ライフサイエンスコーパス: EpCAM

1 EpCAM accumulated on the lateral interfaces of human col

2 EpCAM appears to differentially regulate LC mobility/mig

3 EpCAM appears to promote LC migration from epidermis by

4 EpCAM knockdown resulted in decreases in claudin-7 and c

5 EpCAM overexpression was 98% in both esophageal squamous

6 EpCAM stabilizes claudin-7 in IECs, and HAI-2 regulates

7 EpCAM upregulation occurs in HBV-mediated HCCs and hepat

8 EpCAM(+)MPs in patients with CRSwNP were no different fr

9 EpCAM, PTEN, and p27 were demonstrated as miR-30e-3p add

10 EpCAM-targeted MBs efficiently (85%) and rapidly (within

11 EpCAM-targeted MBs efficiently (88%) isolated frequent t

12 ssociated markers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity following

13 (VEGF-alpha) by a minor subset of activated EpCAM(+)CD59(+)Ly-6D(+) cDC1s.

14 st that, in the absence of strong adjuvants, EpCAM-deficient LCs exhibit increased migration to regio

15 TJ formed readily after EpCAM knockdown; the acquisition of trans-epithelial ele

16 Although EpCAM knockdown decreased claudin-1 and claudin-7 protei

17 This study shows that treatment with an EpCAM neutralizing antibody promotes apoptosis while dec

18 roblasts were associated with E-Cadherin and EpCAM expression and expression of integrin alphavbeta6.

19 e identified by their expression of CD24 and EpCAM, suggesting the potential of exosomes for diagnost

20 has antigen-binding arms that engage CD3 and EpCAM and a constant domain that recruits Fc receptor-be

21 The exosome-associated markers CD63 and EpCAM were enriched in the isolated EVs while markers of

22 of highly specific surface markers CD63 and EpCAM.

23 AM(High) (2.8-3.8 x 10(6) antigens/cell) and EpCAM(Low) (5.2 x 10(4) to 2.2 x 10(5) antigens/cell) ti

24 A knockdown suppresses CpG demethylation and EpCAM expression.

25 increase and become progressively GS(-) and EpCAM(-) .

26 ith elevated expression of Plk1, HOTAIR, and EpCAM.

27 ochemistry scores generated for Keratin7 and EpCAM demonstrated a good correlation with gene expressi

28 Combining OCT4 and EpCAM selection can further enrich the meiotic-competent

29 SC marker expression (e.g., NANOG, OCT4, and EpCAM), expansion of SP, and acceleration of tumor growt

30 whereas other targets such as PTEN, p27, and EpCAM gain relevance and mediate miR-30e-3p oncogenic ro

31 We quantified the size and EpCAM expression of over 2,500 CTCs from 38 patient samp

32 HLA-ABC-/CD49e- (putative spermatogonia) and EpCAM-/HLA-ABC+/CD49e+ (putative MOLT-4) cell fractions.

33 ll and epithelial markers, such as SSEA1 and EpCAM, respectively, are not predictive of reprogramming

34 Anti-EpCAM antibodies were further conjugated on the substrat

35 Anti-EpCAM MBs efficiently (>77%) isolated rare mouse breast

36 e with 90+/-8% efficiency when using an anti-EpCAM-coated array.

37 so achieved by anti-CD63, anti-EGFR and anti-EpCAM modified SPRi array.

38 Biotinylated anti-EpCAM antibody that specifically binds to human cancer c

39 the trifunctional antibody catumaxomab (anti-EpCAM x anti-CD3).

40 nic for T cell recruitment (catumaxomab anti-EpCAM/CD3 and blinatumomab anti-CD19/CD3), increase in t

41 were twice as bright as two commercial anti-EpCAM red fluorophore conjugates, APC and AlexaFluor(R)6

42 (30 mum x 150 mum) channels containing anti-EpCAM antibodies that is scalable in terms of throughput

43 been tested in phase 1 studies so far: anti-EpCAM BiTE((R)) AMG 110, anti-CEA BiTE((R)) MEDI-565/AMG

44 In vitro, RBCs modified with lipophilic anti-EpCAM or anti-CD45 antibodies efficiently bound to cance

45 antiepithelial cell adhesion molecule (anti-EpCAM), provides the specificity for CTC capture.

46 utilized for covalent immobilization of anti-EpCAM antibody.

47 Amino group on anti-EpCAM antibody was covalently bound with succinimidyl gr

48 pture efficiency of a surface with only anti-EpCAM.

49 es with either fibronectin, Matrigel or anti-EpCAM antibody.

50 )) coated with fibronectin, Matrigel or anti-EpCAM.

51 ls (PBMCs) were functionalized with the anti-EpCAM-lipid-CSANs, they were shown to selectively kill a

52 CV results confirm that the anti-EpCAM/LC-SPDP/Au based biosensor could detect MCF-7 cell

53 The anti-EpCAM/LC-SPDP/Au electrodes were exposed to solutions wi

54 These anti-EpCAM/LC-SPDP/Au electrodes were characterized using cyc

55 uman liver cancer cell line Hep3B using anti-EpCAM-CdTe- and anti-GPC3-ZnSe-coated silica nanoparticl

56 microfluidic device functionalized with anti-EpCAM (epithelial cell adhesion molecule) antibodies to

57 NPs were conjugated with anti-EpCAM antibody to the NP surface for immunospecific targ

58 gold electrodes and functionalized with anti-EpCAM.

59 s expressing liver stem cell markers such as EpCAM, CK19, CD133, and Sox9.

60 e optimized to afford discrimination between EpCAM(High) (2.8-3.8 x 10(6) antigens/cell) and EpCAM(Lo

61 Physical interactions between EpCAM and claudins were required for claudin stabilizati

62 novel double-negative feedback loop between EpCAM and ERK that contributes to the regulation of EMT.

63 first time an intricate relationship between EpCAM-regulated transcription and altered biophysical pr

64 o antibodies directed to surface biomarkers (EpCAM and Slex) of human colorectal CTCs.

65 important translational implications as both EpCAM and ERK are currently being targeted in human clin

66 n NSCLC cell lines, positive for E-Cadherin, EpCAM and alphavbeta6 expression, activate normal fibrob

67 Specifically, CCND2, EpCAM, and IGFII expression was elevated at the prolifer

68 ted triple-marker-positive (CD44(+)/CD133(+)/EpCAM(+)) cells of human PC MiaPaCa-2 and L3.6pl cells b

69 analysis showed that CSLCs (CD44(+)/CD133(+)/EpCAM(+)) exhibit differential expression of more than 1

70 Notably, CD133(+)/EpCAM(+) cancer stem cells vanished from the catumaxomab

71 the triple-marker-negative (CD44(-)/CD133(-)/EpCAM(-)) cells.

72 nce-activated cell sorting-enriched CD133(-)/EpCAM(-) (double negative, DN), Huh-7 cells underwent a

73 We previously demonstrated that the CD133(-)/EpCAM(-) hepatoma subpopulation was more metastatic than

74 predominated over epithelial markers (CD133, EpCAM, and LGR5).

75 ion overexpressing CSC markers (CD44, CD166, EpCAM) for all cell lines.

76 everal cancer stemness genes including CD24, EpCAM, and CD133 upregulated by KRAS(G12D).

77 ed distinct CD49f+/EpCAM+ progenitor, CD271+/EpCAM- basal, and ALDEFLUOR+ cell profiles.

78 CD49f(+)/EpCAM(-), CD44(+)/EpCAM(-), CD44(+)/CD24(-), or ALDEFLUOR-positive subpopu

79 CD49f(+)/EpCAM(-), CD44(+)/EpCAM(-), CD44(+)/CD24(-), or ALDEFLUO

80 iated and highly clonogenic ALDH(+)/CD49f(+)/EpCAM(+) luminal progenitors, which express both basal c

81 PAM50 gene-set analyses of ALDH(+)/CD49f(+)/EpCAM(+) populations efficiently identified major and mi

82 ALDH(+)/CD49f(+)/EpCAM(+) tumor and normal cells clustered differently co

83 ary stem cell-enriched basal cells (CD49f(+)/EpCAM(-)/Lin(-)) expressed higher levels of ANTXR1 compa

84 reast with cancer were enriched for CD49f(+)/EpCAM(-), CD44(+)/CD24(-), and CD271(+) cancer stem-like

85 of the same patients showed distinct CD49f+/EpCAM+ progenitor, CD271+/EpCAM- basal, and ALDEFLUOR+ c

86 In epithelial cells, EpCAM regulates expression and distribution of selected

87 nt prostate cancer, isolated via CellSearch (EpCAM(pos)/CK(pos)/CD45(neg)/DAPI(pos)) and subsequent F

88 demonstrated that active matriptase cleaves EpCAM after Arg80 and that loss of HAI-2 in IECs led to

89 -bearing mice enriched for CD133(+)/CXCR4(+)/EpCAM(-) CICs are highly tumorigenic and metastatic.

90 ough the generation of the CD133(+)/CXCR4(+)/EpCAM(-) subset.

91 re contiguous to the surrounding cytoplasmic EpCAM(+)/HNF-4alpha(-) ductular oval cells.

92 the ability of EpCAM aptamer SYL3C to detect EpCAM expression in 170 cases of esophageal cancer (EC)

93 Further evaluation in different EpCAM-expressing cell lines is warranted as well as appl

94 ancer stem cell markers BAMBI, DKK1,2, DLK1, EpCAM, MYC, and proliferation genes CCNA1, CCND2, IGFII,

95 t the promoters of BAMBI, CCND2, DKK2, DLK1, EpCAM, and IGFII was demonstrated by chromatin immunopre

96 UC5AC, MUC6, Das-1, STMN1, TSP1, TSP2, EGFR, EpCAM, GPC1, WNT-2, EphA2, S100A4, PSCA, MUC13, ZEB1, PL

97 activates peritoneal T cells and eliminates EpCAM(+) tumor cells, establishing a molecular and cellu

98 can be caused by mutations in genes encoding EpCAM, a putative adhesion molecule, and HAI-2, a cell s

99 EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype.

100 In a competitive binding experiment, EpCAM aptamer generated a staining pattern similar to th

101 ls containing Matrigel(R) without expressing EpCAM.

102 HCC subset that is classified by an extreme EpCAM(+) AFP(+) gene expression signature and associated

103 or maintaining HCC stemness, is required for EpCAM(+) HCC spheroid formation as well as the maintenan

104 ring EMT, demonstrate an unexpected role for EpCAM in the regulation of ERK and define a novel double

105 etic Notch (synNotch) receptors specific for EpCAM or B7-H3, which are expressed on ROR1(+) tumor cel

106 1AP1 may serve as a key molecular target for EpCAM(+) AFP(+) HCC subtype.

107 RelA site is in a CpG island downstream from EpCAM transcriptional start site (TSS).

108 (+)EpCAM(-) cells, we isolated them as GFP(+)EpCAM(-) cells from DDC-injured livers of Sox9-EGFP mice

109 C-like with high langerin, Birbeck granules, EpCAM, and E-cadherin expression under the same conditio

110 Level 0 single-cell buds are K19(+) /GS(+) /EpCAM(+) /Heppar1(-) .

111 morphologically hepatocytes (K19(-) /GS(+) /EpCAM(+) /Heppar1(+) ).

112 In hepatocytes, EpCAM is silenced by polycomb repressive complex 2 (PRC2

113 inistration to nude BALB/c mice bearing high EpCAM-expressing HT-29 colorectal cancer xenografts.

114 iate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative) xenografts.

115 Interestingly, the human EpCAM gene also has a CpG island downstream from its TSS

116 These results identify EpCAM as a substrate of matriptase and link HAI-2, matri

117 To determine if EpCAM regulates claudins in LC and immune responses to e

118 itical oncoprotein specifically activated in EpCAM(+) AFP(+) HCC.

119 hromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transiti

120 In addition, HCC cells in EpCAM(+) spheroids are more resistant to chemotherapeuti

121 duced translocation and dendrite motility in EpCAM-deficient LC in vivo in contact allergen-treated m

122 nt with its design, MM-131 is more potent in EpCAM-high cells than in EpCAM-low cells, and its potenc

123 1 is more potent in EpCAM-high cells than in EpCAM-low cells, and its potency decreases when EpCAM le

124 in de-repression of PRC2 targets, including EpCAM and pluripotency genes.

125 lls, SOX2 bound the EPCAM promoter to induce EpCAM-p21(Cip1)-cyclin A2 signaling, encouraging cell pr

126 Herein we demonstrate HBx induces EpCAM expression via active DNA demethylation.

127 neck squamous cell cancer FaDu (intermediate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative)

128 To gain insight into EpCAM function in a physiologic context in vivo, we gene

129 ar cell suspensions was performed to isolate EpCAM+/HLA-ABC-/CD49e- (putative spermatogonia) and EpCA

130 ancer stem cell (CSC) markers Aldh1a1, Klf4, EpCAM, and CD133.

131 However, tumor-derived Lineage-EpCAM-CD73+CD90+ cells led to the formation of vessels w

132 ir normal counterpart, tumor-derived Lineage-EpCAM-CD73+CD90+ cells showed enhanced expression of the

133 oth tumor-derived and matched normal Lineage-EpCAM-CD73+CD90+ cells supported the assembly of perfusa

134 ted eDAR for recovery of cells that have low EpCAM expression and developed an immunofluorescence lab

135 gnificantly higher capture efficiency of low-EpCAM cells compared to the commercial method.

136 In addition, these CTCs exhibited lower EpCAM expression.

137 1, CD14 and Gly-A) and the epithelial marker EpCAM.

138 ction strategies rely on cell surface marker EpCAM and intracellular cytokeratins (CKs) for isolation

139 ncreased the expression of stem cell markers EpCAM, Claudin7, and Oct4, as well as decreased E-cadher

140 -1, CD133, Dlk) and liver stem cell markers (EpCAM, CD14, CD24, CD49f); and negative for: hematopoiet

141 te of matriptase and link HAI-2, matriptase, EpCAM, and claudin-7 in a functionally important pathway

142 ore, we hypothesized that HAI-2, matriptase, EpCAM, and claudin-7 were functionally linked.

143 e (EpCAM(+)) SHPC clusters showed membranous EpCAM(+)/HNF-4alpha(+) (hepatocyte nuclear factor-4alpha

144 Evaluation of Met, EpCAM, and HGF levels in human tumor samples reveals tha

145 d spiked-in cancer cells (taken from a model EpCAM(high) cell line) from blood at an efficiency of 95

146 cktail allowed us to reliably detect a model EpCAM(low) cell line for triple negative breast cancer,

147 e proinvasive cell surface adhesion molecule EpCAM.

148 ls in the epithelial cell adhesion molecule (EpCAM(+)) SHPC clusters showed membranous EpCAM(+)/HNF-4

149 ession of epithelial cell adhesion molecule (EpCAM(-)), which also shows the greatest in vitro invasi

150 lpha(neg) epithelial cell adhesion molecule (EpCAM(neg)) CD11b(+) langerin (Lang; CD207)(neg) DCs, bu

151 Epithelial cell adhesion molecule (EpCAM) (CD326) is a surface glycoprotein expressed by in

152 domain of epithelial cell adhesion molecule (EpCAM) (EpEX) significantly increases the levels of plur

153 sed genes epithelial cell adhesion molecule (EpCAM) and pluripotency genes.

154 c for the epithelial cell adhesion molecule (EpCAM) and sorted into four zones of a microfluidic devi

155 ainst the epithelial cell adhesion molecule (EpCAM) and the T-cell antigen CD3, is approved as intrap

156 ponses to Epithelial Cell Adhesion Molecule (EpCAM) antibody and other ligands coated on the sensor c

157 ated anti-epithelial cell adhesion molecule (EpCAM) antibody lead to complete tumour regression in mo

158 with anti-epithelial cell adhesion molecule (EpCAM) antibody.

159 ection of epithelial cell adhesion molecule (EpCAM) antigen, a common marker for tumors of epithelial

160 ession of epithelial cell adhesion molecule (EpCAM) has been implicated in advanced endometrial cance

161 Although epithelial cell adhesion molecule (EpCAM) has previously been shown to promote tumor progre

162 e used an Epithelial Cell Adhesion Molecule (EpCAM) independent fluid biopsy based on cell morphology

163 The epithelial cell adhesion molecule (EpCAM) is closely correlated with the occurrence and dev

164 Epithelial cell adhesion molecule (EpCAM) is expressed at the basolateral membrane of most

165 sitizers, epithelial cell adhesion molecule (EpCAM) on LCs promotes LC dendrite mobility and LC migra

166 s-linking epithelial cell adhesion molecule (EpCAM) on tumor cells with a cluster of differentiation

167 st either epithelial cell adhesion molecule (EpCAM) or epidermal growth factor receptor (EGFR) and th

168 eting epithelial cellular adhesion molecule (EpCAM) present on the MCF-7 cell membrane.

169 ing 4, an epithelial cell adhesion molecule (EpCAM) targeting MMC-immunoconjugate was prepared and du

170 s against epithelial-cell adhesion molecule (EpCAM) via magnetic-activated cell sorting (MACS).

171 CD86(lo), epithelial cell adhesion molecule (EpCAM)(hi), CD45(lo) bone marrow-derived peripheral anti

172 ession of epithelial cell adhesion molecule (EpCAM), a 40-kDa type I transmembrane protein found on e

173 included epithelial cell adhesion molecule (EpCAM), carbonic anhydrase IX (CA9), epidermal growth fa

174 , such as epithelial cell adhesion molecule (EpCAM), human epidermal growth factor receptor-2 (HER-2)

175 e marker, epithelial cell adhesion molecule (EpCAM), is also expressed in human fetal gonads and can

176 richrome, epithelial cell adhesion molecule (EpCAM), K19, CD34, glutamine synthetase (GS), and Ki-67.

177 ha, HNF6, Epithelial cell adhesion molecule (EpCAM), Leucine-rich repeated-containing G-protein coupl

178 n such as epithelial cell adhesion molecule (EpCAM), thereby recruiting T-cell activation to the tumo

179 antigen, epithelial cell adhesion molecule (EpCAM), this study demonstrates that binding affinity an

180 generated epithelial cell adhesion molecule (EpCAM)-positive hepatocytes.

181 including epithelial cell adhesion molecule (EpCAM).

182 known as epithelial cell adhesion molecule (EpCAM).

183 h Met and epithelial cell adhesion molecule (EpCAM).

184 and mouse epithelial cell adhesion molecule (EpCAM; K(D), 21 nM), and with [(89)Zr]Zr-DFO-N-suc-hyS11

185 lial MPs (epithelial cell adhesion molecule [EpCAM](+)MPs, E-cadherin(+)MPs), platelet MPs (CD31(+)CD

186 em cells (epithelial cell adhesion molecule [EpCAM], neural cell adhesion molecule [NCAM], epithelial

187 pressing epithelial cell adhesion molecules (EpCAM) was achieved by functionalizing micropallet surfa

188 showing hepatocytic morphology appeared near EpCAM(+) ductular structures in the livers of mice fed 3

189 epithelial cell adhesion molecule-negative (EpCAM(-)) hepatocyte nuclear factor 4alpha-positive (HNF

190 epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high

191 ic method identifying HBEC as CD45 negative, EpCAM/pan-cytokeratin (pan-CK) double-positive populatio

192 cinoma (EACA) and 100% in metastasis, but no EpCAM overexpression was detected in undifferentiated EC

193 frequently in early-stage NSCLC using a non-EpCAM mediated approach with a wide range noted for a gi

194 and Prominin-1 (OR1.14, P = 0.002), but not EpCAM (OR1.16, P = 0.06), were identified as independent

195 Also, with the percentage of OCT4(+)/EpCAM(+) cells as readout, we demonstrated the synergist

196 Combining BMP4/WNT3A induction and OCT4/EpCAM selection can significantly increase the putative

197 y tested, for the first time, the ability of EpCAM aptamer SYL3C to detect EpCAM expression in 170 ca

198 s, we demonstrated that specific ablation of EpCAM resulted in increased ERK pathway activity and SNA

199 geneous and dynamic expression or absence of EpCAM and/or CKs in CTCs.

200 The absence of EpCAM in normal lymphatics makes it an attractive marker

201 were dramatically reduced in the absence of EpCAM, conditional knockout mice with EpCAM-deficient LC

202 munoprecipitation documented associations of EpCAM with claudin-7 and claudin-1 but not claudin-2 or

203 embly that allows highly specific capture of EpCAM (epithelial cell adhesion molecule) positive CTCs

204 of protein A/G enabled efficient capture of EpCAM antibody on the micropallet surface.

205 Cleavage of EpCAM decreased its ability to associate with claudin-7

206 nsduction triggered cell-surface cleavage of EpCAM, leading to nuclear internalization of its cytopla

207 atriptase activity and efficient cleavage of EpCAM.

208 Here, we demonstrated that culture of EpCAM(+) cells derived from human induced pluripotent st

209 solation techniques rely on the detection of EpCAM to discriminate CTCs from other cells in the blood

210 domain I within the extracellular domain of EpCAM (EpEX) binds EGFR, activating both AKT and MAPK si

211 Thus, genome editing of EpCAM could be associated with altering these nanomechan

212 Elevation of EpCAM enhanced tumorsphere formation and tumor initiatio

213 The enumeration of EpCAM-positive circulating tumor cells (CTCs) has allowe

214 , which correlated with direct expression of EpCAM by DC.

215 n and invasion, whereas forced expression of EpCAM resulted in decreased ERK pathway activity and SNA

216 inversely correlated with the expression of EpCAM.

217 onstrated by the simultaneous immunoassay of EpCAM and GPC3 antigens on the surface of the human live

218 behavior, consistent with the inhibition of EpCAM and Snail expression.

219 r, and PC3 prostate cancer), and one kind of EpCAM negative cancer cell line (293T kidney cancer).

220 cm) were demonstrated to test three kinds of EpCAM positive cancer cell lines (MCF-7 breast cancer, S

221 Knockdown of EpCAM in T84 and Caco-2 cells using shRNAs led to change

222 Knockdown of EpCAM inhibited the expressions of reprogramming factors

223 8) cancer cells expressing various levels of EpCAM and EGFR.

224 rly, HFD female mice express lower levels of EpCAM in lung tissue in comparison with males and lean f

225 nes that express both high and low levels of EpCAM.

226 tumors shed CTCs that express high levels of EpCAM; others release cells that have a low level of the

227 Migration of EpCAM-deficient LC from skin explants was inhibited, but

228 Attenuated migration of EpCAM-deficient LC resulted in enhanced contact hypersen

229 phogenesis and apical expression patterns of EpCAM, a hepatic stem/progenitor cell marker highly expr

230 tion of cells bears the surface phenotype of EpCAM+CD24+CD44+CD133-SCA1- and is closer in its propert

231 ients without malignancy for the presence of EpCAM(+) single cells.

232 Herein we show that in the presence of EpCAM-positive tumor targets, CatmAb markedly enhanced T

233 de important insights into the regulation of EpCAM expression during EMT, demonstrate an unexpected r

234 The capture and release of EpCAM expressing cancer cells using this approach was fo

235 In our studies on the role of EpCAM in cancer biology, we observed that EpCAM expressi

236 four zones of a microfluidic device based on EpCAM expression levels.

237 rms the conventional assay solely relying on EpCAM, as demonstrated by detecting significantly more C

238 (e.g., epithelial cell adhesion molecule or EpCAM) or size to separate them from blood cell populati

239 lecule-positive (EpCAM(+)) cells and overall EpCAM expression.

240 Overexpressed EpCAM was detected in severe dysplasia, but negative in

241 el population of lineage(neg/low), CD45(pos) EpCAM(pos), SCA1(pos), CD117(neg), CD138(neg), MHCII(neg

242 epithelial cell adhesion molecule-positive (EpCAM(+)) cells and overall EpCAM expression.

243 d by the finding that CD44+/CD24- and PROCR+/EpCAM- multi-potent stem cells were elevated significant

244 dividual knockdown was sufficient to promote EpCAM and E-cadherin expression.

245 ociated loss of the cell junctional proteins EpCAM and claudin 7 was also prevented.

246 gical inhibition of the ERK pathway restored EpCAM expression.

247 We demonstrate the ability to select EpCAM positive CTCs from PDAC patients in high purity (>

248 n of SPRi with flow cytometry showed similar EpCAM expression on MCF7, SKBR3 and HS578T cells.

249 Sox9(+)EpCAM(-) cells proliferated and could differentiate to f

250 In addition, Sox9(+)EpCAM(-) cells formed cysts with a small central lumen i

251 Although Sox9(+)EpCAM(-) cells adjacent to expanding ducts likely furthe

252 nverting to cholangiocyte-like cells, Sox9(+)EpCAM(-) cells provide luminal space near expanded ductu

253 know the cellular characteristics of Sox9(+)EpCAM(-) cells, we isolated them as GFP(+)EpCAM(-) cells

254 These results suggest that Sox9(+)EpCAM(-) cells maintaining biphenotypic status can estab

255 the ability of contact allergen-stimulated, EpCAM-deficient LC to exit epidermis in vivo was delayed

256 oncogene-induced ERK2 activation suppressed EpCAM expression, whereas genetic or pharmacological inh

257 ter region, we observed that ERK2 suppresses EpCAM transcription directly by binding to a consensus E

258 Surprisingly, EpCAM appears to modulate ERK activity.

259 contribution from its second arm, targeting EpCAM.

260 nofluorescence-based technology that targets EpCAM to rank aliquots of blood for the presence or abse

261 d on these results, it can be concluded that EpCAM is suitable for use as an EC biomarker, therapeuti

262 l-surface adhesion, here we demonstrate that EpCAM is a regulatory molecule in which its internalizat

263 Furthermore, we demonstrate that EpCAM(+) HCC cells cultured as spheroids are more sensit

264 rative immunoprecipitation demonstrated that EpCAM bound tightly to claudin-7.

265 We demonstrated via FACS that EpCAM is expressed by human spermatogonia but not MOLT-4

266 tome analysis of single cells and found that EpCAM(+) cells from controls expressed transcripts thoug

267 of EpCAM in cancer biology, we observed that EpCAM expression is decreased in mesenchymal-like primar

268 We observed that EpCAM expression is decreased with activation of the ERK

269 Herein, we report that EpCAM regulates the composition and function of tight ju

270 F levels in human tumor samples reveals that EpCAM is expressed at high levels in a wide range of Met

271 Here we show that EpCAM and reprogramming factors (c-Myc, Oct4, Nanog, and

272 These findings suggest that EpCAM modulates adhesion and TJ function by regulating i

273 Together, these findings suggest that EpCAM plays an important role in regulating cancer-initi

274 The EpCAM+/HLA-ABC-/CD49e- fraction was enriched for spermat

275 The EpCAM-/HLA-ABC+/CD49e+ fraction produced tumors followin

276 on into the human genome specifically at the EpCAM, CXCR4 and TFRC gene promoters.

277 ons with proteins and a layer containing the EpCAM antibodies.

278 ding to a consensus ERK2-binding site in the EpCAM promoter and indirectly through activation of EMT-

279 1 and ZEB1, which bind to E-box sites in the EpCAM promoter.

280 the cells, matching with the location of the EpCAM marker.

281 In detailed studies of the EpCAM promoter region, we observed that ERK2 suppresses

282 d by changes in histone modifications of the EpCAM promoter, a target of PRC2 and LSD1/Co-REST/HDAC1

283 ecificity for nonoverlapping epitopes on the EpCAM extracellular domain were chosen for further evalu

284 Treatment with the EpCAM neutralizing antibody, EpAb2-6, inhibited AKT and

285 addition, molecular heterogeneity within the EpCAM(+) population of freshly isolated foetal and adult

286 Using EpCAM targeted MBs CTCs from metastatic cancer patients

287 umulated at the tumor cell surface in viable EpCAM-expressing tumor tissue.

288 Tumor uptake of (89)Zr-AMG 110 was EpCAM-specific and correlated with EpCAM expression.

289 AM-low cells, and its potency decreases when EpCAM levels are reduced by RNAi.

290 s required for association of claudin-1 with EpCAM.

291 G 110 was EpCAM-specific and correlated with EpCAM expression.

292 we generated conditional knockout mice with EpCAM-deficient LC and characterized them.

293 nce of EpCAM, conditional knockout mice with EpCAM-deficient LCs and control LC dendrites docked with

294 munization of conditional knockout mice with EpCAM-deficient LCs with ovalbumin led to increased indu

295 s, we studied conditional knockout mice with EpCAM-deficient LCs.

296 T cells in the tumor and spleen but not with EpCAM expression.

297 was extensively evaluated and optimized with EpCAM-positive HCT116 cells seeded into whole blood.

298 gy for cancer immunotherapy in patients with EpCAM-expressing tumors.

299 atment of malignant ascites in patients with EpCAM-positive carcinomas.

300 that of antibody, but the binding sites with EpCAM were different.