ライフサイエンスコーパス: cancer-associated fibroblast

1 er nonmalignant cells and activate them into cancer-associated fibroblasts.

2 etween RhoA knockout fibroblasts and classic cancer-associated fibroblasts.

3 nuclear cells caused by Cxcl-1 released from cancer-associated fibroblasts.

4 nding stromal cells that acquire features of cancer-associated fibroblasts.

5 l-regulated kinase 1/2 activation in ovarian cancer-associated fibroblasts.

6 uld be counteracted by cytokines secreted by cancer-associated fibroblasts.

7 llate cells (PSC) are a subset of pancreatic cancer-associated fibroblasts.

8 patocarcinoma HepG2 cancer cells, and breast cancer-associated fibroblasts.

9 on of matrix proteins secreted by dermal and cancer-associated fibroblasts.

10 h vimentin and phospho-S6 in Cav-1-deficient cancer-associated fibroblasts.

11 expression is down-regulated in human breast cancer-associated fibroblasts.

12 ) MSFs share many characteristics with human cancer-associated fibroblasts.

13 lls, regulatory T cells and a subtype of pre-cancer-associated fibroblasts.

14 er cells, but also in other cell types, e.g. cancer-associated fibroblasts.

15 ECM remodeling and protumorigenic actions of cancer-associated fibroblasts.

16 en assessed in co-cultures of TNBC cells and cancer-associated fibroblasts.

17 ctive Src-transfected NIH3T3 fibroblasts and cancer-associated fibroblasts.

18 ession exhibited a positive correlation with cancer-associated fibroblasts across all gastrointestina

19 ures of prostate cancer epithelial cells and cancer-associated fibroblasts, active CFL promoted invas

20 unlikely, but the opportunities for studying cancer-associated fibroblast activity in tumor models an

21 esmoplastic microenvironment, which includes cancer-associated fibroblasts [also known as pancreatic

22 ther tumor components, such as immune cells, cancer-associated fibroblasts and differentiated cells,

23 This results in activation of cancer-associated fibroblasts and expression of CXCL16,

24 obiota shape the function and composition of cancer-associated fibroblasts and extracellular matrix c

25 tumor spheroids selectively over surrounding cancer-associated fibroblasts and has excellent pharmaco

26 stic phenotype, which have been described as cancer-associated fibroblasts and have been shown to ind

27 we identified four proteins overexpressed in cancer-associated fibroblasts and linked to Rho GTPase s

28 a pro-tumor microenvironment, with increased cancer-associated fibroblasts and macrophage infiltratio

29 vironment is the heterogeneous population of cancer-associated fibroblasts and myeloid cells that sti

30 increasing pericyte numbers while decreasing cancer-associated fibroblasts and myeloid-derived suppre

31 f biofilm formation on matrices deposited by cancer-associated fibroblasts and osteosarcoma cells.

32 t implications for understanding the role of cancer-associated fibroblasts and RB inactivation in pro

33 ing embryonic development, is upregulated in cancer-associated fibroblasts and regulates cancer cell

34 BL0137 induced ZBP1-dependent necroptosis in cancer-associated fibroblasts and reversed ICB unrespons

35 st time, that Angpts promote accumulation of cancer-associated fibroblasts and tumor angiogenesis in

36 ated blood and lymphatic vessels, pericytes, cancer associated fibroblasts, and cancer stem cells.

37 tion, an increase in mesenchymal markers and cancer-associated fibroblasts, and enlargement of nucleo

38 Although interest in antigen-presenting cancer-associated fibroblasts (apCAFs) is increasing, th

39 Finally, we show that cancer-associated fibroblasts are significantly outnumbe

40 senchymal transition, including signals from cancer-associated fibroblasts, are able to increase the

41 Mesenchymal cells in tumors, called cancer-associated fibroblasts, arise via activation of r

42 ignaling in alphaSMA(+) cells, which include cancer-associated fibroblasts as well as other cells suc

43 othelial cells and reduce alpha-SMA-positive cancer-associated fibroblasts at pharmacologically relev

44 nscriptome significantly overlaps with human cancer-associated fibroblasts; both show a nearly identi

45 TME stroma are multiple and varied, however cancer associated fibroblasts (CAF) and their contributi

46 s, including angiogenesis, inflammation, and cancer-associated fibroblast (CAF) activation.

47 ll RNA sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) and two perivascular-

48 t recruitment to tumours and activation to a cancer-associated fibroblast (CAF) phenotype has been im

49 and sufficient for functional aspects of the cancer-associated fibroblast (CAF) phenotype, including

50 Functional studies identified cancer-associated fibroblast (CAF)-derived EVs (from pat

51 mong the mesenchymal cell subsets, FAP+PDPN+ cancer-associated fibroblasts (CAF) and ACTA2+MCAM+ peri

52 at compared with normal fibroblasts, primary cancer-associated fibroblasts (CAF) and fibroblasts acti

53 n in tumor burden by affecting cancer cells, cancer-associated fibroblasts (CAF) and myeloid cells.

54 ymal stem cells (MSC) can differentiate into cancer-associated fibroblasts (CAF) and promote tumor pr

55 his study, Ang-(1-7) inhibited the growth of cancer-associated fibroblasts (CAF) and reduced fibrosis

56 Cancer-associated fibroblasts (CAF) are a central compon

57 Cancer-associated fibroblasts (CAF) are a major cell typ

58 Cancer-associated fibroblasts (CAF) are a poorly charact

59 rising the tumor microenvironment, of which, cancer-associated fibroblasts (CAF) are a prevalent comp

60 Although cancer-associated fibroblasts (CAF) are abundant in PDAC

61 Cancer-associated fibroblasts (CAF) are abundant in the

62 Cancer-associated fibroblasts (CAF) are among the abunda

63 Cancer-associated fibroblasts (CAF) are crucial players

64 Cancer-associated fibroblasts (CAF) are important consti

65 Cancer-associated fibroblasts (CAF) are key regulators o

66 Cancer-associated fibroblasts (CAF) are known to support

67 Cancer-associated fibroblasts (CAF) are major contributo

68 Cancer-associated fibroblasts (CAF) are prominent player

69 Cancer-associated fibroblasts (CAF) comprise the majorit

70 deletion mouse model, on primary cultures of cancer-associated fibroblasts (CAF) derived from these t

71 Recent results suggest that cancer-associated fibroblasts (CAF) drive progression of

72 Cancer-associated fibroblasts (CAF) engage in tumor prog

73 This led to the observation that cancer-associated fibroblasts (CAF) enhanced invasion in

74 Cancer-associated fibroblasts (CAF) have been reported t

75 Cancer-associated fibroblasts (CAF) have been shown to s

76 Cancer-associated fibroblasts (CAF) have been suggested

77 Cancer-associated fibroblasts (CAF) have many tumor-prom

78 erminant for the tumor-promoting activity of cancer-associated fibroblasts (CAF) in both wild-type (W

79 Metastasis is facilitated by cancer-associated fibroblasts (CAF) in the tumor microen

80 Here, we demonstrate that cancer-associated fibroblasts (CAF) increase the stiffne

81 Notably, cancer-associated fibroblasts (CAF) isolated from patien

82 Signals originating from cancer-associated fibroblasts (CAF) may positively regul

83 Stromal cells and especially cancer-associated fibroblasts (CAF) play a critical biop

84 DNA damage found in prostate cancer-associated fibroblasts (CAF) promotes tumor progr

85 Cancer-associated fibroblasts (CAF) regulate tumor progr

86 Cancer-associated fibroblasts (CAF) represent a major co

87 n-1 and its receptor UNC5B correlates with a cancer-associated fibroblasts (CAF) signature.

88 Cancer-associated fibroblasts (CAF) stimulate tumor grow

89 Cancer-associated fibroblasts (CAF) support tumorigenesi

90 rogression by modulating the contribution of cancer-associated fibroblasts (CAF) that are present in

91 rogenic signaling in breast cancer cells and cancer-associated fibroblasts (CAF) that contribute to c

92 ng TGFbeta signaling prompted the skewing of cancer-associated fibroblasts (CAF) toward an inflammato

93 demonstrating how microvesicles derived from cancer-associated fibroblasts (CAF) transfer miR-221 to

94 rthermore, co-cultures of KYSE-410 cells and cancer-associated fibroblasts (CAF) were investigated.

95 Based on the recognized coevolution of cancer-associated fibroblasts (CAF) with tumor progressi

96 cells (MSC) contribute to stroma in part as cancer-associated fibroblasts (CAF), but a complete unde

97 row-derived mesenchymal stem cells to obtain cancer-associated fibroblasts (CAF)-like features via in

98 racterized by desmoplastic stroma containing cancer-associated fibroblasts (CAF).

99 files of breast cancer cells in contact with cancer-associated fibroblasts (CAF).

100 ion, as it is required for the activation of cancer-associated fibroblasts (CAF).

101 aining an abundance of myofibroblasts termed cancer-associated fibroblasts (CAF).

102 gnaling is a major functional determinant of cancer-associated fibroblasts (CAF).

103 cancer cells and other cell types, including cancer-associated fibroblasts (CAF).

104 i in breast epithelial cells cocultured with cancer-associated fibroblasts (CAF).

105 ir microenvironment to become protumorigenic cancer-associated fibroblasts (CAF).

106 l factor also required for the activation of cancer-associated fibroblasts (CAF).

107 ion was distinctly conserved between MSC and cancer-associated fibroblasts (CAF).

108 y influenced by the tumour stroma, including cancer-associated fibroblasts (CAF).

109 ulture and compared with: 2D co-culture with cancer-associated fibroblasts (CAF); 3D culture in colla

110 s (TEC) can become irreversibly activated as cancer-associated-fibroblasts (CAF) that stimulate oncog

111 Cancer associated fibroblasts (CAFs) are a key component

112 lecular pathways regulating the formation of cancer associated fibroblasts (CAFs) are not well elucid

113 Cancer cells program fibroblasts into cancer associated fibroblasts (CAFs) in a two-step manne

114 Whether it also occurs in Cancer Associated Fibroblasts (CAFs) remains to be caref

115 yer by layer positioning of cancer cells and cancer associated fibroblasts (CAFs) which can replicate

116 d gene expression signatures associated with cancer associated fibroblasts (CAFs), epithelial to mese

117 cancer model lactate released by glycolytic cancer-associated fibroblasts (CAFs) acts on CD4(+) T ce

118 downstream target SMAD2 (pSMAD2) (n=319) in cancer-associated fibroblasts (CAFs) and assessed links

119 Activation of cancer-associated fibroblasts (CAFs) and ensuing desmopl

120 endent upon remodeling 'stroma', composed of cancer-associated fibroblasts (CAFs) and extracellular m

121 ponse to the tumor, suggesting a key role of cancer-associated fibroblasts (CAFs) and fibrosis in its

122 he ANXA6/LRP1/TSP1 complex was restricted to cancer-associated fibroblasts (CAFs) and required physio

123 Desmoplasia, a fibrotic mass including cancer-associated fibroblasts (CAFs) and self-sustaining

124 peritoneal fibroblasts to express markers of cancer-associated fibroblasts (CAFs) and to stimulate gr

125 Cancer-associated fibroblasts (CAFs) are a crucial compo

126 Cancer-associated fibroblasts (CAFs) are a heterogeneous

127 Cancer-associated fibroblasts (CAFs) are a key component

128 Cancer-associated fibroblasts (CAFs) are a key component

129 Cancer-associated fibroblasts (CAFs) are a major cancer-

130 Cancer-associated fibroblasts (CAFs) are a major cellula

131 Cancer-associated fibroblasts (CAFs) are a multifaceted

132 Cancer-associated fibroblasts (CAFs) are abundant compon

133 Cancer-associated fibroblasts (CAFs) are abundantly pres

134 Cancer-associated fibroblasts (CAFs) are activated fibro

135 Cancer-associated fibroblasts (CAFs) are an important co

136 Cancer-associated fibroblasts (CAFs) are an integral com

137 Cancer-associated fibroblasts (CAFs) are associated with

138 Cancer-associated fibroblasts (CAFs) are highly heteroge

139 Cancer-associated fibroblasts (CAFs) are important for t

140 Cancer-associated fibroblasts (CAFs) are integral to the

141 Cancer-associated fibroblasts (CAFs) are key actors in m

142 Among the various components of the TME, cancer-associated fibroblasts (CAFs) are key regulators

143 Cancer-associated fibroblasts (CAFs) are known to contri

144 Cancer-associated fibroblasts (CAFs) are major component

145 Cancer-associated fibroblasts (CAFs) are one of the most

146 Cancer-associated fibroblasts (CAFs) are one of the most

147 Recent studies indicate that cancer-associated fibroblasts (CAFs) are phenotypically

148 Cancer-associated fibroblasts (CAFs) are pivotal in tumo

149 Cancer-associated fibroblasts (CAFs) are recognized pote

150 Cancer-associated fibroblasts (CAFs) are the most abunda

151 Cancer-associated fibroblasts (CAFs) are the most abunda

152 Cancer-associated fibroblasts (CAFs) are the predominant

153 The role of cancer-associated fibroblasts (CAFs) as regulators of tu

154 We identified cancer-associated fibroblasts (CAFs) as the main source

155 Cancer-associated fibroblasts (CAFs) can either suppress

156 We find that cancer-associated fibroblasts (CAFs) can promote antiand

157 Heterogeneous subtypes of cancer-associated fibroblasts (CAFs) coexist within panc

158 wnregulated in 15 out of 16 samples (94%) of cancer-associated fibroblasts (CAFs) compared with match

159 Cancer-associated fibroblasts (CAFs) comprise one of the

160 Cancer-associated fibroblasts (CAFs) comprise the majori

161 Cancer-associated fibroblasts (CAFs) comprise the most f

162 The molecular mechanism by which cancer-associated fibroblasts (CAFs) confer chemoresista

163 Cancer-associated fibroblasts (CAFs) constitute a promin

164 ls are embedded in the tumor stroma of which cancer-associated fibroblasts (CAFs) constitute a promin

165 Here, we demonstrate that cancer-associated fibroblasts (CAFs) constitute the prom

166 Cancer-associated fibroblasts (CAFs) contribute to the p

167 fibroblast growth factor (FGF1) derived from cancer-associated fibroblasts (CAFs) cooperates with can

168 Cancer-associated fibroblasts (CAFs) exert multiple tumo

169 Cancer-associated fibroblasts (CAFs) exhibit spatial and

170 Cancer-associated fibroblasts (CAFs) facilitate therapy

171 Cancer-associated fibroblasts (CAFs) found in primary an

172 Background: Targeting cancer-associated fibroblasts (CAFs) has become an attra

173 Targeting cancer-associated fibroblasts (CAFs) has become an attra

174 Cancer-associated fibroblasts (CAFs) have a pivotal canc

175 Cancer-associated fibroblasts (CAFs) have an important r

176 Cancer-associated fibroblasts (CAFs) have been implicate

177 Cancer-associated fibroblasts (CAFs) have been shown to

178 Cancer-associated fibroblasts (CAFs) have emerged as a d

179 Cancer-associated Fibroblasts (CAFs) have emerged as cri

180 itate the interplay between cancer cells and cancer-associated fibroblasts (CAFs) in head and neck ca

181 deletion of IL-17 signaling specifically in cancer-associated fibroblasts (CAFs) in late-stage tumor

182 in analytics in studying the role of stromal cancer-associated fibroblasts (CAFs) in modulating heter

183 Specialized cancer-associated fibroblasts (CAFs) in the ECM influenc

184 ting the co-existence of distinct subsets of cancer-associated fibroblasts (CAFs) in the microenviron

185 Cancer-associated fibroblasts (CAFs) in the TME possess

186 Interactions between tumor cells and cancer-associated fibroblasts (CAFs) in the tumor microe

187 Cancer-associated fibroblasts (CAFs) in the tumor microe

188 Cancer-associated fibroblasts (CAFs) in triple-negative

189 are coordinated to generate tumour-promoting cancer-associated fibroblasts (CAFs) is not well underst

190 s highly expressed by dermal fibroblasts and cancer-associated fibroblasts (CAFs) isolated from mutan

191 Cancer-associated fibroblasts (CAFs) mediate an immunosu

192 Such cancer-associated fibroblasts (CAFs) modulate the tumor

193 Cancer-associated fibroblasts (CAFs) perform diverse rol

194 Cancer-associated fibroblasts (CAFs) play a pivotal role

195 Cancer-associated fibroblasts (CAFs) play a pivotal role

196 Cancer-associated fibroblasts (CAFs) play a significant

197 Cancer-associated fibroblasts (CAFs) promote tumor malig

198 A-associated scaffold protein Hic-5 in mouse cancer-associated fibroblasts (CAFs) promoted a dramatic

199 Cancer-associated fibroblasts (CAFs) regulate diverse in

200 Cancer-associated fibroblasts (CAFs) represent the most

201 Cancer-associated fibroblasts (CAFs) represent the most

202 :141-155) delineate a novel strategy whereby cancer-associated fibroblasts (CAFs) secrete cytokines t

203 Cancer-associated fibroblasts (CAFs) shape the tumor mic

204 oles in prostate development and cancer, and cancer-associated fibroblasts (CAFs) stimulate tumourige

205 s and convert pancreatic stellate cells into cancer-associated fibroblasts (CAFs) that express inflam

206 tic stellate cells (PSCs) differentiate into cancer-associated fibroblasts (CAFs) that produce desmop

207 ct3/4(+)/Nanog(+) lung CSCs fed with CD90(+) cancer-associated fibroblasts (CAFs) to further advance

208 mal areas and a gene expression signature of cancer-associated fibroblasts (CAFs) were only prognosti

209 Cancer-associated fibroblasts (CAFs) were presumed absen

210 This effect was also confirmed in cancer-associated fibroblasts (CAFs) when co-cultured wi

211 esponded by upregulating S100A4, a marker of cancer-associated fibroblasts (CAFs), and this effect wa

212 t cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms

213 Activated fibroblasts in tumors, or cancer-associated fibroblasts (CAFs), have become a popu

214 Cancer-associated fibroblasts (CAFs), one of the princip

215 Activated stromal fibroblasts, namely cancer-associated fibroblasts (CAFs), play a major role

216 Emerging evidence suggests that cancer-associated fibroblasts (CAFs), the most abundant

217 talk between normal stromal cells, including cancer-associated fibroblasts (CAFs), vascular endotheli

218 k factor 1 (HSF1) is frequently activated in cancer-associated fibroblasts (CAFs), where it is a pote

219 ith known carcinogenic potential, can affect cancer-associated fibroblasts (CAFs), which are a key co

220 ow that the MRTF-SRF pathway is activated in cancer-associated fibroblasts (CAFs).

221 re the secretome of human mammary normal and cancer-associated fibroblasts (CAFs).

222 rget cells, which resembles the phenotype of cancer-associated fibroblasts (CAFs).

223 moting the reprogramming of these cells into cancer-associated fibroblasts (CAFs).

224 ut CIC chemoresistance was also increased by cancer-associated fibroblasts (CAFs).

225 receptor (IL17RC) specifically in IL17A(-/-) cancer-associated fibroblasts (CAFs).

226 haracterized by fibrosis and an abundance of cancer-associated fibroblasts (CAFs).

227 erized by the presence of myofibroblast-like cancer-associated fibroblasts (CAFs).

228 or, MSCs differentiate into S100A4-secreting cancer-associated fibroblasts (CAFs).

229 wed that Hic-5 is primarily expressed in the cancer-associated fibroblasts (CAFs).

230 RCA, we identified two distinct subtypes of cancer-associated fibroblasts (CAFs).

231 n PDAC has evolved, it has become clear that cancer associated fibroblasts can play both tumor promot

232 the tumor microenvironment, and signals from cancer-associated fibroblasts can impinge on mitochondri

233 to accelerate FN assembly in fibroblasts and cancer-associated fibroblasts, cell types that produce a

234 In microarray expression analysis, cancer-associated fibroblasts clustered tightly into one

235 RDEB cancer-associated fibroblasts conferred increased adhesi

236 Cancer-associated fibroblasts constitute a vital subpopu

237 The conditioned media from the cancer-associated fibroblast cultures enhanced prolifera

238 lopment of quinoline-based ligands targeting cancer-associated fibroblasts demonstrated promising pre

239 rmal and IPF fibroblasts, as well as in lung cancer-associated fibroblasts, dermal fibroblasts and he

240 This cancer-associated fibroblast drives tumour growth and in

241 munity revealed new granulocyte-enriched and cancer-associated fibroblast-enriched TCNs specific to h

242 that of cancer-associated fibroblasts, RDEB cancer-associated fibroblasts exhibited a distinct and d

243 Because of upregulated expression on cancer-associated fibroblasts, fibroblast activation pro

244 ely 170 of 22,000 genes were up-regulated in cancer-associated fibroblasts (fold change > 2, P < 0.05

245 sively produced and used by cancer cells and cancer-associated fibroblasts for degrading stromal coll

246 eratin malignant cells and immunosuppressive cancer-associated fibroblasts form an immune exclusionar

247 al trials, chemotherapeutic agents targeting cancer-associated fibroblasts had antitumour properties.

248 ch was expressed in both malignant cells and cancer-associated fibroblasts, had potent anti-tumor act

249 Cancer-associated fibroblasts have a variety of activiti

250 samples, we identify a role for inflammatory cancer-associated fibroblasts (iCAFs) in tumor progressi

251 he distinct molecular expression profiles of cancer-associated fibroblasts in colon cancer metastasis

252 d hepatic stellate cells (aHSC) give rise to cancer-associated fibroblasts in HCC and are considered

253 o, we confirmed COX2 and TGFB2 expression in cancer-associated fibroblasts in metastatic colon cancer

254 e-anchored peptidase, is highly expressed in cancer-associated fibroblasts in more than 90% of epithe

255 ma protein (Rb), through phosphorylation, in cancer-associated fibroblasts in oro-pharyngeal cancer s

256 s cross-talk between breast cancer cells and cancer-associated fibroblasts in the lung metastatic nic

257 nfiltration of inflammatory/immune cells and cancer-associated fibroblasts in the tumor microenvironm

258 stroma, conferring gemcitabine resistance to cancer-associated fibroblasts in vitro and further enhan

259 Cancer-associated fibroblasts induce malignant behavior

260 Fibroblasts in the tumour stroma (cancer-associated fibroblasts) influence tumour progress

261 atrix, either produced by cancer cells or by cancer-associated fibroblasts, influences angiogenesis,

262 bset of the NSCLC cells induced an activated cancer-associated fibroblast-like fibroblast phenotype d

263 ed differential expression of one or several cancer-associated fibroblast markers such as vimentin, f

264 Cancer-associated fibroblasts migrate and invade toward

265 model of the desmoplastic stroma comprising cancer-associated fibroblast-mimicking cells and M2-pola

266 roximity of TGFB1-expressing myofibroblastic cancer-associated fibroblasts (myCAFs) to aggressive 'ba

267 collective cell interactions, proliferation, cancer-associated fibroblasts, myoepithelial cells, and

268 Cancer-associated fibroblasts/myofibroblasts and inflamm

269 FAP is overexpressed by cancer-associated fibroblasts of several tumor entities.

270 activation protein (FAP) is overexpressed in cancer-associated fibroblasts of several tumor entities.

271 rporating other cell types (immune cells and cancer-associated fibroblasts) or species-, organ- or pa

272 ired an activated phenotype or also known as cancer-associated fibroblast phenotype after being in co

273 s with ALL, frequently adopted an activated, cancer-associated fibroblast phenotype.

274 that interleukin 6 (IL6) derived mainly from cancer-associated fibroblasts played the most important

275 ate into myofibroblasts (also referred to as cancer-associated fibroblasts) primarily, but not exclus

276 erent environments, but targeted therapy and cancer-associated fibroblasts qualitatively switch the t

277 EB normal skin fibroblasts resembled that of cancer-associated fibroblasts, RDEB cancer-associated fi

278 t-induced functional diversity of colorectal cancer-associated fibroblasts, representing a non-cell a

279 licited from group I (normal) and group III (cancer-associated) fibroblasts, respectively, approximat

280 Loss of Cav-1 expression in cancer-associated fibroblasts results in an activated tu

281 Cancer-associated fibroblasts secrete growth factors and

282 Activation of the HER2/HER3 axis by cancer-associated fibroblast-secreted NRG1 mediates cast

283 Recently, we reported that human breast cancer-associated fibroblasts show functional inactivati

284 , and E-cadherin expression, with pancreatic cancer-associated fibroblasts showing the opposite expre

285 inducing microenvironment changes, including cancer-associated fibroblasts, T regulatory cells, and i

286 ling pathways exist between cancer cells and cancer-associated fibroblasts that contribute to hypoxic

287 C typically has a prominent stroma including cancer-associated fibroblasts that express fibroblast ac

288 healing, which induces their conversion into cancer-associated fibroblasts that facilitate metastasis

289 expression and activity in cancer cells and cancer-associated fibroblasts that strongly contribute t

290 promote disease pathogenesis, including via cancer-associated fibroblasts, the hematopoietic stem ce

291 CXCL12 expressed by cancer-associated fibroblasts then binds to CXCR4 on tum

292 or xenografts, but they were not produced by cancer-associated fibroblasts, thereby comprising a spec

293 Similarly, when LIMK activity is blocked in cancer-associated fibroblasts, they are unable to lead t

294 o studies indicated that exposure of primary cancer-associated fibroblasts to MEDI-575 can directly a

295 and the metabolic/catabolic reprogramming of cancer-associated fibroblast, to fuel the growth of adja

296 We generated expression profiles of cancer-associated fibroblasts using oligochip arrays and

297 d cancer cells compared with patient-matched cancer-associated fibroblasts, whereas HHT was equally t

298 found to be efficacious even in presence of cancer associated fibroblasts which have been shown to c

299 rounded by a dense stroma that contains many cancer-associated fibroblasts, which promotes their prog

300 he conversion of mesenchymal stem cells into cancer-associated fibroblasts, which secrete stromal-der