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1 le, motile protrusions on the surface of the mammosphere.
2 to proliferate in suspension, as nonadherent mammospheres.
3 xpression was directly controlled by NRF2 in mammospheres.
4 D8's effects on antioxidant genes and ROS in mammospheres.
5 idant genes to enhance gene transcription in mammospheres.
6 ards three-dimensionally cultured breast CSC mammospheres.
7 egation and increase the formation of clonal mammospheres.
8 of single tumor cells as they divide to form mammospheres.
9 way is aberrantly activated in breast cancer mammospheres.
10 increased the ability of these cells to form mammospheres.
11 growth of human breast cancer stem cells as mammospheres.
12 tectable in stem-like cells when expanded as mammospheres.
13 tly compromised the ability of cells to form mammospheres.
14 KP-1) and dephosphorylation of ERK1/2 in the mammospheres.
15 hose cells have an increased ability to form mammospheres, a property associated with mammary epithel
16 (BCSCs), including CD44(+)CD24(-) fractions, mammospheres, ALDH1(+) populations and side population c
17 s of hypoxia on CSC activity, using in vitro mammosphere and holoclone assays as well as in vivo limi
20 he number, size, and replating efficiency of mammospheres and downregulated the stem cell markers ALD
21 cells exhibited an increased ability to form mammospheres and elevated expression of pluripotency-fac
22 -like cells isolated from HMLE cultures form mammospheres and express markers similar to those of HML
23 patient samples that are capable of forming mammospheres and initiating tumors with as few as 10 GD2
26 iferation and self-renewal potential of MCF7 mammospheres and resulted in cell death after <4 weeks o
27 P4-treated breast cancer cells formed larger mammospheres and silencing of CK5 using small hairpin RN
28 ogical inhibition of the Akt pathway in both mammospheres and syngeneic mice bearing tumors was shown
29 an mammary stem/progenitor cells cultured as mammospheres and that these genes are down-regulated whe
30 to the recovery of the capacity to generate mammospheres and to an increase in the number of tumors.
32 ly improves the ability of cMaSCs to grow as mammospheres and, importantly, that this effect is aboli
33 tion blocks the formation and maintenance of mammospheres, and in combination with chemotherapy suppr
34 ercentage of cancer stem cells and number of mammospheres, and its influence upon several glycosphing
38 as compared to non-TICs and in TIC-enriched mammospheres as compared to primary tumor cells depleted
39 howed that McTNs persist in breast stem cell mammospheres as flexible, motile protrusions on the surf
40 or (VDR) was significantly down-regulated in mammospheres, as well as in ALDH(+) breast cancer cells.
41 endent inhibition of bCSC, as evidenced by a mammosphere assay and flow cytometric analysis of aldehy
42 d ALDH1, with further characterisation using mammosphere assay and transplantation into immunodeficie
43 splayed enhanced self-renewal as measured by mammosphere assay compared with CD44(+)/CD24(-)/ANTXR1(-
45 miting dilution transplantation and in vitro mammosphere assay, a Lin(-)CD29(H)CD24(H) subpopulation
46 as able to control cancer cell stemness in a mammosphere assay, anchorage-independent growth in vitro
48 progenitor cells as demonstrated by in vitro mammosphere assays and the expression of stem cell marke
49 alpha3, increased stem cell self-renewal in mammosphere assays and Wnt signaling including the expre
51 mesenchymal transition and generate >100-mum mammospheres bearing markers of cancer-initiating cells.
56 NA methylation of its promoter CpG island in mammosphere-derived epithelial cells on diethylstilbestr
57 tive complexes 2 and 3 readily penetrate CSC mammospheres, enter CSC nuclei, induce genomic DNA damag
58 e altered in epithelial progeny derived from mammospheres exposed to a synthetic estrogen, diethylsti
60 st cancer cells by reducing the formation of mammosphere, expression of pluripotency-factors and alde
62 stem-like properties as indicated by reduced mammosphere formation and aldehyde dehydrogenase activit
63 ties, involving Snail and Slug upregulation, mammosphere formation and aldehyde dehydrogenase activit
67 and mammosphere formation in SUM225, whereas mammosphere formation and Notch1 activity were increased
68 g cell (TIC) fraction was investigated using mammosphere formation and soft-agar colony formation ass
72 es the increase in cancer cell viability and mammosphere formation by equol, and results in a signifi
79 demonstrate that DAPT reduced acini size and mammosphere formation in MCF10DCIS.com whereas there was
83 se reduced cellular migration, invasion, and mammosphere formation of ErbB2-induced mammary tumors.
84 l-to-mesenchymal transition and CCN2-induced mammosphere formation of MCF-7 adenocarcinoma cells.
85 lial cells results in significantly enhanced mammosphere formation that is accelerated in the presenc
87 addition, inhibition of progranulin-induced mammosphere formation was examined and found to be most
89 increased whilst the inhibitor DKK1 reduced mammosphere formation with the greatest inhibitory effec
91 ed cells show mitigated migration, invasion, mammosphere formation, and CD44(+)/CD24(-) population.
92 ed higher levels of migration, invasion, and mammosphere formation, and had a greater proportion of c
93 otch1 abrogated the increase in CSC markers, mammosphere formation, and in vivo tumor-initiating capa
94 mary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the dev
95 in serial transplantations in vivo, reduced mammosphere formation, and reduced the proportion of CD4
96 s the CD44(hi)/CD24(lo) population, enhances mammosphere formation, and upregulates aldehyde dehydrog
97 tion, and increased stem cell generation and mammosphere formation, dependent upon autocrine TGF-beta
98 d anchorage-independent colony formation and mammosphere formation, indicating compromised self-renew
99 cell lines and abrogates NFkappaB-dependent mammosphere formation, indicating that DMF has anti-canc
100 and CD44(+)/CD24(-) CSC subpopulations, and mammosphere formation, indicating that JNK promotes CSC
102 ession in HER2+ BC cells increased secondary mammosphere formation, soft agar colony formation, and %
103 ER+ve and ER-ve breast cancer but not normal mammosphere formation, suggesting that the Wnt pathway i
104 tosis, reversing EMT-signaling and impairing mammosphere formation, thereby blocking the tumor-formin
118 owth, altered morphogenesis in Matrigel, and mammosphere forming ability, when overexpressed in immor
119 8600 treatment suppresses growth, colony and mammosphere forming capacity of BCSCs and induces G2M ar
125 We also undertook cytogenetic analyses of mammosphere-forming cells after prolonged culture, which
126 tes or cytokines increased the proportion of mammosphere-forming cells and of cells expressing stem-l
128 m relative to wild type, suggesting enhanced mammosphere-forming efficiency was due to increased surv
130 enhanced anoikis sensitivity, and suppressed mammosphere generation in mammary epithelial cells.
131 the miR-181 family members were elevated in mammospheres grown in undifferentiating conditions, comp
132 ults indicate that using lipid tethering for mammosphere growth assays can reduce the confounding fac
135 ated that isolated PI-MECs were able to form mammospheres in culture, and upon transplantation, these
136 d MCF7-mCherry cells were seeded, 65% of the mammospheres in lipid-coated wells demonstrated single c
139 ibroblasts, and were also capable of forming mammospheres in suspension culture and subsequent format
140 on of breast cancer (BC) cells that can form mammospheres in suspension, a feature endowed by stem ce
142 samples were cultured in 3D matrigel and as mammospheres in the presence, absence or combination of
143 -like properties such as the ability to form mammospheres in vitro and tumor self-renewal in vivo.
146 Activation of hedgehog signaling increases mammosphere-initiating cell number and mammosphere size,
147 lasia, and modulation of Bmi-1 expression in mammosphere-initiating cells alters mammary development
149 on of new cell surface markers for enriching mammosphere-initiating cells, including endoglin and pri
152 Our findings that PHLDA1 is upregulated in mammospheres (MS) of ER+ breast cancer cells and that PH
153 , breast cancer cells propagated in vitro as mammospheres (MSs) have also been shown to be enriched f
157 analysis of cells isolated from nonadherent mammospheres revealed overlapping genetic programs with
158 eases mammosphere-initiating cell number and mammosphere size, whereas inhibition of the pathway resu
161 helial cells that have undergone an EMT form mammospheres, soft agar colonies, and tumors more effici
162 53 in stem/progenitor cell-containing murine mammospheres, suggesting a potential role for the ER-p53
164 hibits the formation, size, and viability of mammospheres to a better extent than salinomycin, an est
165 Notably, 3 reduces the formation and size of mammospheres to a greater extent than salinomycin, an es
166 ikingly, 1 reduces the formation and size of mammospheres to a greater extent than salinomycin, an es
167 ibly inhibits the formation of free-floating mammospheres to an extent similar to that of salinomycin
168 educes the formation, size, and viability of mammospheres, to a greater extent than salinomycin, a po
173 is study, we examined vitamin D signaling in mammospheres which are enriched in MCSCs from establishe
175 ficient epithelial cells were unable to form mammospheres, which were considered to be derived from m