ライフサイエンスコーパス: choriocarcinoma

1 FLJ22028 (overexpressed in all GCTs, except choriocarcinomas).

2 e tissues, particularly in complete mole and choriocarcinoma.

3 urine of pregnant women and of patients with choriocarcinoma.

4 lateral non-gestational pure primary ovarian choriocarcinoma.

5 ma, embryonal carcinoma, yolk sac tumor, and choriocarcinoma.

6 es, teratoma (TE), yolk sac tumor (YST), and choriocarcinoma.

7 ising and repeat uterine evacuation revealed choriocarcinoma.

8 y included yolk sac, embryonal carcinoma, or choriocarcinoma.

9 Our results show that PMs can transform into choriocarcinoma.

10 partial mole, complete mole and gestational choriocarcinoma.

11 lastic cell line, Rcho-1, derived from a rat choriocarcinoma.

12 al autocrine mechanism in the development of choriocarcinomas.

13 e investigate whether PMs can transform into choriocarcinomas.

14 sclosed testicular carcinoma composed of 90% choriocarcinoma, 9% seminoma, and 1% teratoma.

15 rocess may contribute to the pathogenesis of choriocarcinoma, a highly invasive and lethal form of ca

16 as an essential angiogenic growth factor in choriocarcinoma and melanoma, promoting metastatic growt

17 pports the highly aggressive growth of human choriocarcinoma and possibly of the human trophoblast.

18 ally reduced in both IFN-gamma-treated human choriocarcinoma and primary TBCs compared with HeLa cell

19 re expressed in malignant trophoblasts (i.e. choriocarcinoma) and in the proliferative and in the inv

20 truma ovarii, thyrotropin-secreting tumours, choriocarcinoma, and amiodarone-induced thyrotoxicosis a

21 nd the malignant disorders of invasive mole, choriocarcinoma, and the rare placental-site trophoblast

22 diameter, one patient had a large metastatic choriocarcinoma; and three patients had low-grade astroc

23 Choriocarcinomas are embryonal tumours with loss of impr

24 Choriocarcinoma arising de novo from the ovary is very r

25 To determine whether the choriocarcinoma arose from the PM, DNA from the PM and c

26 enium 2, in the cubilin expressing placental choriocarcinoma BeWo cell line.

27 by which BCRP expression in human placental choriocarcinoma BeWo cells is regulated by progesterone.

28 We demonstrate that in human choriocarcinoma BeWo cells, the PKC activator 12-O-tetra

29 hat TEF-1 represses hCS promoter activity in choriocarcinoma (BeWo) cells, suggesting that TEF-1 inte

30 omic organization of the IGF2-H19 locus in a choriocarcinoma cancer cell line (JEG3).

31 (EC), teratoma (T), yolk sac tumor (YS), and choriocarcinoma (CC) on the basis of the lineage differe

32 have isolated a cDNA from a human placental choriocarcinoma cell cDNA library which, when expressed

33 We used an established choriocarcinoma cell line (BeWo cells) that can be induc

34 enate, biotin, and lipoate, from a placental choriocarcinoma cell line (JAR).

35 ected alpha subunit reporter gene in a human choriocarcinoma cell line (JEG3).

36 59)Fe-hTF into BeWo cells, a human placental choriocarcinoma cell line in culture.

37 on using antisense technology, using the rat choriocarcinoma cell line Rcho-1 as a trophoblastic cell

38 nsient transfection assays in JEG-3 cells, a choriocarcinoma cell line with negligible endogenous NFI

39 that have either moderate (BeWo, a placental choriocarcinoma cell line) or high (MCF-7/MX100, a breas

40 st differentiation and fusion using the BeWo choriocarcinoma cell line, a model of villous cytotropho

41 ation to endoreduplication in the Rcho-1 rat choriocarcinoma cell line.

42 as well as in BeWo cells, a human placental choriocarcinoma cell line.

43 atan sulfate expressed by JAR cells, a human choriocarcinoma cell line.

44 ype-specific, with greatest activity seen in choriocarcinoma cell lines (4-10-fold enhancement).

45 ream enhancer functions in the JEG-3 and JAR choriocarcinoma cell lines but not in adipocytes or HeLa

46 Furthermore, only trophoblast-derived choriocarcinoma cell lines expressed HERV-PTN mRNA where

47 viously reported the identification of human choriocarcinoma cell lines that have very high levels of

48 on analysis in human (BeWo) and rat (Rcho-1) choriocarcinoma cell lines to examine trophoblast cell-s

49 term placentas, purified trophoblast cells, choriocarcinoma cell lines, and human umbilical vein end

50 profiles of transactivation between the two choriocarcinoma cell lines, but maximal activation in bo

51 When DOC-2/hDab2 was transfected into the choriocarcinoma cell lines, Jar, JEG and BeWo, the stabl

52 acentas, term cytotrophoblast cells, and two choriocarcinoma cell lines, JEG-3 and Jar.

53 normal trophoblast cells in culture than in choriocarcinoma cell lines.

54 l pregnancy and that secreted by three human choriocarcinoma cell lines.

55 al analysis in transiently transfected human choriocarcinoma cells (BeWo).

56 ter and Na+ and K+ contents were measured in choriocarcinoma cells (JAr cell line; 96% of which are u

57 riptional regulator that binds to the JRE in choriocarcinoma cells (JEG3 cells).

58 Choriocarcinoma cells and HeLa cells express comparable

59 interaction between Dlx3 and Smad6 in human choriocarcinoma cells and in differentiated trophoblasts

60 from embryonal carcinoma cells, but also in choriocarcinoma cells and in MCF-7 breast carcinoma cell

61 n, the PLE3 element was a strong enhancer in choriocarcinoma cells but not in HeLa cells.

62 the activity of a promoter test fragment in choriocarcinoma cells by 80%.

63 Finally, the JAR choriocarcinoma cells elaborated EPO into the culture me

64 icantly reduced in human trophoblast-derived choriocarcinoma cells relative to HeLa epithelial or fib

65 66 element is shown to be activated in JEG-3 choriocarcinoma cells through synergistic interactions b

66 ophoblastic neoplasias, and is essential for choriocarcinoma cells to survive and escape from apoptos

67 JEG-3 and BeWo choriocarcinoma cells treated with ET-1 displayed an inc

68 behavior of CLIC-5A in vivo, JEG-3 placental choriocarcinoma cells were stably transfected with epito

69 nuclear membranes isolated from JEG-3 human choriocarcinoma cells with epidermal growth factor (EGF)

70 Human choriocarcinoma cells with high endogenous BCRP expressi

71 Treatment of choriocarcinoma cells with the tyrosine phosphatase inhi

72 ass I molecules is abrogated in HSV-infected choriocarcinoma cells, a phenomenon mediated by the vira

73 ed by 27-OHC in COS-1 cells, Y-1 cells, BeWo choriocarcinoma cells, Chinese hamster ovary (CHO) cells

74 The StAR gene promoter is not active in BeWo choriocarcinoma cells, COS-1 cells, HeLa cells, or SK-OV

75 addition, cultured JAR (trophoblast-derived) choriocarcinoma cells, cytotrophoblasts isolated from te

76 in is drastically up-regulated by hypoxia in choriocarcinoma cells, whereas expression of PIGF is not

77 by the overexpression of Ets-2 in human JAr choriocarcinoma cells, which are permissive for IFNT exp

78 ion in syncytializing primary cells and BeWo choriocarcinoma cells.

79 oblasts isolated from term placenta, and JAR choriocarcinoma cells.

80 in vitro but has no effect on that of human choriocarcinoma cells.

81 wn to direct optimal GCAP gene expression in choriocarcinoma cells.

82 he hCGbeta subunit (hCGbeta) promoter in JAr choriocarcinoma cells.

83 sts and NIH 3T3 cells but totally lacking on choriocarcinoma cells.

84 , on cellular proliferation and apoptosis in choriocarcinoma cells.

85 GPR30; a similar effect was observed in JEG3 choriocarcinoma cells.

86 of JAK-2 is compromised in IFN-gamma-treated choriocarcinoma cells.

87 red to placental fibroblasts and human JEG-3 choriocarcinoma cells.

88 ation of this site abolished its activity in choriocarcinoma cells.

89 ssion of growth factor pleiotrophin in human choriocarcinoma cells.

90 via a dynamin-independent mechanism in JEG-3 choriocarcinoma cells.

91 sis of mouse pituitary tumor cells and human choriocarcinoma cells.

92 only a very low level of gene expression in choriocarcinoma cells; the expression does not respond t

93 7 and MDA-MB-231 breast cancer cells and JAR choriocarcinoma cells; we also show for the first time t

94 genetic analysis showed that the subsequent choriocarcinomas contained identical single maternal and

95 A choriocarcinoma-derived cell line (JAr) which, unlike th

96 tly requires treatment with chemotherapy, to choriocarcinoma, for which multi-agent chemotherapy is t

97 d mouse trophoblast cell lines akin to human choriocarcinomas form tumors in syngeneic and immunodefi

98 he depletion of HERV-PTN mRNA prevents human choriocarcinoma growth, invasion, and angiogenesis in mi

99 own previously that PDGF-A overexpression in choriocarcinoma, hepatoma and lung carcinoma cell lines

100 inoma arose from the PM, DNA from the PM and choriocarcinoma in each patient was compared using micro

101 This was identified as choriocarcinoma in three cases.

102 HO and Lec4 cells) and endogenous (placental choriocarcinoma JAR cells) expression systems, we tested

103 Human placental choriocarcinoma (JAR) cells endogenously expressing glyc

104 In human placental choriocarcinoma (JAR) cells, which have been previously

105 phosphorylation and ubiquitination in human choriocarcinoma JEG-3 and mouse pituitary AtT20 cells.

106 otile and invasive in culture as compared to choriocarcinoma JEG-3 cells and normal extravillous trop

107 bal transcriptional effect of PTTG1 in human choriocarcinoma JEG-3 cells by simultaneously assessing

108 g activity when transiently transfected into choriocarcinoma JEG-3 cells in contrast to HeLa cells.

109 Using human choriocarcinoma JEG-3 cells, we found that sustained act

110 no-terminal p300/CBP binding domain in human choriocarcinoma JEG-3 cells.

111 vitro, but neither placental fibroblasts nor choriocarcinoma (malignant trophoblast) cell lines did s

112 se results reveal a route by which malignant choriocarcinoma may arise from molar pregnancies.

113 In a case of choriocarcinoma MCM8 mRNA is aberrant, leading to expres

114 gated the significance of HERV-PTN mRNA in a choriocarcinoma model by targeting this transcript with

115 cinoma (n = 1), yolk sac tumor (n = 107), or choriocarcinoma (n = 1).

116 All choriocarcinomas (n = 33), 90% of epithelioid trophoblas

117 on blocks or markedly reduces the binding of choriocarcinoma nuclear factors to the PLAP promoter, le

118 men were diagnosed of having postgestational choriocarcinoma on the basis of persistently positive hu

119 n HepG2 hepatoma cells, but inactive in JEG3 choriocarcinoma or 3T3 cells.

120 BeWo cells, a human choriocarcinoma placental cell line, behaved as did Menk

121 This group is composed of choriocarcinoma, placental-site trophoblastic tumour, an

122 mouse embryo ectoplacental cone and the rat choriocarcinoma (Rcho-1) cell line, that trophoblast dif

123 protocols for the diagnosis and treatment of choriocarcinoma should be modified to include a compulso

124 Loss-of-function using plgf shRNA in a human choriocarcinoma significantly accelerated tumor growth r

125 lateral non-gestational pure primary ovarian choriocarcinoma that was confirmed by beta human chorion

126 ver previously been proven to transform into choriocarcinoma, the most malignant form of gestational

127 Except for choriocarcinoma, the neoplasms that develop from human t

128 ibits Wilms, rhabdoid, rhabdomyosarcoma, and choriocarcinoma tumor cell growth, and silencing HOTS by

129 o in hormone-sensitive breast, prostate, and choriocarcinoma tumors to slow their growth.

130 lateral non-gestational pure primary ovarian choriocarcinoma was made.

131 patient nearly died before the diagnosis of choriocarcinoma was made.

132 The histology of both PM and ensuing choriocarcinoma was reviewed and flow cytometry used to

133 atients with a PM who developed a subsequent choriocarcinoma were identified from our GTD database.

134 Viable tumor included embryonal carcinoma, choriocarcinoma, yolk sac carcinoma, seminoma, and terat