MPMs, but they are dispersed throughout the literature,

236 overexpressed and activated in a majority of MPMs.

237 and image correlation spectroscopy (ICS) on MPM, scanning electron, and darkfield microscopy images.

238 not related to the amount of EGFR present on MPM cells or to the degree of inhibition of EGFR phospho

239 growth) bearing subcutaneous and orthotopic MPM tumors by using HER1- and HER2-targeted indium 111 (

240 Other MPM features included elongated tumor cells in the epide

241 observed in at least one tumor from 49 other MPM patients.

242 is antigen mannosyl-beta1-phosphomycoketide (MPM).

243 from 115 patients with histologically proven MPM.

244 Methods Patients with microscopically proven MPM were identified within the National Cancer Database

245 tion without ERK activity diminishes IP(3)R1 MPM-2 reactivity and [Ca2+](i) responses.

246 es demonstrated that EPCR expression renders MPM cells highly susceptible to IFNgamma + TNFalpha-indu

247 We report MPM-1-TIFSIX, a molecular porous material (MPM) based up

248 e found that relative to 3T3 cells, resident MPM and tg-MPM express low amounts of caveolin-1 (45 and

249 S-MPM exhibited excellent discrimination (C statistic, 0.8

250 The 9-point S-MPM (Surgical Mortality Probability Model) 30-day mortal

251 lower mutation rates observed in sarcomatoid MPM (P < 0.001).

252 uvate carboxykinase (PEPCK)-GFP mice, serial MPM found PEC-to-podocyte migration and nanotubule conne

253 om gene duplication and fusion of the single MPM motif of a bacterial K(+) channel subunit.

254 hough the channels are formed by four single-MPM motif subunits, the transmembrane KdpA subunit and t

255 ymporters has remained closest to the single-MPM ancestor protein.

256 cal and pathological characteristics of SPM, MPM, and both in Cox proportional hazards regression mod

257 igate the mechanism by which EPCR suppresses MPM tumor growth and evaluate whether EPCR gene therapy

258 nd intrapleural EPCR gene therapy suppresses MPM progression.

259 t relative to 3T3 cells, resident MPM and tg-MPM express low amounts of caveolin-1 (45 and 15% of tho

260 ells examined, with highest expression in tg-MPM and the lowest in J774 cells.

261 te-elicited mouse peritoneal macrophages (tg-MPM) and in the J774 mouse macrophage cell line by RT-PC

262 Loading of tg-MPM with cholesterol or variations in unesterified chole

263 We conclude that MPM and ICS are an effective combination to assess bulk

264 These data indicate that MPM-2 recognizes a Cdk2-regulated protein that assembles

265 Cell viability results showed that MPM cells were highly sensitive to crizotinib, BKM120 an

266 The MPM images were compared with histopathologic findings.

267 nt in histone deletion embryos, although the MPM-2 foci are smaller, and some Lsm11 foci are not asso

268 centromeric histone H3-like protein and the MPM-2 antibody, which identifies a kinetochore-associate

269 l cycle-regulated proteins recognized by the MPM-2 antibody were not detectable in anoxic embryos.

270 We show that in Drosophila embryos the MPM-2 monoclonal antibody, raised against a phosphoepito

271 CBL was significantly higher in the MPM group when compared with that of the OM group at bot

272 opathology criteria can be identified in the MPM images.

273 and 9 months, respectively, in favor of the MPM-treated sites.

274 At 6- and 9-month observation periods, the MPM-treated sites showed a statistically significant imp

275 hicker SPM was greater than that for thicker MPM.

276 mm, 13.56 [95% CI, 6.47-28.40]) than thicker MPM (2.93 [1.17-7.30]).

277 This MPM is amenable to room-temperature synthesis and activa

278 tial of Gli as a therapeutic target to treat MPM.

279 ovel, clinically effective approach to treat MPM.

280 pathway is an effective strategy in treating MPM as compared to a single agent.

281 entify potential driver mutations underlying MPM.

282 Using MPM-2 and anti-Lsm11 antibodies, we demonstrate that the

283 djusted for probability of survival by using MPM-0 scores showed nosocomial infection to occur at con

284 patient population, that noninvasive in vivo MPM imaging can provide label-free contrast that reveals

285 In vivo MPM-2 staining and in vitro kinase assays established th

286 colony formation (41-89% at 10 microM) when MPM cells were grown in soft agarose.

287 and some Lsm11 foci are not associated with MPM-2 foci, suggesting that the histone locus is importa

288 y-seven patients (23 male, four female) with MPM were treated on five escalating dose levels.

289 eural lavage showed that mice implanted with MPM cells expressing EPCR had elevated levels of IFNgamm

290 and TNFalpha compared to mice implanted with MPM cells lacking EPCR.

291 cific antibody, MPM-2, and co-localized with MPM-2 immunoreactivity in AD neurons.

292 Forty-four resectable patients with MPM underwent pleurectomy, followed by a 1-hour lavage o

293 Results Of 20,561 patients with MPM, 6,645 were identified in the matched cohort, among

294 ed with high-dose intensity in patients with MPM.

295 otinib in previously untreated patients with MPM.

296 fective therapeutic option for patients with MPM.

297 ies to be associated at high prevalence with MPM.

298 one phosphatase-sensitive band reacted with MPM-2 antibody that recognizes a phosphoepitope phosphor

299 type p16INK4A, 2.6% (7 of 271) in those with MPM, and 2.9% (2 of 69) in the probands of families with

300 In patients with MPMs, ACC was the most frequent initial malignancy.