ライフサイエンスコーパス: MPM

1 MPM development spanned across decades and crucially dep

2 MPM images corresponding to dysplastic nevi and melanoma

3 MPM imaging identified in vivo and noninvasively the mai

4 MPM is a rare but aggressive disease with poor treatment

5 MPM is largely unresponsive to conventional chemotherapy

6 MPM nodules, protruding into the pleural cavity may have

7 MPM with moxifloxacin was demonstrated in various cell l

8 MPM, a noninvasive imaging modality that facilitates con

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

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

11 MPMs project population dynamics based on the reproducti

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

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

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

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

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

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

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

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

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

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

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

23 paradigm for patients with locally advanced MPM.

24 d be an important target for therapy against MPM.

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

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

27 T2A gene expression could be detected in all MPM cell lines, showing the highest expression in NCI-H2

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

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

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

31 teric heat of adsorption yet reported for an MPM.

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

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

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

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

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

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

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

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

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

41 ng three with either sarcomatoid or biphasic MPM.

42 0 reduced survival and proliferation in both MPM cell lines and primary cells and showed synergistic

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

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

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

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

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

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

49 Conclusion MPM is an aggressive and rapidly fatal disease.

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

51 To determine risk factors for developing MPMs and compare the survival of patients with MPMs to t

52 ated to gender and histology appear to drive MPM.

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

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

55 11, a total of 529 patients with epithelioid MPM underwent complete resection by EPP as part of a mul

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

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

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

59 or NSCLC and by modified RECIST criteria for MPM.

60 uestioned the safety and efficacy of EPP for MPM.

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

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

63 obviate unnecessary invasive procedures for MPM.

64 Surgery for MPM has shifted from extra-pleural pneumonectomy to PDC

65 athway is a potential therapeutic target for MPM.

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

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

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

69 nfirm microstructural measurements made from MPM images.

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

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

72 The outputs from MPMs have direct biological interpretations, facilitatin

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

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

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

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

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

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

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

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

81 In MPM cells, GHRH antagonists also regulated activity and

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

83 ne resulted in moderate clinical activity in MPM.

84 abundant both in cultured aggregates and in MPM surgical specimens.

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

86 benefit precludes additional development in MPM.

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

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

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

90 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

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

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

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

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

95 d CD36 expression and foam cell formation in MPM.

96 no mutated gene was previously implicated in MPM.

97 influnine, a novel microtubule inhibitor, in MPM.

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

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

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

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

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

103 t wall metastases (CWM) after a procedure in MPM.

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

105 erlying mechanism of cisplatin resistance in MPM.

106 host immunity may play an important role in MPM development.

107 ncluding lung cancer; however, their role in MPM remains unknown.

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

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

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

111 ic model was reported to predict survival in MPM.

112 ional for targeting the actomyosin system in MPM.

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

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

115 antagonists MIA-602 and MIA-690 in vitro in MPM cell lines and in primary MPM cells, and in vivo in

116 nes and in primary MPM cells, and in vivo in MPM xenografts.

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

118 , RNA helicase and p53 signaling pathways in MPMs.

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

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

121 Patients with invasive MPMs had increased risk of melanoma-specific death both

122 graphic metrics that can be derived from its MPMs.

123 IV-MPM represents a powerful tool to study leukocytes in co

124 Furthermore, IV-MPM analyses revealed alterations in both the CD11c(+) D

125 hrough intravital multiphoton microscopy (IV-MPM), allowing the means to accumulate critical spatial

126 emic brain and mouse peritoneal macrophages (MPM).

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

128 and risk for multiple primary malignancies (MPMs).

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

130 The median MPM of clinically relevant organisms was 1,533, versus 2

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

132 Multiple primary melanoma (MPM) has been associated with a higher 10-year mortality

133 271 patients with multiple primary melanoma (MPM) without mutations affecting p16INK4A (wild-type p16

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

135 ents who develop multiple primary melanomas (MPMs).

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

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

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

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

140 Malignant pleural mesothelioma (MPM) has an overall poor prognosis and unsatisfactory tr

141 atients with malignant pleural mesothelioma (MPM) has been a widespread practice across Europe, altho

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

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

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

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

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

147 Malignant pleural mesothelioma (MPM) is a rare, but aggressive tumor with dismal prognos

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

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

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

151 Malignant pleural mesothelioma (MPM) is an aggressive malignancy associated with exposur

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

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

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

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

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

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

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

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

160 atients with malignant pleural mesothelioma (MPM).

161 epithelioid malignant pleural mesothelioma (MPM).

162 activity in malignant pleural mesothelioma (MPM).

163 unresectable malignant pleural mesothelioma (MPM).

164 y studied in malignant pleural mesothelioma (MPM).

165 treatment of malignant pleural mesothelioma (MPM).

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

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

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

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

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

171 molecules of microbial cfDNA per microliter (MPM) of plasma.

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

173 Multiphoton microscopy (MPM) has emerged as one of the most powerful and widespr

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

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

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

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

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

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

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

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

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

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

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

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

186 cently developed multistate parabolic model (MPM).

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

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

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

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

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

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

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

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

195 first unbiased view of the genomic basis of MPM.

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

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

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

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

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

201 Here we review the last decade of MPM development and highlight how in vivo imaging has ma

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

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

204 /d for 4 wk strongly inhibited the growth of MPM xenografts in mice, along with reduction of tumor in

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

206 hance the clinical outcome and management of MPM in the future.

207 ld be further evaluated in the management of MPM.

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

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

210 iptional deregulation in the pathogenesis of MPM.

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

212 primary melanomas, new markers predictive of MPM risk are needed.

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

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

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

216 immunomodulatory genes modulate the risk of MPM compared to patients with SPM or healthy controls.

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

218 sessment can enhance the clinical staging of MPM.

219 ntly lacking in the AJCC clinical staging of MPM.Supplemental material is available for this article.

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

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

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

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

224 Treatment of MPM cells with these inhibitors also significantly decre

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

226 the latest developments in the treatment of MPM.

227 , may offer an approach for the treatment of MPM.

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

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

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

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

232 overexpressed and activated in a majority of MPMs.

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

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

235 Other MPM features included elongated tumor cells in the epide

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

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

238 90 in vitro in MPM cell lines and in primary MPM cells, and in vivo in MPM xenografts.

239 ) classification models: maximum projection (MPM), multislice (MSM), and fused (FM).

240 from 115 patients with histologically proven MPM.

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

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

243 ovide our own opinion on how the most recent MPM developments can be leveraged at scale to enable the

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

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

246 uantitative comparisons between the reviewed MPM instruments.

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

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

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

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

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

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

253 nd intrapleural EPCR gene therapy suppresses MPM progression.

254 elop spontaneously in the majority of tested MPM cell lines when cultured at high cell density.

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

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

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

258 The MPM images were compared with histopathologic findings.

259 ain splice variant SV1 were found in all the MPM cell types examined.

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

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

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

263 opathology criteria can be identified in the MPM images.

264 ongest induction of apoptosis in each of the MPM cell lines, but in different markedness.

265 The MT gene- and protein expression of the MPM-cell lines MSTO-211H, NCI-H2052 and NCI-H2452 and th

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

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

268 d those that returned negative, nor were the MPMs different between pretreated and untreated organism

269 hicker SPM was greater than that for thicker MPM.

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

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

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

273 ovel, clinically effective approach to treat MPM.

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

275 entify potential driver mutations underlying MPM.

276 odified RECIST in patients with unresectable MPM.

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

278 e propose a computational model for in vitro MPM nodule development.

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

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

281 ession of SPI1, was strongly associated with MPM risk reduction (OR = 0.60; 95% CI = 0.45-0.81; p = 0

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

283 expression of BATF3, is also associated with MPM-specific survival (HR = 3.42; 95% CI = 1.57-7.42; p

284 y primary melanomas and also associates with MPM survival.

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

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

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

288 rgoing a chest wall procedure, patients with MPM were randomly assigned to receive prophylactic radio

289 Nineteen patients with MPM were studied before and after 2 cycles (6 wk) of che

290 Patients with MPM who underwent uniform-protocol preoperative MRI betw

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

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

293 otinib in previously untreated patients with MPM.

294 chest wall procedure sites in patients with MPM.

295 ies to be associated at high prevalence with MPM.

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

297 Ms and compare the survival of patients with MPMs to those with single primary melanomas, a prospecti

298 ngle primary melanomas and 305 patients with MPMs were identified.

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

300 omas and 8.8 +/- 5.9 years for patients with MPMs.