ライフサイエンスコーパス: OPC

1 OPC migration in vivo was disrupted in mice with defecti

2 OPCs also produced the majority of myelinating Schwann c

3 suggesting that Sox2 expression in activated OPCs also primes these cells to eventually undergo diffe

4 ls during myelination and in activated adult OPCs responding to demyelination, and is also detected i

5 e and rats, it is neither expressed by adult OPCs nor by oligodendrocytes (although it is expressed b

6 We find that adult OPCs have a transcriptome more similar to that of oligod

7 ontributed to neurodegeneration by affecting OPC viability and/or development.

8 selective synthesis of the preclinical agent OPC 51803.

9 AMPA-kainate receptor inhibition alleviates OPC loss and IVH-induced inflammation and restores myeli

10 vivo cerebellar slices demonstrated altered OPC migratory responses to neurotransmitter stimulation

11 Prediction Outcome Prediction Challenge (AML-OPC), a crowdsourcing effort designed to promote the dev

12 der stem cell conditions as compared with an OPC-like cell.

13 eroxisome biogenesis, lipid homeostasis, and OPC differentiation during white matter development and

14 lpha/IFN-gamma toxicity in both neuronal and OPC cultures.

15 S60 through the promotion of OL survival and OPC differentiation.

16 of myelin membrane formation, in vitro, and OPC differentiation in fibronectin aggregate containing

17 GFP(+) mice were treated with cuprizone, and OPCs were sorted from the corpus callosum.

18 Here, we used post-natal rat derived OLs and OPCs to assess the impact of RNS60 on the response of OL

19 ion also reduced the population of apoptotic OPCs, levels of several cytokines (TNFalpha, IL-beta, IL

20 As OPC clinker-generating mixtures, six clay-containing bin

21 replacement practice, end points included as OPC, follow-up terms for specific OPC, patient populatio

22 emphasize the ability of glial cells such as OPCs to positively respond to moderate intensity SMF sti

23 omavirus (HPV)-related oropharyngeal cancer (OPC) generally present with more advanced disease but ha

24 chemotherapy to treat oropharyngeal cancer (OPC) is supported by evidence from prospective clinical

25 worldwide incidence of oropharyngeal cancer (OPC).

26 quired to prevent oropharyngeal candidiasis (OPC) in mice and humans.

27 Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused

28 ntributes to oligodendrocyte precursor cell (OPC) damage and hypomyelination in both neonatal and adu

29 ty determine oligodendrocyte precursor cell (OPC) differentiation and myelination.

30 to control oligodendroglial precursor cell (OPC) differentiation through a combination of fiber topo

31 gin, promote oligodendrocyte precursor cell (OPC) production after hypoxic-ischemic (HI) injury, the

32 th decreased oligodendrocyte precursor cell (OPC) proliferation and diminished levels of active RhoA,

33 equired for oligodendrocyte progenitor cell (OPC) development, we generated an inducible conditional

34 teps during oligodendrocyte progenitor cell (OPC) development.

35 adult human oligodendrocyte progenitor cell (OPC) differentiation, in addition to its immune regulato

36 n, arrested oligodendrocyte progenitor cell (OPC) maturation, and reduced myelination of the white ma

37 perturbing oligodendrocyte progenitor cell (OPC) maturation.

38 the role of oligodendrocyte progenitor cell (OPC) microRNAs (miRNAs) during remyelination and develop

39 trated that oligodendrocyte progenitor cell (OPC) proliferation is crucial for oligodendrocyte (OL) r

40 tion of ciliary IFT80 in OB precursor cells (OPC) in mice results in growth retardation and markedly

41 ls (NSC) or oligodendrocyte precursor cells (OPC).

42 numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neur

43 ail because oligodendrocyte precursor cells (OPCs) do not completely migrate into demyelinated areas

44 imary mouse oligodendrocyte precursor cells (OPCs) in vitro and that genetically inhibiting the ISR i

45 after which oligodendrocyte precursor cells (OPCs) migrate and proliferate before differentiating int

46 evelop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain a

47 m Pdgfra(+) oligodendrocyte precursor cells (OPCs) to distinct mature oligodendrocytes.

48 xpressed in oligodendrocyte precursor cells (OPCs) together with other SoxE factors and we show here

49 Human oligodendrocytes precursor cells (OPCs) were stimulated with moderate intensity SMF (0.3 T

50 oliferating oligodendrocyte precursor cells (OPCs), and a dense extracellular matrix.

51 oliferative oligodendrocyte precursor cells (OPCs).

52 ocytes from oligodendrocyte precursor cells (OPCs).

53 Oligodendrocyte precursor cells (OPCs; PDGFRalpha+) produced oligodendrocytes responsible

54 f cultured oligodendrocyte progenitor cells (OPCs) also caused an increase in OPC migration.

55 pathway in oligodendrocyte progenitor cells (OPCs) and suppresses remyelination.

56 ination by oligodendrocyte progenitor cells (OPCs) can restore these deficits.

57 uration of oligodendrocyte progenitor cells (OPCs) during the remyelination process is essential to d

58 ly derived oligodendrocyte progenitor cells (OPCs) ectopically exit the spinal cord and myelinate per

59 gration of oligodendrocyte progenitor cells (OPCs) from a ventral site.

60 nmental manipulation of OL progenitor cells (OPCs) has profound effects on the establishment of funct

61 occurs in oligodendrocyte progenitor cells (OPCs) in rodent models during myelination and in activat

62 n of oligodendrocyte (OLG) progenitor cells (OPCs) into mature OLGs are key to understanding myelinat

63 uration of oligodendrocyte progenitor cells (OPCs) involve the assembly and disassembly of actin micr

64 eurons and oligodendrocyte progenitor cells (OPCs) it induces cellular death.

65 nsplanting oligodendrocyte progenitor cells (OPCs) or by mobilizing endogenous progenitors, holds gre

66 ression in oligodendrocyte progenitor cells (OPCs) or in premyelinating oligodendrocytes, we reveal t

67 pressed in oligodendrocyte progenitor cells (OPCs) preparing to undergo differentiation, allowing the

68 Oligodendrocyte progenitor cells (OPCs) that are positive for the cell surface antigen rec

69 ion of rat oligodendrocyte progenitor cells (OPCs) via modulation of PKCalpha.

70 sions have oligodendrocyte progenitor cells (OPCs) within their borders.

71 In oligodendrocyte progenitor cells (OPCs), Lrp1 is required for cholesterol homeostasis and

72 ied murine oligodendrocyte progenitor cells (OPCs), the remyelinating cells of the adult CNS, to obta

73 gration of oligodendrocyte progenitor cells (OPCs), the resident myelinating glial cell of the CNS, i

74 uration of oligodendrocyte progenitor cells (OPCs), thereby impeding remyelination, in the demyelinat

75 ve as oligodendrocyte (OL) progenitor cells (OPCs), we examined here whether their infection by neuro

76 is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by t

77 recruited oligodendrocyte progenitor cells (OPCs), which, early after lesion induction, sense neuron

78 tiation of oligodendrocyte progenitor cells (OPCs).

79 tiation of oligodendrocyte progenitor cells (OPCs).

80 rentiating oligodendrocyte progenitor cells (OPCs).

81 pansion of oligodendrocyte progenitor cells (OPCs).

82 tiation of oligodendrocyte progenitor cells (OPCs).

83 he pool of oligodendrocyte progenitor cells (OPCs).

84 production of both ordinary Portland cement (OPC) and calcium sulfoaluminate (CSA) cement, and (ii) p

85 ed from 3 to 5 mg L(-1) as Cl2, compromising OPC assessments.

86 duct (DBP) organic precursor concentrations (OPCs) are crucial to assess and improve DBP control proc

87 ly, eya and so are also sufficient to confer OPC-like identity, and, in parallel with hth, the OPC-sp

88 tients with nonmetastatic (M0) p16-confirmed OPC treated with radiotherapy with or without chemothera

89 The optical phase conjugation (OPC) through photonic nanostructures in coherent optics

90 er understanding of the factors that control OPC maturation in order to stimulate this pool of progen

91 Conversely, OPC-specific HIF1/2alpha loss of function leads to insuf

92 and propose that this signaling coordinates OPC migration with differentiation.

93 the basis of objective performance criteria (OPC).

94 arge-area, orientationally pure crystalline (OPC) methylammonium lead iodide (MAPbI3) hybrid perovski

95 This reduction results from decreased OPC proliferation, rather than increased cell death or a

96 on, while Sox2 knockout results in decreased OPC proliferation and survival, suggesting that Sox2 con

97 Lrp1-deficient OPC/OLs show a strong increase in the sterol-regulatory

98 stores OB differentiation of IFT80-deficient OPCs by disrupting actin stress fibres and promoting cil

99 steogenic differentiation of IFT80-deficient OPCs by inhibiting non-canonical Hh-RhoA-Cofilin/MLC2 si

100 We report that delamanid (OPC-67683), an approved drug for multi-drug resistant tu

101 ss the safety of engrafted stem cell-derived OPCs, as well as approaches by which to modulate their d

102 ically inhibiting the ISR in differentiating OPCs increases their susceptibility to in vitro hypoxia.

103 and microRNA reverse transfection to direct OPC differentiation.

104 ssion of cell activity marker (c-fos), early OPC (Olig1, Olig2.

105 er is compromised in the presence of ectopic OPCs.

106 mostly unaffected in the presence of ectopic OPCs.

107 mbined, cholesterol and pioglitazone enhance OPC differentiation into mature OLs.

108 leading to dissociation of E2F1 and enhanced OPC proliferation.

109 ional culture, nanofiber topography enhanced OPC differentiation by inducing 2-fold increase in RIP(+

110 tion and that VDR agonist vitamin D enhances OPC differentiation.

111 ng the use of this new surgical approach for OPC.

112 ation and is an essential Ca(2+) channel for OPC maturation during the remyelination of the adult bra

113 studies demonstrate that PLP is critical for OPC responses to glutamate signaling and has important i

114 enhances actin dynamics and is essential for OPC morphogenesis and differentiation.

115 These factors are essential for OPC specification and neurogenesis control.

116 signaling and has important implications for OPC responses when levels of glutamate are high in the e

117 ese OPC apply, and (statistical) methods for OPC development.

118 calcium channels (L-VGCCs) are required for OPC development during remyelination, we generated an in

119 th the vascular endothelium are required for OPC migration.

120 Cancer Control (UICC) TNM staging system for OPC was developed for HPV-unrelated OPC.

121 However, it is recommended that formal OPC be applied for approval of new-generation THVs for u

122 A second Pdgfra(+) population, distinct from OPCs, was found along vessels.

123 provide evidence that deletion of Tsc1 from OPCs, but not differentiating oligodendrocytes, is benef

124 nevertheless provide more information on how OPC differentiation is controlled and therefore enriches

125 ne system in CNS regeneration, revealing how OPCs themselves contribute to the postinjury inflammator

126 Therefore, understanding how OPCs respond to glutamate has important implications for

127 However, OPCs fail to mature into oligodendrocytes (OLs) even in

128 Although HPV-OPC has favorable prognosis, 10% to 25% of HPV-OPCs recu

129 mavirus-related oropharyngeal carcinoma (HPV-OPC) is increasing in incidence in the United States.

130 t diagnosis but rare after treatment for HPV-OPC.

131 e cohort study of patients with incident HPV-OPC diagnosed from 2009 to 2013 at 4 academic tertiary r

132 cohort of 157 participants with incident HPV-OPC treated with curative intent, 124 had 1 or more post

133 V) DNA in oral rinses is associated with HPV-OPC, but its potential as a prognostic biomarker is uncl

134 C has favorable prognosis, 10% to 25% of HPV-OPCs recur.

135 lomavirus-associated oropharynx cancer (HPVA-OPC) is rapidly increasing in incidence and has unique e

136 undertreating the poorer-risk subset in HPVA-OPC, and validated biomarkers are needed to identify pat

137 re mitigates the favorable prognosis of HPVA-OPC.

138 nt risk of morbidity, and patients with HPVA-OPC have a younger median age.

139 g of clinical trials, and patients with HPVA-OPC should be offered clinical trial options whenever th

140 demonstration of its activity on adult human OPCs, leads us to propose dual PDE7-GSK3 inhibition, and

141 n vivo and whether complex formation impacts OPC migration in the brain.

142 mental myelination, there were no changes in OPC or oligodendrocyte numbers in either model.

143 ctive on the role of NgR1 ligand function in OPC fate in the context of a specific and common type of

144 itor cells (OPCs) also caused an increase in OPC migration.

145 there is a approximately 6-fold increase in OPC number within the lesions and a reduced proportion o

146 one deacetylase Sirt1 as a Cdk2 regulator in OPC proliferation and response to HX.

147 -17 stimulation induces NOTCH1 activation in OPCs, contributing to Th17-mediated demyelinating diseas

148 er sex, we establish that Cav1.2 deletion in OPCs leads to less efficient remyelination of the adult

149 ults reveal a key role of Sox2 expression in OPCs responding to demyelination, enabling them to effec

150 Conditional ablation of Gpr56 in OPCs leads to a reduced number of mature oligodendrocyte

151 ally when the Cav1.2 deletion was induced in OPCs during the first 2 postnatal weeks.

152 ncreases the intracellular calcium influx in OPCs as well as the gene expression of L-type channel su

153 suggest that voltage-gated Ca(2+) influx in OPCs is critical for remyelination.

154 ctivin A receptor type I (ACVR1) knockout in OPCs.

155 show that RXR-gamma binds to several NRs in OPCs and OLGs, one of which is vitamin D receptor (VDR).

156 reducing beta-catenin-dependent signaling in OPCs creates an environment that is permissive to axonal

157 ed a conditional knockout mouse for VGCCs in OPCs.

158 st that Ca(2+) influx mediated by L-VOCCs in OPCs is necessary for normal myelination.

159 at of surgical heart valves by incorporating OPC and provides several considerations and recommendati

160 he composition and bioactivity of individual OPCs and more generally highlight the potential of tradi

161 tion in vivo suppresses basal and HX-induced OPC proliferation.

162 We demonstrate that Noggin-induced OPC production requires Olig1 function.

163 aches we show that RXR-VDR signaling induces OPC differentiation and that VDR agonist vitamin D enhan

164 s phosphorylation of Smad 1/5/8 and inhibits OPC differentiation into myelinating oligodendrocytes (O

165 Hyaluronan (HA) inhibits OPC maturation and complexes with the heavy chain (HC) o

166 n signaling is critical for both the initial OPC reactivation step and late-stage tumor cell prolifer

167 l activity and release of glutamate instruct OPCs to differentiate into new myelinating oligodendrocy

168 a Cre reporter, we establish that Cav1.2(KO) OPCs display a reduced maturational rate through the ent

169 Specifically, Cav1.2(KO) OPCs mature slower and produce less myelin than control

170 by a Cre reporter, we found that Cav1.2(KO) OPCs produce less mature oligodendrocytes than control c

171 ion, in a mouse line in which the Cav1.2(KO) OPCs were identified by a Cre reporter, we establish tha

172 nsgenic mouse in which all of the Cav1.2(KO) OPCs were tracked by a Cre reporter, we found that Cav1.

173 Treatment of Lrp1(-/-) OPCs with cholesterol or activation of peroxisome prolif

174 Methods (SM) 5710-B/D - are used to measure OPCs.

175 Whereas neuroepithelial cells in the medial OPC directly convert into neuroblasts, in an IPC subdoma

176 Migrating OPCs crawl along and jump between vessels.

177 feration and, at a late stage, by modulating OPC maturation.

178 2 miRNA, miR-297c-5p, increased during mouse OPC differentiation in vitro and during callosal develop

179 Mouse OPCs with genetic Wnt dysregulation (high tone) express

180 Loss of function in cultured mouse OPCs also results in an impaired ability to undergo norm

181 s intense therapy compared with HPV-negative OPC.

182 to that of oligodendrocytes than to neonatal OPCs, but revert to a neonatal-like transcriptome when a

183 Tsc1 deletion from NG2(+) OPCs accelerated remyelination.

184 acellular Ca(2+) signaling, whereas PLP null OPCs did not reduce GluR2 at the cell surface or increas

185 migration rate of wild-type but not PLP null OPCs.

186 O4(+) OPCs can be isolated by cell sorting for myelination stu

187 was largely due to a profound attenuation of OPC recruitment and likely also due to impaired differen

188 be taken into account in the construction of OPC include the maturity of THV technology, variability

189 ng, tamoxifen emerges as a potent inducer of OPC differentiation in vitro.

190 ounteract fibronectin-mediated inhibition of OPC maturation.

191 linating oligodendrocytes and in the rate of OPC proliferation.

192 linating oligodendrocytes and in the rate of OPC proliferation.

193 okine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signa

194 otein 1 (LINGO-1) is a negative regulator of OPC differentiation.

195 has been shown to be a positive regulator of OPC differentiation.

196 describes miR-297c-5p, a novel regulator of OPC function.

197 miR-297c-5p as both a negative regulator of OPC proliferation and a positive regulator of OL maturat

198 cate that Sirt1 is an essential regulator of OPC proliferation and OL regeneration after neonatal bra

199 material for the synthesis of two series of OPC and CSA clinkers, obtained from mixes heated in a la

200 Live imaging studies of OPC migration in ex vivo cerebellar slices demonstrated

201 minal-B (Abd-B) caused the transformation of OPC to IPC neuroepithelial identity.

202 mportant, given our lack of understanding of OPC miRNA regulatory networks and their potential clinic

203 ents the distribution and differentiation of OPCs at an early, but narrow, window of time during feta

204 ofile, proliferation, and differentiation of OPCs by altering the expression of regulatory cytoplasmi

205 ces the proliferation and differentiation of OPCs in the developing CNS.

206 ng that Sox2 contributes to the expansion of OPCs during the recruitment phase of remyelination.

207 Co-localization of OPCs with the presynaptic protein VGluT2 in MS lesions i

208 ter, which results in arrested maturation of OPCs and myelination failure.

209 and CCL2, which enhance the mobilization of OPCs.

210 was a significant decrease in the number of OPCs and mature oligodendrocytes throughout postnatal de

211 This smaller pool of OPCs results from altered cell cycle and reduced cell pr

212 Surprisingly, in the presence of OPCs, perineurial glia exited the CNS normally.

213 er tracts in Olig1-null mice lacked Olig2(+) OPCs, and instead proliferating neuronal precursors and

214 ent deprivation, referred to as 'NG') and on OPC differentiation capacity.

215 hibiting effect of aggregated fibronectin on OPC maturation by activating a PKA-dependent signaling p

216 hibiting effect of aggregated fibronectin on OPC maturation, both in vitro and in vivo, by activating

217 omotes remyelination via CXCR4 activation on OPCs, resulting in their differentiation into myelinatin

218 GD1a exerts its effect on OPCs by inducing their proliferation and, at a late stag

219 e did not affect survival, proliferation, or OPC progenitor marker expression but suppressed certain

220 ompletely migrate into demyelinated areas or OPCs in lesions may not mature into myelinating oligoden

221 isual system, two neuroepithelia, the outer (OPC) and inner (IPC) proliferation centers, generate neu

222 riginate from two neuroepithelia, the outer (OPC) and inner (IPC) proliferation centers.

223 wn-regulates NgR1 inhibitors during the peak OPC maturation block.

224 Patients with newly diagnosed HPV-positive OPC (by p16 immunohistochemistry or in situ hybridizatio

225 Patients with HPV-positive OPC have distinct risk factor profiles and generally hav

226 A total of 661 patients with HPV-positive OPC met the inclusion criteria.

227 s better separate patients with HPV-positive OPC with respect to survival than does the current AJCC/

228 growing subset of patients with HPV-positive OPC.

229 modality for many patients with HPV-positive OPC.

230 ease progression, patients with p16-positive OPC had significantly improved survival rates compared w

231 C isoform Cav1.2 was deleted in NG2-positive OPCs (Cav1.2(KO)).

232 v1.2 was postnatally deleted in NG2-positive OPCs.

233 urification of oligomeric proanthocyanidins (OPCs) derived from grape seed extract yielded pure OPC d

234 o the establishment of methods for producing OPCs and oligodendrocytes from embryonic stem cells and

235 Oligodendrocyte progenitors (OPCs) are electrically responsive cells receiving synapt

236 d to injury, as oligodendrocyte progenitors (OPCs) proliferate.

237 Increased proliferating OPCs and elevated MAPK activity were also observed durin

238 It also promoted OPC maturation, myelination, and neurological recovery.

239 scovered that anti-LINGO-1 antibody-promoted OPC differentiation was accompanied by upregulation of c

240 ion, whereas overexpression of cGSN promoted OPC differentiation in vitro and remyelination in vivo F

241 dium from FSD-C10-treated microglia promoted OPC survival and oligodendrocyte maturation.

242 Inhibition of Sirt1 also promotes OPC differentiation after HX.

243 e treatment represses inflammation, promotes OPC maturation, and restores myelination and neurologica

244 Furthermore, we show that RNS60 promotes OPC differentiation under physiological conditions.

245 studies suggest that while the ISR protects OPCs from hypoxia in vitro, it does not appear to play a

246 derived from grape seed extract yielded pure OPC dimer, trimer, tetramer, and their gallates (pOPCs).

247 Chemotaxis assays of purified OPCs revealed that AMPA stimulation was neither attracti

248 in both mouse embryonic fibroblasts and rat OPCs (rOPCs), cell cycle analysis revealed that miR-297c

249 s study, we used chromatin isolated from rat OPCs and immature oligodendrocytes, to characterize the

250 Overexpression of Sox2 in rat OPCs in vitro maintains the cells in a proliferative sta

251 Treating rat OPCs with cGSN siRNA reduced OPC differentiation, wherea

252 Treating rat OPCs with cGSN siRNA reduced OPC differentiation, whereas overexpression of cGSN prom

253 Cl2) at pH 7.0 (the AM) accurately reflected OPCs.

254 roteolipid protein is critical to regulating OPC migratory responses to the neurotransmitter glutamat

255 .004) but not for patients with HPV-related OPC (stage I, II, III, and IV 5-year OS: 88%, 78%, 71%,

256 hort comprised 573 patients with HPV-related OPC and 237 patients with HPV-unrelated OPC, with a medi

257 M1 as stage IV) is proposed for HPV-related OPC as a result of significantly improved survival predi

258 RPA divided HPV-related OPC into RPA-I (T1-3N0-2b), RPA-II (T1-3N2c), and RPA-II

259 For HPV-related OPC, recursive partitioning analysis (RPA) derived new R

260 redict outcomes of patients with HPV-related OPC.

261 Cancer Control TNM framework for HPV-related OPC.

262 lecular tool to boost maturation of resident OPCs to overcome remyelination failure and halt disease

263 oligosaccharide administration would restore OPC maturation, myelination, and neurological function i

264 ibition suppresses inflammation and restores OPC maturation, myelination, and neurologic recovery in

265 uclear E2F1 during differentiation of rodent OPC into oligodendrocytes (OLs) in developing white matt

266 ncluded as OPC, follow-up terms for specific OPC, patient populations to which these OPC apply, and (

267 in formation and/or repair and by suspending OPCs in a state of persistent susceptibility to excitoto

268 These findings indicate that OPC-intrinsic HIF signaling couples postnatal white matt

269 We argue that OPCs have the potential to develop both astrocytic and o

270 Here, we demonstrate that OPCs, but not OLs, are major CNS targets of both FrCasE

271 We observed that OPCs of the embryonic mouse brain and spinal cord, as we

272 We show that OPCs require the vasculature as a physical substrate for

273 The OPC maturation block after white matter stroke is in par

274 Although both marks were present at the OPC stage, only H3K9me3 marks (but not H3K27me3) were fo

275 ike identity, and, in parallel with hth, the OPC-specific neurogenesis mode on the IPC.

276 gonist administered after stroke reduces the OPC astrocytic transformation and improves poststroke ol

277 We find that the OPC films spontaneously form periodic microarrays that a

278 e that the EGFP signal co-localizes with the OPC markers throughout the brain.

279 ific OPC, patient populations to which these OPC apply, and (statistical) methods for OPC development

280 in which the PCO unit has been isomerized to OPC.

281 work highlights the importance of miRNAs to OPC biology and describes miR-297c-5p, a novel regulator

282 d TCR-delta(-/-) mice were both resistant to OPC.

283 nantly control IL-17R-dependent responses to OPC through regulation of BD3 expression.

284 stently, Defb3(-/-) mice were susceptible to OPC.

285 t MLV infection is not directly cytotoxic to OPCs but rather acts to interfere with OL differentiatio

286 ed new stage groupings with both traditional OPC regional lymph node (N) categories and nasopharyngea

287 egories as an alternative to the traditional OPC N categories in the new AJCC/UICC TNM staging system

288 or 5-year survival than RPA with traditional OPC N categories.

289 AMPA receptor stimulation of wild-type OPCs caused decreased cell-surface expression of the Glu

290 was evident for patients with HPV-unrelated OPC (stage I, II, III, and IV 5-year OS: 70%, 58%, 50%,

291 patients with HPV-related and HPV-unrelated OPC separately.

292 ated OPC and 237 patients with HPV-unrelated OPC, with a median follow-up of 5.1 years.

293 stem for OPC was developed for HPV-unrelated OPC.

294 er survival than patients with HPV-unrelated OPC.

295 pithelial default state is IPC-like, whereas OPC identity is derived.

296 Using zebrafish mutants in which OPCs migrate out of the spinal cord and myelinate periph

297 e a two-hit scenario where interference with OPC differentiation combined with glial Env-induced neur

298 s (OECs) and in tongue tissue from mice with OPC.

299 ss ongoing clinical trials for patients with OPC.

300 ion and proliferation of subventricular zone OPCs is decreased in the Cav1.2(KO) mice.