ライフサイエンスコーパス: embryonal carcinoma

1 ith good clinical prognosis in patients with embryonal carcinoma.

2 may share a common pathway involving p53 in embryonal carcinomas.

3 e urinary bladder (6 of 6 cases), testicular embryonal carcinoma (1 of 1 case), colonic adenocarcinom

4 As an example, human embryonal carcinoma 2102 cells display strong adhesion t

5 lated in cell-free lysates prepared from P19 embryonal carcinoma and C6 glioma cell lines and after c

6 ity and trophoblast differentiation of mouse embryonal carcinoma and embryonic stem cells.

7 Presence of vascular invasion together with embryonal carcinoma and rete testis invasion in the test

8 the pluripotent cells (embryonic stem cells, embryonal carcinomas and induced pluripotent cells).

9 that exhibited coordinated overexpression in embryonal carcinomas and seminomas, which included the k

10 lain the differences in pluripotency between embryonal carcinomas and seminomas.

11 -cm tumor that was 95% yolk sac tumor and 5% embryonal carcinoma, and retroperitoneal lymph node diss

12 We further identified the embryonal carcinoma antigen podocalyxin-like protein 1 (

13 and nonseminomas, which include pluripotent embryonal carcinomas as well as other histologic subtype

14 erentiated human GCTs, such as seminomas and embryonal carcinoma, but not in normal testis or in diff

15 beta) in neurons (NT2N) derived from a human embryonal carcinoma cell line (NT2) by steady state meta

16 rated that NT2N neurons derived from a human embryonal carcinoma cell line (NT2) constitutively proce

17 Treatment of the undifferentiated parental embryonal carcinoma cell line NT2 with soluble Tax1 did

18 rans-retinoic acid (RA) treatment, the human embryonal carcinoma cell line NT2/D1 exhibits a progress

19 In the embryonal carcinoma cell line NT2/D1, ectopic DeltaN-p63

20 oth mouse embryonic stem cells and the human embryonal carcinoma cell line NT2/D1.

21 After RA-treatment the multipotent human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1)

22 iggers terminal differentiation in the human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1),

23 Differentiation of the human embryonal carcinoma cell line NTERA-2 is characterized b

24 oters in mouse central nervous system and an embryonal carcinoma cell line P19 was confirmed in a rib

25 xamined in transgenic mouse embryos, a mouse embryonal carcinoma cell line P19, and a mouse embryonic

26 ct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves recept

27 quired for suppressive activity in the mouse embryonal carcinoma cell line P19.

28 Incubation of a human embryonal carcinoma cell line with NMM reduces its stem

29 transactivation function of p53 in the human embryonal carcinoma cell line, NT2/D1, in a retinoid rec

30 Both species are repressed when the human embryonal carcinoma cell line, NT2/D1, is induced to dif

31 Here we show that a embryonal carcinoma cell line, P19, transfected with a S

32 clude two regions of promoter activity in an embryonal carcinoma cell line, Tera2EC.

33 r into a de novo methylation-competent mouse embryonal carcinoma cell line.

34 ell lines, five normal human tissues, and an embryonal carcinoma cell line.

35 significantly greater levels in human ES and embryonal carcinoma cell lines than in control samples.

36 Comparison of human embryonal carcinoma cell lines with breast/ovarian cance

37 nd no alpha subunit message, is expressed in embryonal carcinoma cell lines, F9 and Nulli-SSC1, and i

38 alyzed the activity of 4HPR on a panel of F9 embryonal carcinoma cell lines, which includes wild-type

39 pattern of ARP1 in several mouse tissues and embryonal carcinoma cell lines.

40 ines showed many similarities with the human embryonal carcinoma cell samples and more distantly with

41 pluripotent embryonic stem cells (ESCs) and embryonal carcinoma cells (ECCs) have some but not all c

42 the Hoxa1, RARbeta2, and Cyp26A1 RAREs in F9 embryonal carcinoma cells (teratocarcinoma stem cells) d

43 (IPE) element that is inactive in murine F9 embryonal carcinoma cells and active in the parietal end

44 predominant form in embryonic stem cells and embryonal carcinoma cells and can also be detected from

45 lated during neuronal differentiation in P19 embryonal carcinoma cells and epigenetic changes play an

46 or beta2 (RAR(beta2)) gene expression in P19 embryonal carcinoma cells and for reporters driven by th

47 y the activation of STAT1 and STAT3 in mouse embryonal carcinoma cells and human T cells.

48 ted knockdown of USP2a in NTERA-2 testicular embryonal carcinoma cells and MCF7 breast cancer cells c

49 re methylated de novo to a high level in the embryonal carcinoma cells and that the B1 elements acted

50 rget of GATA-6 regulation in differentiating embryonal carcinoma cells and that, in vivo, the express

51 These studies employed F9 embryonal carcinoma cells and their differentiated cells

52 Undifferentiated human embryonal carcinoma cells are characterized by high expr

53 , new markers, eg, FGF4, CD30, and OCT-4, of embryonal carcinoma cells are identifying alternative wa

54 protein synthesis-independent manner in P19 embryonal carcinoma cells by inactivation of NF-kappa B.

55 P19 mouse embryonal carcinoma cells can be stimulated to different

56 wn of Cripto-1 expression in human and mouse embryonal carcinoma cells desensitized the ligand-induce

57 protein affects mdm-2 gene expression as F9 embryonal carcinoma cells differentiate into parietal en

58 FoxA proteins are induced when F9 embryonal carcinoma cells differentiate into visceral en

59 c acid (RA)-induced differentiation of human embryonal carcinoma cells engages p53.

60 on of Pax3 expression in differentiating P19 embryonal carcinoma cells have been localized.

61 rmation of primitive endoderm from mouse P19 embryonal carcinoma cells in response to retinoic acid,

62 Differentiation of P19 embryonal carcinoma cells in response to the morphogen r

63 neural cells derived from embryonic stem and embryonal carcinoma cells in vitro and neural stem cells

64 st cancer cells and suppressed the growth of embryonal carcinoma cells in vitro.

65 ression following transfection into mouse F9 embryonal carcinoma cells indicated that only Adh-2 poss

66 L1 RNA in extracts from both mouse and human embryonal carcinoma cells indicated that ORF1 protein bi

67 Studies of miR-125b function in mouse P19 embryonal carcinoma cells induced to develop into neuron

68 erization partner E12, can convert mouse P19 embryonal carcinoma cells into differentiated neurons.

69 e Bmp2 mRNA during the differentiation of F9 embryonal carcinoma cells into parietal endoderm.

70 s demonstrated that differentiation of mouse embryonal carcinoma cells leads to transcriptional up-re

71 of the expressing differentiated cells with embryonal carcinoma cells or by treatment of the differe

72 Removal of endogenous OAZ from pluripotent embryonal carcinoma cells prevents the induction of Smad

73 Here, we report that human embryonal carcinoma cells proliferate and produce differ

74 that overexpressing Hoxa2 in cultures of P19 embryonal carcinoma cells reduced the frequency of spont

75 ion of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cispla

76 Embryonal carcinoma cells represent the pluripotent enti

77 t growth factor 4 (FGF-4) gene expression in embryonal carcinoma cells requires a synergistic interac

78 rentiation, whereas studies with pluripotent embryonal carcinoma cells suggest that this pathway prom

79 ed large sets of genes in embryonic stem and embryonal carcinoma cells that are associated with the t

80 bers of the MEF2 family are expressed in P19 embryonal carcinoma cells that have been induced to form

81 which regulates inducibility of the gene in embryonal carcinoma cells through a pattern of DNA-prote

82 Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm a

83 we demonstrate that differentiation of mouse embryonal carcinoma cells to parietal endoderm-like cell

84 the action of retinoic acid, inducing these embryonal carcinoma cells to primitive endoderm.

85 tutive levels of this BH3-only protein prime embryonal carcinoma cells to undergo rapid and massive a

86 ffold protein (GRASP), was isolated from P19 embryonal carcinoma cells using a subtractive screening

87 hylation upon stable transfection into mouse embryonal carcinoma cells was examined.

88 o DNA methylation-associated inactivation in embryonal carcinoma cells were transfected into differen

89 We showed previously that HL-60 and F9 mouse embryonal carcinoma cells will take up and deblock perac

90 In P19 embryonal carcinoma cells, activation of EphB1 (ELK) by

91 use embryonic stem cells, in differentiating embryonal carcinoma cells, and in transgenic mice.

92 sttranscriptionally in embryonic stem cells, embryonal carcinoma cells, and primary tumors.

93 cardiomyocyte differentiation in pluripotent embryonal carcinoma cells, and we show that this involve

94 d in mES cells and in Ntera-2 or NCCIT human embryonal carcinoma cells, as compared with cells growin

95 ot only in differentiated cells derived from embryonal carcinoma cells, but also in choriocarcinoma c

96 Sox-2 is also highly expressed in F9 embryonal carcinoma cells, but becomes undetectable foll

97 In P19 mouse embryonal carcinoma cells, expression of the MOR was gre

98 ansfection of TFIIB and IRF-1 cDNAs into P19 embryonal carcinoma cells, further demonstrating functio

99 footprinting analysis was performed with P19 embryonal carcinoma cells, in which transcription of the

100 we show that in mouse embryoid bodies or F9 embryonal carcinoma cells, RARs occupy a large repertoir

101 f RA-induced neuronal differentiation of p19 embryonal carcinoma cells, supporting a role for this pr

102 We show here, using P19 embryonal carcinoma cells, that the combination of RA an

103 coupled to the effective maturation of human embryonal carcinoma cells, the described co-transfection

104 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-nega

105 We have studied the function of LINC in F9 embryonal carcinoma cells, which are distinguished by a

106 mElf-3 mRNA during the differentiation of F9 embryonal carcinoma cells.

107 y recombinant nodal protein treatment of P19 embryonal carcinoma cells.

108 of retinoic acid-induced differentiation of embryonal carcinoma cells.

109 potent mouse embryonic stem cells or NTERA-2 embryonal carcinoma cells.

110 ferentiation and cell cycle control of human embryonal carcinoma cells.

111 ng retinoid-induced differentiation of human embryonal carcinoma cells.

112 ferentiation and growth suppression of human embryonal carcinoma cells.

113 tion signals has been devised with mouse P19 embryonal carcinoma cells.

114 fic inhibitor of histone deacetylase, on P19 embryonal carcinoma cells.

115 ic stem cells or their malignant equivalent, embryonal carcinoma cells.

116 noic acid/cAMP induced differentiation of F9 embryonal carcinoma cells.

117 ional activation of the same reporter in P19 embryonal carcinoma cells.

118 ng RA-driven differentiation of human NT2/D1 embryonal carcinoma cells.

119 nd murine mammary stem/progenitor cells, and embryonal carcinoma cells.

120 ouse embryonic stem (mES) cells and in human embryonal carcinoma cells.

121 erum/cytokine-free expansion of leukemic and embryonal carcinoma cells.

122 ctodermal differentiation of pluripotent P19 embryonal carcinoma cells.

123 colocalizing with OCT4 in Ntera2 testicular embryonal carcinoma cells.

124 ons of dorsal root ganglion (DRG) and in P19 embryonal carcinoma cells.

125 platin in testicular germ cell-derived human embryonal carcinoma cells.

126 vity that accompanies the differentiation of embryonal carcinoma cells.

127 s the specificity of RNA interference in p19 embryonal carcinoma cells.

128 f RA-induced neuronal differentiation in p19 embryonal carcinoma cells.

129 fferentiation and cell cycle arrest in human embryonal carcinoma cells.

130 Viable tumor included embryonal carcinoma, choriocarcinoma, yolk sac carcinoma

131 These results show that human embryonal carcinoma-derived progeny interact with mouse

132 ribosomal frameshifting signal of the mouse embryonal carcinoma differentiation regulated (Edr) gene

133 protein-coupled receptor is regulated during embryonal carcinoma differentiation.

134 ryogenesis, is expressed in undifferentiated embryonal carcinoma (EC) and embryonic stem (ES) cells.

135 (NSE), the latter including the pluripotent embryonal carcinoma (EC) and its differentiated derivati

136 Pluripotent cells within embryonal carcinoma (EC) can differentiate in vivo or in

137 used the well-characterized pluripotent P19 embryonal carcinoma (EC) cell culture model of neuro-ect

138 NTera-2 (NT2) cells are a human embryonal carcinoma (EC) cell line derived from a terato

139 rentiating cultures of the pluripotent human embryonal carcinoma (EC) cell line NTERA-2.

140 e to all-trans retinoic acid (RA), the human embryonal carcinoma (EC) cell line, NT2/D1, differentiat

141 derived from the retinoic acid-treated human embryonal carcinoma (EC) cell line, NTERA-2.

142 Using human embryonal carcinoma (EC) cells as bait, approximately 3

143 Embryonal carcinoma (EC) cells have served as a model to

144 et of neuroectodermal differentiation in P19 embryonal carcinoma (EC) cells three independent techniq

145 OCT4 levels and increases the resistance of embryonal carcinoma (EC) cells to cisplatin and bleomyci

146 y, it has been shown that differentiation of embryonal carcinoma (EC) cells turns on the expression o

147 therapy, and testicular cancer-derived human embryonal carcinoma (EC) cells undergo a p53-dominant tr

148 n between mDab1 and Src is observed when P19 embryonal carcinoma (EC) cells undergo differentiation i

149 Mouse embryonal carcinoma (EC) cells were then stably transfec

150 silenced genes in cancer cells; however, in embryonal carcinoma (EC) cells, CBX7 can initiate stable

151 bryonic stem (ES) cells and can give rise to embryonal carcinoma (EC) cells, the stem cells of testic

152 Retinoids cause differentiation in embryonal carcinoma (EC) cells, thus mimicking events in

153 ession of the TGF-beta2 gene, we employed F9 embryonal carcinoma (EC) cells, which express TGF-beta2

154 s induced by retinoic acid (RA) in mouse P19 embryonal carcinoma (EC) cells.

155 erentiated cells, but not in the parental F9 embryonal carcinoma (EC) cells.

156 wn that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with

157 tion stimulated by retinoic acid (RA) in the embryonal carcinoma (EC) line P19 is accompanied by upre

158 ed mouse embryonic stem (ES) cells and mouse embryonal carcinoma (EC) lines.

159 de of Noxa reduced the apoptotic response of embryonal carcinoma (EC) NTERA2 cells to cisplatin.

160 us GCTs (NSGCTs) can be further divided into embryonal carcinoma (EC), teratoma (T), yolk sac tumor (

161 Pluripotent embryonal carcinomas (EC) are the malignant counterparts

162 Embryonal carcinomas (EC) comprise a subset of TGCTs tha

163 n is restricted in vitro to undifferentiated embryonal carcinomas (ECs).

164 Using volume of embryonal carcinoma in the orchiectomy specimen, lymph n

165 ion of several stem cell-associated genes in embryonal carcinoma, including several core "stemness" g

166 Embryonal carcinoma is a model of embryonic development

167 ates 9 of 15 genes in this pathway in the F9 embryonal carcinoma model and 11 of 15 pathway genes in

168 inoma (n = 20), malignant teratoma (n = 55), embryonal carcinoma (n = 1), yolk sac tumor (n = 107), o

169 apoptosis in wild-type p53-containing human embryonal carcinoma NT-2 cells and in p53-null promyeloc

170 When comparing undifferentiated human embryonal carcinoma NT2- cells and differentiated NT2N n

171 acute promyelocytic leukemic (NB4) and human embryonal carcinoma (NTERA-2) cells exposed to all-trans

172 Required histology included yolk sac, embryonal carcinoma, or choriocarcinoma.

173 of neural progenitor cells, using the mouse embryonal carcinoma P19 cell line as a model system.

174 id receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic ac

175 Using mouse embryonal carcinoma P19 cells as a neural differentiatio

176 X protein levels are also increased in mouse embryonal carcinoma P19 cells during retinoic acid (RA)-

177 Stimulation of endogenous EphB1 in embryonal carcinoma P19 cells with its ligand ephrinB1 i

178 ne by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic

179 R) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by ret

180 d malignant tumors, with yolk sac tumors and embryonal carcinomas positive for alpha-fetoprotein, cyt

181 knockdown Smn gene expression in the murine embryonal carcinoma stem cell line P19, which can be dif

182 We used an embryonal carcinoma stem cell model and show here that (

183 tutively expressed in postnatal day 19 (P19) embryonal carcinoma stem cells and is suppressed by NO d

184 We identified mRNA subsets from P19 embryonal carcinoma stem cells by using mRNA-binding pro

185 Cs across species and between human ESCs and embryonal carcinoma stem cells suggest that while plurip

186 r the differentiation of cultured P19 murine embryonal carcinoma stem cells to beating cardiac myocyt

187 quired for the differentiation of murine P19 embryonal carcinoma stem cells to beating cardiac myocyt

188 primitive endoderm formation from mouse P19 embryonal carcinoma stem cells, a process that includes

189 ern virus replication in monocytic THP-1 and embryonal carcinoma (Tera-2) cells.

190 ed for 95 previously untreated patients with embryonal carcinoma with or without other germ cell comp

191 Comparison of embryonal carcinoma with seminomas revealed relative ove

192 t there is a subgroup of NSGCT patients with embryonal carcinoma (with or without other histologies)

193 btypes included immature teratoma, seminoma, embryonal carcinoma, yolk sac tumor, and choriocarcinoma