ライフサイエンスコーパス: mammosphere

1 le, motile protrusions on the surface of the mammosphere.

2 to proliferate in suspension, as nonadherent mammospheres.

3 way is aberrantly activated in breast cancer mammospheres.

4 increased the ability of these cells to form mammospheres.

5 growth of human breast cancer stem cells as mammospheres.

6 tectable in stem-like cells when expanded as mammospheres.

7 tly compromised the ability of cells to form mammospheres.

8 KP-1) and dephosphorylation of ERK1/2 in the mammospheres.

9 hose cells have an increased ability to form mammospheres, a property associated with mammary epithel

10 (BCSCs), including CD44(+)CD24(-) fractions, mammospheres, ALDH1(+) populations and side population c

11 s of hypoxia on CSC activity, using in vitro mammosphere and holoclone assays as well as in vivo limi

12 drogenase 1 (ALDH1) expression, and decrease mammosphere and progenitor colony formation.

13 CD133NPs effectively decreased the number of mammospheres and colonies formed.

14 he number, size, and replating efficiency of mammospheres and downregulated the stem cell markers ALD

15 cells exhibited an increased ability to form mammospheres and elevated expression of pluripotency-fac

16 -like cells isolated from HMLE cultures form mammospheres and express markers similar to those of HML

17 patient samples that are capable of forming mammospheres and initiating tumors with as few as 10 GD2

18 ER2(+)/PIK3CA tumors more efficiently formed mammospheres and lung metastases.

19 significant decrease in the overall size of mammospheres and reduced tumor volume in nude mice.

20 iferation and self-renewal potential of MCF7 mammospheres and resulted in cell death after <4 weeks o

21 P4-treated breast cancer cells formed larger mammospheres and silencing of CK5 using small hairpin RN

22 ogical inhibition of the Akt pathway in both mammospheres and syngeneic mice bearing tumors was shown

23 an mammary stem/progenitor cells cultured as mammospheres and that these genes are down-regulated whe

24 to the recovery of the capacity to generate mammospheres and to an increase in the number of tumors.

25 of miR-181, exhibited reduced expression in mammospheres and upon TGF-beta treatment.

26 ly improves the ability of cMaSCs to grow as mammospheres and, importantly, that this effect is aboli

27 tion blocks the formation and maintenance of mammospheres, and in combination with chemotherapy suppr

28 Importantly, mammospheres are enriched for cells that regenerate an e

29 We demonstrate that nonadherent mammospheres are enriched in early progenitor/stem cells

30 Here, we used progenitor-containing mammospheres as an in vitro exposure model to study this

31 as compared to non-TICs and in TIC-enriched mammospheres as compared to primary tumor cells depleted

32 howed that McTNs persist in breast stem cell mammospheres as flexible, motile protrusions on the surf

33 or (VDR) was significantly down-regulated in mammospheres, as well as in ALDH(+) breast cancer cells.

34 endent inhibition of bCSC, as evidenced by a mammosphere assay and flow cytometric analysis of aldehy

35 d ALDH1, with further characterisation using mammosphere assay and transplantation into immunodeficie

36 splayed enhanced self-renewal as measured by mammosphere assay compared with CD44(+)/CD24(-)/ANTXR1(-

37 miting dilution transplantation and in vitro mammosphere assay, a Lin(-)CD29(H)CD24(H) subpopulation

38 as able to control cancer cell stemness in a mammosphere assay, anchorage-independent growth in vitro

39 drogenase 1, side population and by in vitro mammosphere assay.

40 progenitor cells as demonstrated by in vitro mammosphere assays and the expression of stem cell marke

41 alpha3, increased stem cell self-renewal in mammosphere assays and Wnt signaling including the expre

42 mesenchymal transition and generate >100-mum mammospheres bearing markers of cancer-initiating cells.

43 nase (ALDH(+)) had increased ability to form mammospheres compared to ALDH(-) cells.

44 Mammospheres, containing enriched breast progenitors, we

45 TPH was induced by PRL in mammosphere cultures and by milk stasis in nursing dams,

46 ible model of cellular transformation and in mammosphere-derived breast CSCs.

47 NA methylation of its promoter CpG island in mammosphere-derived epithelial cells on diethylstilbestr

48 e altered in epithelial progeny derived from mammospheres exposed to a synthetic estrogen, diethylsti

49 These mammospheres expressed MCSC-specific markers and generat

50 st cancer cells by reducing the formation of mammosphere, expression of pluripotency-factors and alde

51 s expands the stem cell population, augments mammosphere formation and accelerates EMT.

52 ties, involving Snail and Slug upregulation, mammosphere formation and aldehyde dehydrogenase activit

53 to a non-CSC, which was detected by reduced mammosphere formation and cell motility.

54 ssion and enriched for CSCs, as indicated by mammosphere formation and CSC markers.

55 with stem cells assessed by gene expression, mammosphere formation and lineage markers.

56 and mammosphere formation in SUM225, whereas mammosphere formation and Notch1 activity were increased

57 g cell (TIC) fraction was investigated using mammosphere formation and soft-agar colony formation ass

58 ARTN also enhanced mammosphere formation and the ALDH1+ population in estro

59 DUSP4 loss increased mammosphere formation and the expression of the CSC-prom

60 Loss of miR-141 enhanced both mammosphere formation and tumor initiation.

61 es the increase in cancer cell viability and mammosphere formation by equol, and results in a signifi

62 PL also inhibited mammosphere formation by tumor cells from patient-derive

63 se aldehyde dehydrogenase-positive BCSCs and mammosphere formation capacity in SUM149.

64 er cell motility and metastasis, and greater mammosphere formation efficiency.

65 Mammosphere formation in cell lines and human primary DC

66 demonstrate that DAPT reduced acini size and mammosphere formation in MCF10DCIS.com whereas there was

67 hanced migration and invasion, and increased mammosphere formation in methylcellulose.

68 Lapatinb reduced acini size and mammosphere formation in SUM225, whereas mammosphere for

69 uPAR overexpression increased mammosphere formation in vitro and tumor formation in an

70 se reduced cellular migration, invasion, and mammosphere formation of ErbB2-induced mammary tumors.

71 Inhibition of ALDH1 activity and/or mammosphere formation upon DATS treatment was significan

72 Both drug resistance and enhanced mammosphere formation were reversed by treatment with a

73 increased whilst the inhibitor DKK1 reduced mammosphere formation with the greatest inhibitory effec

74 otch1 abrogated the increase in CSC markers, mammosphere formation, and in vivo tumor-initiating capa

75 mary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the dev

76 in serial transplantations in vivo, reduced mammosphere formation, and reduced the proportion of CD4

77 s the CD44(hi)/CD24(lo) population, enhances mammosphere formation, and upregulates aldehyde dehydrog

78 tion, and increased stem cell generation and mammosphere formation, dependent upon autocrine TGF-beta

79 cell lines and abrogates NFkappaB-dependent mammosphere formation, indicating that DMF has anti-canc

80 and CD44(+)/CD24(-) CSC subpopulations, and mammosphere formation, indicating that JNK promotes CSC

81 Mammosphere formation, inhibited by EZH2 depletion, was

82 ER+ve and ER-ve breast cancer but not normal mammosphere formation, suggesting that the Wnt pathway i

83 tosis, reversing EMT-signaling and impairing mammosphere formation, thereby blocking the tumor-formin

84 (CIP1) attenuated oncogene-induced BT-IC and mammosphere formation.

85 in parallel with decreased CD44(hi)/CD24(lo) mammosphere formation.

86 increased the expression of CSC markers and mammosphere formation.

87 cyclin D1 expression, cell proliferation or mammosphere formation.

88 ke cells and promoted cell growth as well as mammosphere formation.

89 important for cellular growth, invasion and mammosphere formation.

90 ectively, and a reduction by 2.6-fold of the mammospheres formation.

91 null cells abrogated invasion, migration and mammosphere-formation.

92 owth, altered morphogenesis in Matrigel, and mammosphere forming ability, when overexpressed in immor

93 stem cell properties, which included reduced mammosphere-forming ability and tumor initiation.

94 ATRA reduced mammosphere-forming ability of a subset of breast cancer

95 /CD24(-) stem cells, and a 3.2-fold enhanced mammosphere-forming capacity.

96 We also undertook cytogenetic analyses of mammosphere-forming cells after prolonged culture, which

97 tes or cytokines increased the proportion of mammosphere-forming cells and of cells expressing stem-l

98 SMO activation also increased the mammosphere-forming efficiency of primary mammary epithe

99 m relative to wild type, suggesting enhanced mammosphere-forming efficiency was due to increased surv

100 enhanced anoikis sensitivity, and suppressed mammosphere generation in mammary epithelial cells.

101 the miR-181 family members were elevated in mammospheres grown in undifferentiating conditions, comp

102 ng proteins important for breast cancer cell mammosphere growth.

103 MMTV-neu;Nedd9(-/-) mammospheres had striking defects in morphology and cell

104 ated that isolated PI-MECs were able to form mammospheres in culture, and upon transplantation, these

105 pe and form well-organized prostaspheres and mammospheres in Matrigel.

106 feration and a decreased ability to generate mammospheres in normal mammary glands.

107 ibroblasts, and were also capable of forming mammospheres in suspension culture and subsequent format

108 on of breast cancer (BC) cells that can form mammospheres in suspension, a feature endowed by stem ce

109 The ability of MCF-10A(arom) cells to form mammospheres in the absence of serum was increased.

110 samples were cultured in 3D matrigel and as mammospheres in the presence, absence or combination of

111 -like properties such as the ability to form mammospheres in vitro and tumor self-renewal in vivo.

112 ary gland cells that are capable of forming "mammospheres" in vitro.

113 Activation of hedgehog signaling increases mammosphere-initiating cell number and mammosphere size,

114 lasia, and modulation of Bmi-1 expression in mammosphere-initiating cells alters mammary development

115 Overexpression of Gli2 in mammosphere-initiating cells results in the production o

116 on of new cell surface markers for enriching mammosphere-initiating cells, including endoglin and pri

117 Snail was up-regulated in mammospheres isolated from breast cancer cells.

118 Down-regulation of p63 in ErbB2 mammospheres markedly restricts self-renewal and expansi

119 Our findings that PHLDA1 is upregulated in mammospheres (MS) of ER+ breast cancer cells and that PH

120 , breast cancer cells propagated in vitro as mammospheres (MSs) have also been shown to be enriched f

121 SCF rescued the c-Jun-deficient mammosphere production.

122 stem-like cells, offsetting the formation of mammospheres relative to nontransduced T cells.

123 analysis of cells isolated from nonadherent mammospheres revealed overlapping genetic programs with

124 eases mammosphere-initiating cell number and mammosphere size, whereas inhibition of the pathway resu

125 RNA abolished this P4-dependent increase in mammosphere size.

126 CK5+ cells and prevented the P4 increase in mammosphere size.

127 helial cells that have undergone an EMT form mammospheres, soft agar colonies, and tumors more effici

128 53 in stem/progenitor cell-containing murine mammospheres, suggesting a potential role for the ER-p53

129 ly transformed line that forms self-renewing mammospheres that contain cancer stem cells.

130 ikingly, 1 reduces the formation and size of mammospheres to a greater extent than salinomycin, an es

131 ibly inhibits the formation of free-floating mammospheres to an extent similar to that of salinomycin

132 educes the formation, size, and viability of mammospheres, to a greater extent than salinomycin, a po

133 Mammospheres were relatively insensitive to treatment wi

134 metastatic breast cancer samples, only ER-ve mammospheres were responsive to the ligand Wnt3a.

135 is study, we examined vitamin D signaling in mammospheres which are enriched in MCSCs from establishe

136 Notably, in MCF-7 cell mammospheres, which display a well-defined acinus-like s

137 ficient epithelial cells were unable to form mammospheres, which were considered to be derived from m