ライフサイエンスコーパス: cancer stem cell

1 he characterization of metabolic activity in cancer stem cells.

2 eivably due to tumor initiating cells (TICs)/cancer stem cells.

3 umors has emerged as a driver for growth via cancer stem cells.

4 therapeutics that target the resurrection of cancer stem cells.

5 suring the ratios of mRNA splice variants in cancer stem cells.

6 is essential for self-renewal of normal and cancer stem cells.

7 pulation of tumor-initiating cells (TIC), or cancer stem cells.

8 ty and phagocytosis checkpoints by apoptotic cancer stem cells.

9 py based on lack of CDX2 expression in their cancer stem cells.

10 umor-initiating cells (BTICs), also known as cancer stem cells.

11 ase alpha (IKKalpha)-BMI1 module in prostate cancer stem cells.

12 coexpressed with Lgr5, also marks intestinal cancer stem cells.

13 to maintain the subpool of Lgr5(+)/Dclk1(+) cancer stem cells.

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

15 hways preferentially killing transformed and cancer stem cells.

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

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

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

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

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

21 The measurement of cancer stem cell abundance and intra-tumour heterogeneit

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

23 ancer efficacy by 8-fold and increasing anti-cancer stem cell activity by 50-fold.

24 Cancer stem cells also possess resistant phenotypes that

25 e, but the tumor cells themselves, including cancer stem cells, also influence the surrounding cells.

26 ave become a well-recognized exemplar of the cancer stem cell and have been characterized extensively

27 theories of disease progression, such as the cancer stem cell and plasticity models.

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

29 lammatory cytokine expression, enrichment of cancer stem cells and acquired resistance to paclitaxel

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

31 he former is expressed dominantly in hepatic cancer stem cells and correlates significantly to a poor

32 ression appears to be associated with breast cancer stem cells and endocrine resistance.

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

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

35 mour of an individual patient, is related to cancer stem cells and is also considered a potential pro

36 experiments from 'Wnt activity defines colon cancer stem cells and is regulated by the microenvironme

37 from 'The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing

38 ll lines, aldehyde dehydrogenase-positive MM cancer stem cells and patient specimens.

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

40 gnostic power is driven by genes involved in cancer stem cells and treatment resistance.

41 head Box Protein C2 (FOXC2) known to promote cancer stem-cells and metastasis.

42 alysis are enriched for oncogenic, stem cell/cancer stem cell, and early development loci--including

43 anges in gene expression, the development of cancer stem cells, and immunomodulation are plausible un

44 Cancer stem cells are capable of transformation after ap

45 Mechanisms that maintain cancer stem cells are crucial to tumour progression.

46 Cancer stem cells are particularly tolerant to DNA damag

47 Many types of normal and cancer stem cells are resistant to killing by genotoxins

48 Cancer stem cells are responsible for tumor progression,

49 Malignant stem cells, or cancer stem cells, are a subpopulation of tumor cells th

50 l cells increased the proportion of prostate cancer stem cells as characterized by gene expression, e

51 e hFL-HCC tumour line is highly enriched for cancer stem cells as indicated by limited dilution tumou

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

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

54 rties in malignant cells by enhancing breast cancer stem cell (BCSC) phenotype.

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

56 oral hypoxia stimulates enrichment of breast cancer stem cells (BCSC), which are critical for metasta

57 study demonstrates that DATS targets breast cancer stem cells (bCSC).

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

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

60 Chemotherapy induces enrichment of breast cancer stem cells (BCSCs), which are responsible for tum

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

62 m cell antigen Sca-1 is implicated in murine cancer stem cell biology and breast cancer models, but t

63 Wnt signaling drives colorectal cancer stem cells, but effective therapeutics targeting

64 tion, confers upon tumor cells the traits of cancer stem cell by augmenting self-renewal, chemoresist

65 ogy and analyzed the oncogenic signatures of cancer stem cells by quantitating both aldehyde dehydrog

66 tion occurs in HBV-mediated HCCs and hepatic cancer stem cells, by a mechanism not understood.

67 nitiation and metastasis properties of these cancer stem cells can be uncoupled.

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

69 Like normal stem cells, cancer stem cells can undergo self-renewal and different

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

71 el LncRNA, Lnc34a, that is enriched in colon cancer stem cells (CCSCs) and initiates asymmetric divis

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

73 irectly suppresses Numb in early-stage colon cancer stem cells (CCSCs), forming an incoherent feedfor

74 ent of hepatic tumors composed of cells with cancer stem cell characteristics.

75 -215 expression is depleted in FACS-enriched cancer stem cells compared with unsorted samples.

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

77 Colorectal cancer stem cells (CRCSC) comprise a rare self-renewing

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

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

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

81 Activation of sonic hedgehog (Shh) in cancer stem cell (CSC) has been demonstrated with aggres

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

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

84 infection causes induction of several tumors/cancer stem cell (CSC) markers and is known to be a majo

85 Cancer stem cell (CSC) markers, including CD133, CD24, S

86 iveness, and an increase in cells expressing cancer stem cell (CSC) markers.

87 326 regulated expression of multiple EMT and cancer stem cell (CSC) pathway genes.

88 up protein BMI1 is an important regulator of cancer stem cell (CSC) phenotype and is often overexpres

89 ) cells that survived chemotherapy exhibited cancer stem cell (CSC) phenotypes based on growth potent

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

91 The breast cancer stem cell (CSC) potency of a series of copper(II)

92 ined the impact of hypoxia on EMT-associated cancer stem cell (CSC) properties, by culturing transfor

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

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

95 Here, we show VEGF promotes breast and lung cancer stem cell (CSC) self-renewal via VEGF receptor-2

96 utes to the reprogramming and maintenance of cancer stem cell (CSC) states that are activated by epit

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

98 ion and metastasis, confers tumor cells with cancer stem cell (CSC)-like characteristics, and increas

99 esistance to TORC1/2 inhibition is driven by cancer stem cell (CSC)-like populations that could be ta

100 A cancer stem cell (CSC)-like subpopulation in neuroblasto

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

102 rarchies that are driven by tumor-initiating cancer stem cells (CSC) and rely on complex interactions

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

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

105 debate on the concepts and challenges of the cancer stem cells (CSC) as well as CSC-centered scientif

106 ed that AGR2 was overexpressed in pancreatic cancer stem cells (CSC) compared with non-stem cancer ce

107 umulating evidence suggests a major role for cancer stem cells (CSC) in chemoresistance, although the

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

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

110 Cancer stem cells (CSC) present a formidable clinical ch

111 The degree of heterogeneity among cancer stem cells (CSC) remains ill-defined and may hind

112 arcinomas are hierarchically organized, with cancer stem cells (CSC) residing at the top of the hiera

113 relapse can be attributed to a population of cancer stem cells (CSC) that survives radiotherapy, anal

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

115 ion and validation of mammary stem cells and cancer stem cells (CSC), but the signaling pathways that

116 ulation of chemoresistant and radioresistant cancer stem cells (CSC).

117 lar processes in multiple cell types such as cancer stem cells (CSC).

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

119 of the malignant subpopulation of so-called cancer stem cells(CSC), as these cells are exclusively a

120 ion of IRE1alpha decreased stemness of colon cancer stem cells (CSCs) and attenuated growth of intest

121 Cancer stem cells (CSCs) are a promising target for canc

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

123 Cancer stem cells (CSCs) are considered responsible for

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

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

126 easing evidence supports the hypothesis that cancer stem cells (CSCs) are resistant to antiproliferat

127 Previous studies have demonstrated that cancer stem cells (CSCs) are selectively enriched after

128 Cancer stem cells (CSCs) are tumor cells that have the p

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

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

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

132 al pathways and epigenetic programs in which cancer stem cells (CSCs) can drive tumour growth and giv

133 rived HSC-3 cells contain a subpopulation of cancer stem cells (CSCs) characterized by a high level o

134 Cancer stem cells (CSCs) contribute to tumour heterogene

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

136 Liver cancer stem cells (CSCs) have been identified and shown

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

138 Cancer stem cells (CSCs) have key roles in treatment res

139 ote tumor growth involved the acquisition of cancer stem cells (CSCs) in cancer population.

140 We characterized cancer stem cells (CSCs) in CCA subtypes and evaluated t

141 Targeting cancer stem cells (CSCs) in colorectal cancer (CRC) rema

142 tenance, their role in maintaining MaSCs and cancer stem cells (CSCs) in constantly replenishing mamm

143 We report that self-renewing cancer stem cells (CSCs) in glioblastoma have low TLR4 e

144 cular mechanisms that underlie modulation of cancer stem cells (CSCs) in NPC remain unclear.

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

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

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

148 extracellular matrix impacts the function of cancer stem cells (CSCs) is a significant but poorly und

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

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

151 Cancer stem cells (CSCs) may be responsible for tumour d

152 Because most cancers have a clonal origin, cancer stem cells (CSCs) must generate phenotypically di

153 The cancer stem cells (CSCs) of glioblastoma multiforme (GBM

154 report a microfluidics method that enriches cancer stem cells (CSCs) or tumor-initiating cells on th

155 ma, their role in regulation of osteosarcoma cancer stem cells (CSCs) remains unknown.

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

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

158 th resultant efficient elimination of breast cancer stem cells (CSCs) resulting in abrogation of tumo

159 umor and contains self-renewing, tumorigenic cancer stem cells (CSCs) that contribute to tumor initia

160 Cancer stem cells (CSCs) with enhanced tumorigenicity an

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

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

163 ; (iii) impaired the proliferation of glioma cancer stem cells (CSCs), more resistant to chemotherape

164 Cancer stem cells (CSCs), or tumor-initiating cells, com

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

166 The discovery of cancer stem cells (CSCs), which are responsible for self

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

168 the formation, maintenance, and expansion of cancer stem cells (CSCs), which have the capacity for se

169 They are significantly enriched in cancer stem cells (CSCs), which makes claudin-low tumor

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

171 tant, self-renewing CD133(hi)/ER(lo)/IL6(hi) cancer stem cells (CSCs).

172 in primary tumors, which are referred to as cancer stem cells (CSCs).

173 tumor initiation, properties associated with cancer stem cells (CSCs).

174 expressed in and required for maintenance of cancer stem cells (CSCs).

175 plus 5 genes reported to be overexpressed in cancer stem cells (CSCs).

176 how this combined effect can be used against cancer stem cells (CSCs).

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

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

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

180 we highlight current advances in identifying cancer stem cells, detail the interactions of these cell

181 When these cancer stem cells differentiated into their chemosensiti

182 colorectal cancers that selectively induces cancer stem cell differentiation through HOXA5 expressio

183 rreversible deleterious mutations, symmetric cancer stem cell division that increases the cancer stem

184 dentify a limited subpopulation of epidermal cancer stem cells (ECS cells), in squamous cell carcinom

185 disease (cytokeratin 19 [CK19]), identifying cancer stem cells (epithelial cell adhesion molecule [Ep

186 myeloid leukemia progenitors that may inform cancer stem cell eradication strategies.

187 Cancer stem cells exert enormous influence on neoplastic

188 We report that melanoma-specific CD133(+) cancer stem cells exhibit increased tumor-initiating pot

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

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

191 ll proliferation, targeted both the bulk and cancer stem cell fraction, and strongly attenuated xenog

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

193 rcinoma in PR-SET7-deficient mice displays a cancer stem cell gene signature specified by the co-expr

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

195 CD133 (PROM1), a marker of cancer stem cells, has been shown to facilitate EMT in v

196 Cancer stem cells have been postulated to represent a th

197 Cancer stem cells have been shown to form vascular mimic

198 l biomarkers in a number of malignancies and cancer stem cells, highlighting the need for the identif

199 umor initiating cells (BTICs), also known as cancer stem cells, hijack high-affinity glucose uptake a

200 The cancer stem cell hypothesis, that a small population of

201 ssible applications in the investigations on cancer stem cells, immunity and immune modulators, appli

202 n supports the survival and proliferation of cancer stem cells in an NFAT-dependent manner and promot

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

204 which are required for enrichment of breast cancer stem cells in response to hypoxia or chemotherapy

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

206 These cells show characteristics of cancer stem cells in vitro, as well as enhanced tumorige

207 mesenchymal transition and the generation of cancer stem cells, indicating that SET9 plays a role in

208 or (VA4) was also shown to inhibit epidermal cancer stem cell invasion with an EC50 of 3.9 muM, repre

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

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

211 ation and conversion into a dedifferentiated cancer stem cell-like phenotype depends on opposing leve

212 lls highly migratory and invasive, attaining cancer stem cell-like phenotype.

213 motes tumour formation in vivo and maintains cancer stem cell-like populations.

214 ression and potentiated the cytokine-induced cancer stem cell-like properties.

215 he mCXCL1-mTORC1 pathway as crucial in liver cancer stem cell maintenance and highlights it as a nove

216 nable IMPs to play a potentially key role in cancer stem cell maintenance and tumor growth.

217 transition, motility, invasion, metastasis, cancer stem cell maintenance, immune evasion, and resist

218 surveillance, survival, invasion as well as cancer stem cell maintenance.

219 ALDHs enzymatic activity has been used as a cancer stem cell marker and seems to correlate with tumo

220 We identified ALDH1A1, a cancer stem cell marker as being overexpressed in OC sph

221 a directly regulates alternative splicing of cancer stem cell marker CD44 through a phosphorylated T1

222 on resulted in the expression of Sox2, a GBM cancer stem cell marker, and was obligatory for tumor fo

223 liferation makers (BrdU, cyclin D1, p53) and cancer stem cell markers (CD133 and nanog) are significa

224 g, markedly suppressed the expression of the cancer stem cell markers c-Myc, CD133, and nestin, which

225 re for the frequency of cells expressing the cancer stem cell markers CD44, CD133, and c-Met and the

226 evidence that contests the observations that cancer stem cell markers reliably identify the subset of

227 , such as sphere formation and expression of cancer stem cell markers, including BMI1.

228 ent survival, and, at the single-cell level, cancer stem cell markers.

229 etastasis and fewer cells expressing mammary cancer stem cell markers.

230 ith high levels of Wnt activity also express cancer stem cell markers.

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

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

233 Thus, normal or cancer stem cells may rely primarily on lipid reserves f

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

235 erapeutic implications for the management of cancer stem cell-mediated melanoma progression.

236 This cancer stem cell model offers an explanation for chemoth

237 o glioma development, offer insight into the cancer stem cell model, help refine classifications, and

238 as at single-cell resolution and support the cancer stem cell model, with substantial implications fo

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

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

241 al-mesenchymal transition and by enriching a cancer stem cell phenotype in tumor epithelial cells.

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

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

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

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

246 s unique trait allows for maintenance of the cancer stem cell pool and facilitates differentiation in

247 cancer stem cell division that increases the cancer stem cell pool, and telomere length and erosion a

248 on of RANK signaling drastically reduces the cancer stem cell pool, decreases tumor and metastasis in

249 llows non-cancer stem cells to replenish the cancer stem cell pool, initiate tumorigenesis, and escap

250 goal by combination therapy that erodes the cancer stem cell pool.

251 could inhibit the cancer cell proliferation, cancer stem cell population and EMT, hence suppressed th

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

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

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

255 tumor cells by targeting the CD44(+)CD24(-) cancer stem cell population.

256 dies have suggested coexistence of different cancer stem cell populations within a tumor mass, where

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

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

259 of DeltaNp63alpha, leading to maintenance of cancer stem cell properties and enhanced tumor formation

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

261 critically important for the acquisition of cancer stem cell properties, including self-renewal, tum

262 unique population of HGSOC cancer cells with cancer stem cell properties, p53 protein aggregation is

263 here formation, indicating that DMF has anti-cancer stem cell properties.

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

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

266 Expression profiling for cancer stem cell-related genes suggested that FoxQ1 may

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

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

269 s implicated in breast cancer metastasis and cancer stem cell renewal.

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

271 Breast cancer stem cells represent the tumor subpopulation invo

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

273 specific markers have led to an explosion of cancer stem cell research.

274 ic epithelial-to-mesenchymal transition-like cancer stem cells resulting in tumors whose gene express

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

276 These cancer 'stem cells (SCs)' have been shown to maintain tu

277 However, diverse cancer stem cell signatures are difficult for physicians

278 tein supports cancer hallmarks including the cancer stem cell state.

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

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

281 quired for epidermal squamous cell carcinoma cancer stem cell survival.

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

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

284 demonstrated that SCD1 is important in lung cancer stem cells survival and propagation.

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

286 intracellular drug targeting, gene delivery, cancer stem cell therapy, magnetic drug targeting and ul

287 Efforts to induce the differentiation of cancer stem cells through treatment with all-trans retin

288 Plasticity allows non-cancer stem cells to replenish the cancer stem cell pool

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

290 OX2 and NANOG; sustains the manifestation of cancer stem cell traits; and drives metastatic reactivat

291 sphere formation of colon and head and neck cancer stem cells under nonadherent conditions.

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

293 Remarkably, the self-renewal capacity of cancer stem cells was blocked by LF3 in concentration-de

294 adhesive capacity, and the enrichment of the cancer stem cells was confirmed by flow cytometry biomar

295 intenance of the neoplastic phenotype and in cancer stem cells, which may allude to its additional in

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

297 derstanding distinctive pathways relating to cancer stem cells will provide insight into early diagno

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 mediated survival pathway in MM cells and MM cancer stem cells within the context of microenvironment