ライフサイエンスコーパス: cancer stem cell

1 Synergy was also observed against breast cancer stem cells.

2 , cell lines, and a genetic model of ovarian cancer stem cells.

3 almodulin-like kinase 1 (DCLK1), a marker of cancer stem cells.

4 in breast cancer significantly inhibits the cancer stem cells.

5 crucial for the biology of adult normal and cancer stem cells.

6 ty and phagocytosis checkpoints by apoptotic cancer stem cells.

7 induce Wnt-beta-catenin signals that expand cancer stem cells.

8 ay be a novel method of reducing endometrial cancer stem cells.

9 hways preferentially killing transformed and cancer stem cells.

10 EMT), and expressed markers related to colon cancer stem cells.

11 sion of side-population cells, also known as cancer stem cells.

12 es breast cancer initiation, metastasis, and cancer stem cells.

13 mesenchymal transition, and the emergence of cancer stem cells.

14 acids metabolism as a key regulator of lung cancer stem cells.

15 he characterization of metabolic activity in cancer stem cells.

16 possible role for PADI4 in regulating breast cancer stem cells.

17 vity, immune response, and the population of cancer stem cells.

18 ericytes, cancer associated fibroblasts, and cancer stem cells.

19 ates that this population contains potential cancer stem cells.

20 erapeutic targets for GBM subtype-restricted cancer stem cells.

21 riants are overexpressed in many cancers and cancer stem cells.

22 increased in view of its high expression in cancer stem cells, a population of cancer cells with str

23 ulation, providing a novel mechanism whereby cancer stem cells acquire metastatic potential.

24 arcinoma cells, including invasive behavior, cancer stem cell activity, and greater resistance to che

25 - resistant ovarian cancer cells and ovarian cancer stem cells and (ii) downregulation of beta-cateni

26 d their metastases depend on Bmi1-expressing cancer stem cells and AP1 signaling and that simultaneou

27 XPHOS dependency is frequently a hallmark of cancer stem cells and cells resistant to chemotherapy an

28 nsights relevant for experimental studies on cancer stem cells and for clinical protocols for the dia

29 trength of adhesive attachment could provide cancer stem cells and hematopoietic stem cells with a me

30 ROM1 (CD133) is detected in both somatic and cancer stem cells and is also expressed in terminally di

31 s from the paper 'Wnt activity defines colon cancer stem cells and is regulated by the microenvironme

32 The percent of cancer stem cells and number of formed mammospheres was

33 to its effect in reducing the percentage of cancer stem cells and number of mammospheres, and its in

34 rug target due to its role in maintenance of cancer stem cells and potential to eliminate cancer rela

35 transformations in Lgr5-expressing (Lgr5(+)) cancer stem cells and promote an adenoma-to-adenocarcino

36 4 as a tumor suppressor in regulating breast cancer stem cells and provide insight into context-speci

37 he mesenchymal state is also associated with cancer stem cells and resistance to chemotherapy.

38 bitor has the potential to eradicate ovarian cancer stem cells and to prevent ovarian cancer recurren

39 d transcriptomic experiments in the areas of cancer, stem cell and islet biology.

40 regenerative capacity of treatment-resistant cancer stem cells, and challenges in achieving high conc

41 growth factor beta signaling, maintenance of cancer stem cells, and modulation of the extracellular m

42 Cancer stem cells are particularly tolerant to DNA damag

43 n of tumor cells, called tumor initiating or cancer stem cells, are responsible for metastatic dissem

44 mammary tumor growth, reduces the number of cancer stem cells, as well as decreases tumor-initiating

45 n of cisplatin-induced senescence-associated cancer stem cells, as well as tumor relapse after cispla

46 and helps regulate the expression of several cancer stem cell associated markers including aldehyde d

47 o the maintenance of a chemoresistant breast cancer stem cell (BCSC) population.

48 hat Rad51ap1 plays a critical role in breast cancer stem cell (BCSC) self-renewal.

49 PHA5 deficiency effectively increases breast cancer stem cell (BCSC)-like properties, including NANOG

50 Breast cancer stem cells (BCSCs) are unique in their ability to

51 Breast cancer stem cells (BCSCs) play a critical role in cancer

52 T has been linked to the formation of breast cancer stem cells (BCSCs) that confer both tumor cell he

53 d that p62 expression was elevated in breast cancer stem cells (BCSCs), including CD44(+)CD24(-) frac

54 genase kinase 1 (PDK1) is enriched in breast cancer stem cells (BCSCs), whereas depletion of PDK1 rem

55 e and drug resistance is supported by breast cancer stem cells (BCSCs).

56 of apoptosis and promotion of proliferation, cancer stem cell biology, and epithelial-to-mesenchymal

57 ch-mediated function of Norrin in regulating cancer stem cell biology.

58 ve as a cell of origin for cancers, and that cancer stem cells can be key in driving the continued gr

59 Apoptotic cancer stem cells can evade cell death by undergoing cel

60 ediated epigenetic regulation of human colon cancer stem cells (CCSC).

61 Circulating cancer stem cells (CCSCs), a rare circulating tumor cell

62 temness, NANOG and OCT4, specifically in the cancer stem cell compartment, by reducing the transcript

63 The second International Cancer Stem Cell Conference in Cleveland, Ohio, on Septe

64 Increased cancer stem cell content during development of resistanc

65 Evidence indicates that a subpopulation of cancer stem cells contributes to therapy resistance and

66 epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) acquisitions.

67 its to an epithelial phenotype and inhibited cancer stem cell (CSC) activity.

68 The breast cancer stem cell (CSC) and bulk breast cancer cell poten

69 form of breast cancer that displays profound cancer stem cell (CSC) and mesenchymal features that pro

70 The discovery of colorectal (CR) cancer stem cell (CSC) as the cell compartment responsib

71 Ectopic expression of DOCK6 promoted GC cancer stem cell (CSC) characteristics and chemo- or rad

72 Recent research into the cancer stem cell (CSC) concept has driven progress in th

73 peutic treatment, and possessed the greatest cancer stem cell (CSC) content.

74 The HectH9/HK2 pathway regulates cancer stem cell (CSC) expansion and CSC-associated chem

75 epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) formation are two paramount proce

76 findings may have important implications for cancer stem cell (CSC) functions and therapeutic strateg

77 epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) maintenance resulting in tumor pr

78 breast cancer tumorigenesis, metastasis, and cancer stem cell (CSC) maintenance.

79 Here we report that splice isoforms of the cancer stem cell (CSC) marker CD44 exhibit strikingly op

80 M animals revealed a significant decrease in cancer stem cell (CSC) markers Aldh1a1, Klf4, EpCAM, and

81 inib combination resulted in upregulation of cancer stem cell (CSC) markers and susceptibility to FAK

82 th higher tumor grade and with expression of cancer stem cell (CSC) markers, including Notch pathway

83 326 regulated expression of multiple EMT and cancer stem cell (CSC) pathway genes.

84 esized that ERK2, but not ERK1, promotes the cancer stem cell (CSC) phenotype and metastasis in TNBC.

85 of a mesenchymal phenotype that results in a cancer stem cell (CSC) phenotype in PCa was described.

86 ate vs differentiation state) to control the cancer stem cell (CSC) pool remains elusive.

87 CK5+ cells are enriched in cancer stem cell (CSC) properties, can be induced by pro

88 are therapy resistant and exhibit increased cancer stem cell (CSC) properties.

89 l-mesenchymal plasticity, and acquisition of cancer stem cell (CSC) properties.

90 Notably, we demonstrate that ITGB4(+) cancer stem cell (CSC)-enriched mesenchymal cells reside

91 Tumor-repopulating cells (TRCs) are cancer stem cell (CSC)-like cells with highly tumorigeni

92 , plays a critical role in the regulation of cancer stem cell (CSC)-like characteristics.

93 pharmacological inhibition of YAP repressed cancer stem cell (CSC)-like properties, including tumors

94 We hypothesized that AR maintains a cancer stem cell (CSC)-like tumor-initiating population

95 dently of molecular markers such as putative cancer stem cell (CSC)-specific genes.

96 ipid expression differs between human breast cancer stem cells (CSC) and cancer non-stem cells (non-C

97 on of PPARdelta induces expansion of colonic cancer stem cells (CSC) and promotes colorectal cancer l

98 Cancer stem cells (CSC) appear to have increased metasta

99 Cancer stem cells (CSC) are a subset of tumour cells end

100 Prostate cancer stem cells (CSC) are implicated in tumor initiati

101 n to being refractory to treatment, melanoma cancer stem cells (CSC) are known to suppress host antit

102 Cancer stem cells (CSC) drive growth, therapy resistance

103 These cancer stem cells (CSC) function as putative drivers of

104 PADI4 activity limited the number of cancer stem cells (CSC) in multiple breast cancer models

105 n be used to sort marker-based heterogeneous cancer stem cells (CSC) into mechanically stiff and soft

106 transfer converts noncancer stem cells into cancer stem cells (CSC) leading to therapy resistance re

107 Cancer stem cells (CSC) maintain both undifferentiated s

108 mal human colonic SC niche to understand how cancer stem cells (CSC) may arise.

109 intracellular heterogeneity with subsets of cancer stem cells (CSC) that sustain tumor growth, recur

110 of tumor cells that have been designated as cancer stem cells (CSC).

111 pression is suppressed in ovarian tumors and cancer stem cells (CSC).

112 Emerging evidence demonstrates that cancer stem cells (CSCs) and cellular metabolism play a

113 Tumors comprise cancer stem cells (CSCs) and their heterogeneous progeny

114 Cancer stem cells (CSCs) are a class of cancer cells cha

115 Cancer stem cells (CSCs) are a small subpopulation of qu

116 Cancer stem cells (CSCs) are a subpopulation of cancer c

117 Cancer stem cells (CSCs) are capable of sustaining tumor

118 Cancer stem cells (CSCs) are cells within tumors that ma

119 Cancer stem cells (CSCs) are found in many cancer types,

120 esent study provides the first evidence that cancer stem cells (CSCs) are one of the key sources of C

121 Since cancer stem cells (CSCs) are radioresistant and metastas

122 Cancer stem cells (CSCs) are rare types of cells respons

123 It is not clear how pancreatic cancer stem cells (CSCs) are regulated, resulting in ine

124 We have shown that salivary gland cancer stem cells (CSCs) are resistant to platinum-based

125 Human colorectal cancer stem cells (CSCs) are tumour initiating cells tha

126 (2020) identify residual cancer stem cells (CSCs) as a mechanism of immunotherapy

127 ased levels of unsaturated lipids in ovarian cancer stem cells (CSCs) as compared to non-CSCs.

128 ked individual cells that express markers of cancer stem cells (CSCs) as well as of epithelial/mesenc

129 The fact that cancer stem cells (CSCs) become enriched in humans follo

130 a by autophagy, positively regulates hepatic cancer stem cells (CSCs) by suppressing the tumor suppre

131 immature subpopulation of tumor-propagating cancer stem cells (CSCs) differentiates into non-tumorig

132 t only significantly reduces self-renewal of cancer stem cells (CSCs) from NSCLC but also decreases S

133 Cancer stem cells (CSCs) have been hypothesized to repre

134 Putative cancer stem cells (CSCs) have been identified in HNSCC,

135 Cancer stem cells (CSCs) have been isolated from human o

136 Cancer stem cells (CSCs) have features such as the abili

137 Cancer stem cells (CSCs) have important roles in tumour

138 Cancer stem cells (CSCs) have the ability to self-renew

139 es HDAC1 and HDAC7 are necessary to maintain cancer stem cells (CSCs) in both breast and ovarian tumo

140 intenance of embryonic stem cells (ESCs) and cancer stem cells (CSCs) in prostate cancer (PCa).

141 ationships between EMT and the generation of cancer stem cells (CSCs) in prostate cancer.

142 ment have been attributed to the presence of cancer stem cells (CSCs) in tumors, and there is current

143 XEN445 inhibited the self-renewal of cancer stem cells (CSCs) in vitro and TNBC tumor formati

144 molecule and therapeutic target for various cancer stem cells (CSCs) including those driven by MLL f

145 Elimination of self-renewing cancer stem cells (CSCs) is necessary to permanently era

146 g three platinum atoms, Pt-3, towards breast cancer stem cells (CSCs) is reported.

147 demonstrated that DACH1 inversely related to cancer stem cells (CSCs) markers, epithelial-mesenchymal

148 Cancer stem cells (CSCs) may be responsible for treatmen

149 Cancer stem cells (CSCs) or CSC-like cells play crucial

150 Cancer stem cells (CSCs) play critical roles in cancer,

151 Cancer stem cells (CSCs) proactively remodel their micro

152 egulates epigenetic alterations to influence cancer stem cells (CSCs) remain to be explored.

153 These cancer stem cells (CSCs) represent a significant clinica

154 Effective targeting of cancer stem cells (CSCs) requires neutralization of self

155 Cancer stem cells (CSCs) subpopulation within the tumour

156 Recurrent tumors originate from cancer stem cells (CSCs) that survive conventional treat

157 sts that this is driven by subpopulations of cancer stem cells (CSCs) with tumor-initiating potential

158 There is evidence that cancer stem cells (CSCs) within breast tumours are capab

159 Cancer stem cells (CSCs), a subpopulation of cancer cell

160 Although the role of cancer stem cells (CSCs), a subset of tumor cells with t

161 urvival of these, treatment-resistant breast cancer stem cells (CSCs), allowing for relapse.

162 omers in rare subpopulations of resting- and cancer stem cells (CSCs), and these monomers were not in

163 Stem cells, including cancer stem cells (CSCs), require niches to maintain ste

164 f a subset of PDAC cells known as pancreatic cancer stem cells (CSCs), which are more resistant to cu

165 carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell-like f

166 s depends on a subset of tumor cells, called cancer stem cells (CSCs), with SC-like properties.

167 tatic cells called tumor initiating cells or cancer stem cells (CSCs).

168 ng phenotypes that have been associated with cancer stem cells (CSCs).

169 in tumor metastasis and the accumulation of cancer stem cells (CSCs).

170 chemotherapy, properties that are shared by cancer stem cells (CSCs).

171 r initiating and metastatic capacity, termed cancer stem cells (CSCs).

172 T) gene signature and are often enriched for cancer stem cells (CSCs).

173 including the ability to kill BT-474 breast cancer stem cells (CSCs).

174 n, L-GAELs display superior activity to kill cancer stem cells (CSCs).

175 pate in the acquisition of the properties of cancer stem cells (CSCs).

176 negative mesenchymal-like cells (enriched in cancer stem cells-CSCs) could promote a luminal-like dif

177 duced number of tumor-associated MSCs, fewer cancer stem cells, decreased tumor vasculature, and an i

178 e in the expression of genes associated with cancer stem cells downstream of Wnt/beta-catenin signali

179 ovel functions of B7-H3 in regulating breast cancer stem cell enrichment.

180 function conversely curbs tumour growth and cancer stem cell expansion, restores chemosensitivity an

181 e due to the presence of a sub-population of cancer stem cells expressing the multi-drug efflux trans

182 atinum-tolerant cell population with partial cancer stem cell features, characterized by FZD7 express

183 a (AML) have been advanced paradigms for the cancer stem cell field.

184 rticular emphasis on mechanisms relevant for cancer stem cell formation (CSC) and function.

185 tumor cell proliferation, angiogenesis, and cancer stem cell function.

186 ease the understanding of the role of glioma cancer stem cells (GCSCs) in the virulence of gliomas.

187 epithelial transition, in tumour metastasis, cancer stem cell generation and maintenance, and therape

188 Y cells and proved even to efficiently block cancer stem cell growth.

189 n the treatment of BC/TNBC along with breast cancer stem cells have been discussed in details.

190 Hepatic cancer stem cells (HCSCs) are considered as main players

191 map the molecular dependencies of pancreatic cancer stem cells, highly therapy-resistant cells that p

192 and therapeutic targets of rare cells (e.g., cancer stem cells); however, these studies remain challe

193 As therapy against cancer stem cells in endometrial cancer is lacking, the

194 fferentiation pathways were used to identify cancer stem cells in leukemia and gliomas.

195 In addition, we explore the role of cancer stem cells in promoting radiation resistance, and

196 The role of breast cancer stem cells in the recurrence of BC and TNBC has a

197 Chemotherapy has been shown to enrich cancer stem cells in tumors.

198 dase activity, is required for TG2-dependent cancer stem cell invasion, migration and tumour formatio

199 Investigation of the metabolic regulation of cancer stem cells is an emerging field that offers promi

200 istics of the malignant phenotype, including cancer stem cell like features in neuroblastoma PDXs, ma

201 2-positive breast cancers through regulating cancer stem cell-like properties.

202 origenesis proceeds through Wnt-differential cancer stem cell-like subpopulations before differentiat

203 chondrial reactive oxygen species clearance, cancer stem cell maintenance, and HIF/mTOR/RHEB signalin

204 ontent and is required for expression of the cancer stem cell marker ALDH1A3 and Wnt signalling activ

205 Notably, overexpression of the cancer stem cell marker CD44 enhanced the stability of S

206 nd transcriptionally activates expression of cancer stem cell marker CD44 in PC cells.

207 ify integrin alpha(v)beta(5) as a functional cancer stem cell marker essential for GBM maintenance an

208 HCC patients demonstrated CTCs positive for cancer stem cell marker, CD44, suggesting that the major

209 mical disruption had a reduced expression of cancer stem cell markers (CD133, CD90, CD49f) and a dimi

210 oenvironment correlates with Notch and other cancer stem cell markers and can be targeted by a novel,

211 nt after chemotherapy, reduced expression of cancer stem cell markers, and increased chemosensitivity

212 As of VEGF or neuropilin-1 (NRP-1) attenuate cancer stem cell markers, inhibit the tumor-initiating c

213 uated DNA repair signaling and expression of cancer stem cells markers and sensitized chemoresistant

214 nt after chemotherapy, reduced expression of Cancer-Stem-Cell markers, and increased chemosensitivity

215 nt studies demonstrated that the presence of cancer stem cells may lead to the failure of chemotherap

216 ased invasiveness of xenografts derived from cancer stem cells may not be clearly detected by standar

217 transformation of normal LSCs to metastatic cancer stem cells (mCSCs).

218 eres revealed enriched signatures related to cancer stem cells, metastasis, and recurrence and showed

219 This cancer stem cell model offers an explanation for chemoth

220 of iron handling in tumor-initiating cells (cancer stem cells), novel contributions of the tumor mic

221 Persistence of ovarian cancer stem cells (OCSC) at the end of therapy may be re

222 ing guanine exchange factor, specifically in cancer stem cells of transition zone tumors.

223 s had human immunodefiency virus (HIV)/AIDS, cancer, stem cell or organ transplantation, nonsteroid i

224 nical significance of eradicating pancreatic cancer stem cells (PCSC) and its components using a pan-

225 ed studies of viability, type of cell death, cancer stem cell percent and glycosphingolipid expressio

226 asis is required for induction of the breast cancer stem cell phenotype in response to hypoxia or cyt

227 se data establish that DAB2IP suppresses the cancer stem cell phenotype via inhibition of WNT5B-induc

228 Although Glut3 is a known driver of a cancer stem cell phenotype, direct targeting is complica

229 es, including ALDH1A1 and SOX2, leading to a cancer stem cell phenotype, which is implicated in disea

230 ting beta-catenin signaling and inducing the cancer stem cell phenotype.

231 ations of varying potency and drug resistant cancer stem-cell phenotypes, including those derived fro

232 es, providing a means to identify normal and cancer stem-cell phenotypes.

233 es the effects of radiation by targeting the cancer stem cell pool.

234 t upregulation of B7-H3 increases the breast cancer stem cell population and promotes cancer developm

235 of tumor stroma crosstalk, and enrichment of cancer stem cell population during tumorigenesis.

236 Here, we identify a highly tumorigenic cancer stem cell population in a mouse model of transiti

237 Our findings define a quiescent cancer stem cell population in glioblastoma that may be

238 hase experiments demonstrated a perivascular cancer stem cell population in Pten/Trp53 double mutant

239 e is great interest in understanding how the cancer stem cell population may be maintained in solid t

240 cing revealed that the stemness of a bladder cancer stem cell population was inhibited by decitabine

241 diverse mechanisms including maintaining the cancer stem cell population, enhancing DNA damage repair

242 ion, tumorsphere formation and ALDH-positive cancer stem cell population, in vitro.

243 ight be similarly important as targeting the cancer stem cell population.

244 can alter the metabolic requirements of the cancer stem cell population.

245 Cancer stem cells possess the capacity for self-renewal

246 at differential MAPK signaling balances EMT, cancer stem cell potential, and tumor growth in colorect

247 , malignancy, immunosuppression, metastasis, cancer stem cell production, and modulation of the tumor

248 factor, as a critical regulator of a breast cancer stem cell program that enables metastatic coloniz

249 RBP is a central regulator of translation of cancer stem cell programs.

250 Regulation of Sox2 by Six2 enhanced cancer stem cell properties and increased metastatic col

251 The MNK1/NODAL axis promoted cancer stem cell properties and invasion in vitro.

252 s mesenchymal breast cancer populations with cancer stem cell properties in vitro.

253 R-141 in CD44(+) and bulk PCa cells inhibits cancer stem cell properties including holoclone and sphe

254 lial-mesenchymal transition in promoting the cancer stem cell properties needed for metastasis initia

255 esenchymal or mesenchymal cells that possess cancer stem cell properties, promoting multidrug resista

256 y promoting EZH2-mediated gene silencing and cancer stem cell property compared with PARPi-untreated

257 om studies on intratumoral heterogeneity and cancer stem cells raise the possibility that multiple br

258 e methyltransferase SMYD2 and the pancreatic cancer stem cell regulator RORC in all three ASCPs, and

259 Overcoming drug resistance and targeting cancer stem cells remain challenges for curative cancer

260 ors that regulate self-renewal of normal and cancer stem cells remains limited.

261 the RNA-binding proteins (RBPs) that govern cancer stem cells remains poorly characterized.

262 uivalents of blastomeres, the most primitive cancer stem cells reported to date.

263 Breast cancer stem cells represent the tumor subpopulation invo

264 Glycolysis is critical for cancer stem cell reprogramming; however, the underlying

265 epithelial monolayers generated from gastric cancer stem cells retained high levels of ST6Gal-I and r

266 al heterogeneity and selective resistance of cancer stem cell (SC) subpopulations to molecularly targ

267 emonstrates that FTO plays critical roles in cancer stem cell self-renewal and immune evasion and hig

268 r growth and metastasis by regulating breast cancer stem cell self-renewal.

269 transformed traits and for acquisition of a cancer stem cell state by otherwise more benign cells.

270 to-mesenchymal transition or transition to a cancer stem cell state.

271 n of immuno-regulatory signals by pancreatic cancer stem cells, suggesting that autoimmune drugs shou

272 ated with numerous human diseases, including cancer stem cell survival and metastatic phenotype.

273 ype 2 transglutaminase (TG2) is an important cancer stem cell survival protein that exists in open an

274 n tumor initiation, chemotherapy resistance, cancer stem cell survival, and tumor metastasis.

275 transamidase site-specific inhibitors reduce cancer stem cell survival.

276 as a GTP-binding GTPase and is required for cancer stem cell survival.

277 Cancer stem cells sustain propagation of the deadly prim

278 nhibition had a higher synergistic effect in cancer stem cells than in bulk cancer cells, compensatin

279 e formation, and had a greater proportion of cancer stem cells than PT.

280 therapy and was effective in killing ovarian cancer stem cells that contribute to both platinum-resis

281 rphase pool of KIF11 present in glioblastoma cancer stem cells that drives tumor cell invasion.

282 model of tumor growth involving slow-cycling cancer stem cells that give rise to fast-proliferating p

283 dentify molecular dependencies of pancreatic cancer stem cells that may be exploited therapeutically.

284 ical disease, as well as provide support for cancer stem cell theories of glioma.

285 'Cancer stem cell theory' purports that a minor populatio

286 llinating enzyme PADI4 in suppressing breast cancer stem cells through epigenetic repression of stemn

287 ioblastoma offers a reliable cancer to study cancer stem cells to better model the human disease and

288 els of pre-neoplastic mammary epithelial and cancer stem cells to reveal the connection between cell

289 s, compensating for the lower sensitivity of cancer stem cells to the individual drugs.

290 sion of YAP is sufficient to reprogram Lgr5+ cancer stem cells to this state and thereby suppress tum

291 cells and patient-derived human glioblastoma cancer stem cells) to demonstrate how vital the informat

292 ht be a good candidate for therapy for liver cancer stem cells together with liver cirrhosis.

293 ed destruction of Nanog, leading to elevated cancer stem cell traits and PrCa progression.

294 f both mesenchymal-epithelial transition and cancer stem cell traits in disseminated tumour cells is

295 transcription factors and miRNAs coordinate cancer stem cell tumor-propagating capacity are unclear.

296 modulating tumor cell motility and invasion, cancer stem cell viability and differentiation, resistan

297 ncer cell's proteomic profiles and eliminate cancer stem cells while preserving non-malignant cells.

298 Hence, targeting epithelial cancer stem cells with rapid tumorigenesis signatures in

299 ing the characteristic features of migratory cancer stem cells with tumorigenic property is important

300 Recent studies have implicated cancer stem cells within glioblastoma (glioma stem cells