ライフサイエンスコーパス: CAF

1 CAF +/- HAL are studied on RYR1 single-channel currents

2 CAF-derived SFRP1, driven by CD105 signaling, was necess

3 CAF-triggered Ca(2+) release and its influences on skele

4 CAFs also invaded a Matrigel matrix following a glutamin

5 CAFs clustered into two states: the first with features

6 CAFs moving toward Gln presented a polarized Akt2 distri

7 pletion of the chromatin assembly complex-1 (CAF-1) complex, a histone chaperone that is required for

8 stone chaperone Chromatin Assembly Factor 1 (CAF-1), which is recruited to DNA replication forks thro

9 bly mediated by CHROMATIN ASSEMBLY FACTOR 1 (CAF-1).

10 C [4.13 +/- 1.22 (CAF + EMD); 3.95 +/- 1.11 (CAF + CM + EMD); 2.94 +/- 0.77 (CAF + CM); 2.72 +/- 0.81

11 owed a superior length of NC [4.13 +/- 1.22 (CAF + EMD); 3.95 +/- 1.11 (CAF + CM + EMD); 2.94 +/- 0.7

12 mpared with the other groups [1.09 +/- 0.26 (CAF + EMD); 1.04 +/- 0.34 (CAF + CM); and 1.14 +/- 0.29

13 1.04 +/- 0.34 (CAF + CM); and 1.14 +/- 0.29 (CAF), P = 0.03].

14 s [1.09 +/- 0.26 (CAF + EMD); 1.04 +/- 0.34 (CAF + CM); and 1.14 +/- 0.29 (CAF), P = 0.03].

15 ); 3.01 +/- 0.56 (CAF + EMD); 2.15 +/- 0.47 (CAF + CM); 2.29 +/- 0.82 (CAF), P = 0.005].

16 21 +/- 0.68 (CAF + CM + EMD); 3.01 +/- 0.56 (CAF + EMD); 2.15 +/- 0.47 (CAF + CM); 2.29 +/- 0.82 (CAF

17 0.81 (CAF), P = 0.02] and NB [3.21 +/- 0.68 (CAF + CM + EMD); 3.01 +/- 0.56 (CAF + EMD); 2.15 +/- 0.4

18 95 +/- 1.11 (CAF + CM + EMD); 2.94 +/- 0.77 (CAF + CM); 2.72 +/- 0.81 (CAF), P = 0.02] and NB [3.21 +

19 D); 2.94 +/- 0.77 (CAF + CM); 2.72 +/- 0.81 (CAF), P = 0.02] and NB [3.21 +/- 0.68 (CAF + CM + EMD);

20 D); 2.15 +/- 0.47 (CAF + CM); 2.29 +/- 0.82 (CAF), P = 0.005].

21 However, little is known about CAF subtypes, the roles they play in cancer progression,

22 onditioned media from radiotherapy-activated CAFs increased iNOS/NO signaling in tumor cells through

23 e of a difference in KTW gain between ADMG + CAF and SCTG + CAF.

24 ween acellular dermal matrix grafts (ADMG) + CAF and SCTG + CAF or between enamel matrix derivative (

25 ive targeting of both the A(2B)-mediated ADO-CAF-CD73 feedforward circuit and A(2A)-mediated immune s

26 hat oncogenic Kras and CXCR2 signaling alter CAFs, producing a secretory CAF phenotype with low fibro

27 ted strategies to disrupt interactions among CAFs, the immune system, and cancer cells, focusing on a

28 index, defined as the number of amoxicillin CAF standard units divided by the total number of CAF st

29 The CAF and CAF + CM groups showed a superior epithelial length when

30 mesenchymal markers in epithelial cells and CAF.

31 dvanced flap (CAF); CAF + CM; CAF + EMD; and CAF + CM + EMD (split-mouth design).

32 Notably, the VEX2-orthologue and CAF-1 in mammals are also implicated in exclusion and in

33 that direct contact between cancer cells and CAFs triggers the expression of a wide range of inflamma

34 coculture experiments of tumor organoids and CAFs showed that CAFs shape the epithelial-to-mesenchyma

35 kin Squamous Cell Carcinoma (SCC)-associated CAFs, in which CSL is decreased.

36 In turn, this metabolic-based CAF-immunomodulated environment exerts a pro-invasive ef

37 We tested both liposomal and emulsion based CAFs with solid and fluid phase lipids, with or without

38 study shows a novel interaction axis between CAF and immune cells and reveals the central role of CAF

39 Ab inhibited intercellular signaling between CAF and cancer cells by modulating CAF-mediated expressi

40 Strong pharmacological synergism between CAF and HAL is demonstrated in both single-channel and m

41 At 2 years of follow up, both CAF+CTG and TUN+CTG resulted in significant clinical and

42 We further reveal that histone deposition by CAF-1 is required for efficient H3K9me2 enrichment at re

43 TAD5 and subsequent nucleosome deposition by CAF-1.

44 citabine resistance of PDAC cells induced by CAF-derived hepatocyte growth factor.

45 ler Class I or II GR defect, were treated by CAF+CTG (control; n = 19) or TUN+CTG (test; n = 20) and

46 oducing enzyme NOX4, which is upregulated by CAF in many human cancers, and compared this with TGFbet

47 r inhibition of CDH11, which is expressed by CAFs in the pancreatic tumor stroma, reduces growth of p

48 four groups: coronally advanced flap (CAF); CAF + CM; CAF + EMD; and CAF + CM + EMD (split-mouth des

49 Dietary caffeine (CAF) is the most commonly consumed psychoactive compound

50 ion protein (FAP), coexist within the CD49e+ CAF compartment in high-grade serous ovarian cancers.

51 ps: coronally advanced flap (CAF); CAF + CM; CAF + EMD; and CAF + CM + EMD (split-mouth design).

52 in vivo findings showed that Prrx1-deficient CAFs remain constitutively activated.

53 sts to generate a predominant SOX2-dependent CAF population expressing the WNT regulator Sfrp2 as its

54 By using EAC patient-derived CAFs, organoid cultures, and xenograft models we identif

55 sed to investigate the influences of dietary CAF on both peripheral and central responses before and

56 We hypothesize that dietary CAF achieving blood levels measured in human plasma exac

57 subcutaneous electrodes reveals that dietary CAF does not alter baseline electroencephalogram (EEG) t

58 odel of MH susceptibility exposed to dietary CAF, a modifiable lifestyle factor that may mitigate ris

59 er, CD49e, and demonstrate that two distinct CAF states, distinguished by expression of fibroblast ac

60 ital imaging, we observe that these dominant CAFs delay cancer cell response to chemotherapy.

61 s prevented Akt2 polarization and Gln-driven CAF invasion.

62 Glutamine dependence drove CAF migration toward this amino acid when cultured in lo

63 re randomly assigned to be treated by either CAF (n = 18) or LPF (n = 18).

64 cal trial comparing CTG combined with either CAF or TUN in the treatment of single maxillary gingival

65 found for SCTG + CAF when compared to EMD + CAF (MD: -1.06 mm), and SCTG + CAF when compared to GTR

66 or between enamel matrix derivative (EMD) + CAF and SCTG + CAF.

67 nd microenvironmental signals, and establish CAF-derived FGF1 as a novel paracrine regulator of oncog

68 cation-associated chromatin assembly factor, CAF-1, binds to and specifically maintains VEX1 compartm

69 opy combined with the novel CUBIC Acid-Fast (CAF) staining procedure enables a quantitative approach

70 lammation, and cancer-associated fibroblast (CAF) activation.

71 s revealed two cancer-associated fibroblast (CAF) and two perivascular-like (PVL) subpopulations.

72 aspects of the cancer-associated fibroblast (CAF) phenotype, including the expression of CAF markers

73 lls as well as cancer-activated fibroblasts (CAF) that facilitate epithelial tumor cell invasion.

74 ried, however cancer associated fibroblasts (CAF) and their contribution to the TME are important in

75 Carcinoma-associated fibroblasts (CAF) are a potential therapeutic target for both direct

76 Although cancer-associated fibroblasts (CAF) are abundant in PDAC tumors, the effects of radioth

77 Cancer-associated fibroblasts (CAF) are prominent players in the microenvironment of br

78 prostatic carcinoma-associated fibroblasts (CAF) contribute to tumor progression and resistance to a

79 ervation that cancer-associated fibroblasts (CAF) enhanced invasion in 3D by inducing expression of a

80 Cancer-associated fibroblasts (CAF) have many tumor-promoting functions and promote imm

81 nd especially cancer-associated fibroblasts (CAF) play a critical biophysical role in cancer progress

82 elates with a cancer-associated fibroblasts (CAF) signature.

83 oevolution of cancer-associated fibroblasts (CAF) with tumor progression, we tested the role of cance

84 activation of cancer-associated fibroblasts (CAF).

85 tween MSC and cancer-associated fibroblasts (CAF).

86 ma, including cancer-associated fibroblasts (CAF).

87 by glycolytic cancer-associated fibroblasts (CAFs) acts on CD4(+) T cells, shaping T-cell polarizatio

88 Activation of cancer-associated fibroblasts (CAFs) and ensuing desmoplasia play an important role in

89 , composed of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), which plays a crit

90 Cancer-associated fibroblasts (CAFs) are a heterogeneous population of mesenchymal cell

91 Cancer associated fibroblasts (CAFs) are a key component of the tumor microenvironment.

92 Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment

93 Cancer-associated fibroblasts (CAFs) are activated fibroblasts that constitute the majo

94 Cancer-associated fibroblasts (CAFs) are an important component of the tumor microenvir

95 Cancer-associated fibroblasts (CAFs) are an integral component of the tumor microenviro

96 Cancer-associated fibroblasts (CAFs) are key actors in modulating the progression of ma

97 Cancer-associated fibroblasts (CAFs) are known to contribute to poor outcome by conferr

98 formation of cancer associated fibroblasts (CAFs) are not well elucidated.

99 Cancer-associated fibroblasts (CAFs) are one of the most significant components in the

100 indicate that cancer-associated fibroblasts (CAFs) are phenotypically and functionally heterogeneous.

101 Cancer-associated fibroblasts (CAFs) can either suppress or support T lymphocyte activi

102 We find that cancer-associated fibroblasts (CAFs) can promote antiandrogen resistance in mouse model

103 s subtypes of cancer-associated fibroblasts (CAFs) coexist within pancreatic cancer tissues and can b

104 onstrate that cancer-associated fibroblasts (CAFs) constitute the prominent CD73(hi) population in hu

105 derived from cancer-associated fibroblasts (CAFs) cooperates with cancer cell-autonomous signals to

106 Cancer-associated fibroblasts (CAFs) facilitate therapy resistance and metastasis.

107 nd: Targeting cancer-associated fibroblasts (CAFs) has become an attractive goal for diagnostic imagi

108 Targeting cancer-associated fibroblasts (CAFs) has become an attractive goal for diagnostic imagi

109 Cancer-associated fibroblasts (CAFs) have been shown to display a high degree of interc

110 ct subsets of cancer-associated fibroblasts (CAFs) in the microenvironment of murine carcinomas, each

111 our-promoting cancer-associated fibroblasts (CAFs) is not well understood.

112 Cancer-associated fibroblasts (CAFs) perform diverse roles and can modulate therapy res

113 Cancer-associated fibroblasts (CAFs) promote tumor malignancy, but the precise transcri

114 lso occurs in Cancer Associated Fibroblasts (CAFs) remains to be carefully investigated.

115 ategy whereby cancer-associated fibroblasts (CAFs) secrete cytokines that stimulate glycogen breakdow

116 te cells into cancer-associated fibroblasts (CAFs) that express inflammatory cytokines at high levels

117 signature of cancer-associated fibroblasts (CAFs) were only prognostic in specific tumor stages.

118 cer cells and cancer associated fibroblasts (CAFs) which can replicate tumor microenvironment.

119 regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined.

120 sociated with cancer associated fibroblasts (CAFs), epithelial to mesenchymal transition, mesenchymal

121 abundance of cancer-associated fibroblasts (CAFs).

122 broblast-like cancer-associated fibroblasts (CAFs).

123 to the trapezoidal coronally advanced flap (CAF) and CTG combination.

124 ically treated with coronally advanced flap (CAF) associated with SCTG harvested by: double blade sca

125 sue grafts (SCTG) + coronally advanced flap (CAF) compared to guided tissue regeneration with resorba

126 on the outcomes of coronally advanced flap (CAF) for treating multiple adjacent gingival recessions

127 ned to four groups: coronally advanced flap (CAF); CAF + CM; CAF + EMD; and CAF + CM + EMD (split-mou

128 extension on the outcomes of MAGRs following CAF with or without a connective tissue graft (CTG).

129 Whereas beta-catenin is dispensable for CAF-mediated ECM remodelling, cancer cell growth and inv

130 40 +/- 40 ng/L for CBZ, 180 +/- 110 ng/L for CAF, 4 +/- 3 ng/L for DCF, and 310 +/- 70 ng/L for ILA a

131 A superior STT was observed for CAF + CM + EMD group (1.5 +/- 0.33) when compared with t

132 We then examined the potential for CAF targeting, focusing on the ROS-producing enzyme NOX4

133 Cationic adjuvant formulations (CAFs) have been previously investigated as an adjuvant f

134 (defined as child-appropriate formulations [CAFs]) using wholesale data from the IQVIA-Multinational

135 RNA sequencing of CD8(+) T cells from CAF-rich murine tumors and immunochemistry analysis of h

136 Lastly, profiling of miRs from CAF exosomes showed alterations of several exosomal miRs

137 Here we generated CAF-rich murine tumor models (TC1, MC38, and 4T1) to inv

138 sis of patient-derived and de-novo generated CAFs demonstrated widespread loss of cytosine methylatio

139 oted vimentin collapse in Hic-5 heterozygous CAFs.

140 Clinically, high CAF abundancy in CRC tissues correlates strongly with el

141 cific transcription factor TCF21 in FAP-high CAFs decreases their ability to promote invasion, chemor

142 dels (TC1, MC38, and 4T1) to investigate how CAFs influence the immune microenvironment and affect re

143 The action of DDR2 in mouse and human CAFs, and tumors in vivo, was found to influence mechano

144 CAFs derived from cKO mice as well as human CAFs showed that FAK is required for their activity to p

145 otein most increased in abundance in hypoxic CAFs.

146 ogenic and pro-migratory function of hypoxic CAFs by decreasing secretion of the pro-angiogenic facto

147 in the neoplastic compartment, and identify CAFs as the specific source of FGF1 in the tumor microen

148 human mammary CAFs promoted angiogenesis in CAF-endothelial cell cocultures in vitro.

149 on PCa epithelial inhibition of catalase in CAF.

150 g of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some ant

151 nergistically enhances antitumor immunity in CAF-rich tumors.

152 We identify neuregulin 1 (NRG1) in CAF supernatant, which promotes resistance in tumor cell

153 +) T-cell exclusion was similarly present in CAF-rich human tumors.

154 nhibition restored immunotherapy response in CAF-rich tumors.

155 tial role and mechanisms of FAK signaling in CAF to promote breast cancer metastasis in vivo.

156 geted by TLR9-induced NF-kappaB signaling in CAF.

157 e cancer cells, and netrin-1 upregulation in CAF was associated with increased cancer cell stemness.

158 , and the inactivation of Sox2 or Sfrp1/2 in CAFs impaired the induction of migration and invasion of

159 We further showed that FAK ablation in CAFs decreased exosome functions to promote tumor cell m

160 Wnt activity in CAFs was linked with distinct subtypes, where low and hi

161 ing a potential undescribed role of CXCR2 in CAFs.

162 the action of the collagen receptor DDR2 in CAFs controls tumor stiffness by reorganizing collagen f

163 tically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2

164 Mechanistically, DKK3 in CAFs acts via canonical Wnt signalling by interfering wi

165 We report Osx expression in CAFs and by using Osx-cre;TdTomato reporter mice we conf

166 ne amplification and increased expression in CAFs are an attractive target for stroma-focused anti-ca

167 RNA and protein were significantly higher in CAFs than in pancreatic cancer epithelial cells, human o

168 We discuss how inactivation of IFNAR1 in CAFs acts to stimulate stromagenesis and tumor growth.

169 O) secretion were significantly increased in CAFs secretome following radiotherapy.

170 2 is expressed by tumor cells and induced in CAFs derived from synthetic fibroblasts.

171 Expression of NNMT in CAFs led to depletion of S-adenosyl methionine and reduc

172 rotein (FAP) is overexpressed selectively in CAFs, drawing interest in FAP as a stromal target.

173 lts identify a new role for FAK signaling in CAFs that regulate their intercellular communication wit

174 that TRAF6 was significantly upregulated in CAFs adjacent to melanoma cells.

175 o be distinctly expressed by tumor-inductive CAF, which was further demonstrated to occur in a CD105-

176 e enriched with neutrophils and inflammatory CAFs in a p63-dependent manner.

177 igation of gene signatures from inflammatory-CAFs and differentiated-PVL cells in independent TNBC pa

178 causes conversion of dermal fibroblasts into CAFs.

179 Targeting the EVs-ITGBL1-CAFs-TNFAIP3-NF-kappaB signaling axis provides an attrac

180 ion of the RhoGTPase Cdc42 in Hic-5 knockout CAFs rescued the vimentin collapse, while pan-formin inh

181 and high levels induced an inflammatory-like CAF (iCAF) subtype or contractile myCAFs, respectively.

182 by the ability of FAP-high, but not FAP-low, CAFs to aggressively promote proliferation, invasion and

183 Both colon and lung CAF secreted netrin-1 when cocultured with respective ca

184 tient derived xenograft (PDX) cells and lung CAFs co-cultures.

185 We found that hypoxic human mammary CAFs promoted angiogenesis in CAF-endothelial cell cocul

186 xia-induced molecular alterations in mammary CAFs.

187 oring distinct alterations in p53 manipulate CAFs.

188 Mechanistically, CAF-CD73 expression is enhanced via an ADO-A(2B) recepto

189 This work shows that Prrx1-mediated CAF plasticity has significant impact on PDAC biology an

190 However, the role of TRAF6 in melanoma CAFs remains unclear.

191 functions among the DNA methyltransferases, CAF-1, and histone-modifying enzymes.

192 are present in ongoing attempts to modulate CAFs for therapeutic benefit.

193 g between CAF and cancer cells by modulating CAF-mediated expression of cytokines such as IL6.

194 nt and bi-directional interactions with MSCs/CAFs and M2-TAMs.

195 minin-overexpressing cells admixed with MSCs/CAFs grew faster, metastasized earlier, especially to lu

196 dermal progenitor cells into a myofibroblast/CAF phenotype and is, therefore, a therapeutic target in

197 through multiple mechanisms, but as yet, no CAF-specific inhibitors are clinically available.

198 [GKT137831 (Setanaxib)] of NOX4 "normalized" CAF to a quiescent phenotype and promoted intratumoral C

199 miR-148a enriched in exosomes from FAK-null CAFs contribute to the reduced tumor cell activities and

200 rations of several exosomal miRs in FAK-null CAFs, and further analysis suggested that miR-16 and miR

201 emerges as a critical step in the control of CAF pro-tumorigenic potential.

202 Deletion of CAF-1 p150 subunit impairs the silencing of many genes i

203 (CAF) phenotype, including the expression of CAF markers and the secretion of cytokines and oncogenic

204 asis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement ou

205 and colleagues investigate the influence of CAF on the immune environment of tumors, specifically fo

206 access percentage, defined as the number of CAF standard units of Access antibiotics divided by the

207 s antibiotics divided by the total number of CAF standard units; amoxicillin index, defined as the nu

208 tandard units divided by the total number of CAF standard units; and access-to-watch index, defined a

209 d clinical trials evaluating the outcomes of CAF in the treatment of MAGRs was performed using mixed

210 NNMT is a central, metabolic regulator of CAF differentiation and cancer progression in the stroma

211 on of TGFbeta in vivo leads to remodeling of CAF dynamics, greatly reducing the frequency and activit

212 immune cells and reveals the central role of CAF in establishing a hospitable inflammatory niche in l

213 Here, we aim to elucidate the role of CAF plasticity and its impact on PDAC biology.

214 stromal cells (MSC) are a possible source of CAF following myofibroblastic differentiation, and we ha

215 We found that the large subunit of CAF-1, Chaf1a, requires the N-terminal KER domain to ass

216 The overall median volume of CAF antibiotic standard units sold in 2015 per country w

217 in melanoma cells affected the activation of CAFs.

218 Analyses of CAFs derived from cKO mice as well as human CAFs showed

219 t modulates the pro-tumorigenic behaviour of CAFs in vitro and in vivo.

220 To characterize the impact of CAFs on tumor differentiation and response to chemothera

221 ations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being de

222 This SnapShot summarizes the origins of CAFs, their diverse functions, and how this relates to h

223 mutant p53 educate a dominant population of CAFs that establish a pro-metastatic environment for GOF

224 f oncolytic viruses(2); however, the role of CAFs in this context remains unclear.

225 mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant

226 ntegrin alpha (ITGA) 11-expressing subset of CAFs that negatively associated with survival.

227 ized the concurrence of multiple subtypes of CAFs with diverse roles, fibrogenic, and secretory.

228 PDAC tumors, the effects of radiotherapy on CAFs and the response of PDAC cells to radiotherapy are

229 NOX4 potentiates immunotherapy by overcoming CAF-mediated CD8(+) T-cell exclusion.

230 " Here, we identify a novel cell surface pan-CAF marker, CD49e, and demonstrate that two distinct CAF

231 l stem cells, was diminished in high passage CAF.

232 , we identify an integrin alpha11/PDGFRbeta+ CAF subset displaying tumor-promoting features in BC.

233 HET mice receiving CAF (plasma CAF 893 ng/ml) have significantly shorter times to respi

234 nvasion induced by integrin alpha11-positive CAFs.

235 or invasion by fibroblasts required previous CAF activation, which involved the TGFbeta/Snail1 signal

236 elated serum-borne marker for IL-6-producing CAFs, and serum levels of this marker predicted unfavora

237 t defining pathways and molecules to program CAF composition for cancer therapy.

238 onstrate that glutamine deprivation promotes CAF migration and invasion, which in turn facilitates th

239 rentiation of MSC towards a tumour-promoting CAF phenotype in vivo.

240 ibition of netrin-1 may reduce proneoplastic CAF-cancer cell cross-talk, thus inhibiting cancer plast

241 We found that prostatic CAF expressed DEC205, which was not expressed by normal

242 HET mice receiving CAF (plasma CAF 893 ng/ml) have significantly shorter ti

243 ions of PCNA residues involved in recruiting CAF-1 to the chromatin also result in defects in differe

244 1 inhibition could prevent, but not reverse, CAF differentiation.

245 m), and SCTG + CAF when compared to GTR rm + CAF (MD: -1.77 mm).

246 eration with resorbable membranes (GTR rm) + CAF (mean difference [MD]: -0.37 mm).

247 dermal matrix grafts (ADMG) + CAF and SCTG + CAF or between enamel matrix derivative (EMD) + CAF and

248 ared to EMD + CAF (MD: -1.06 mm), and SCTG + CAF when compared to GTR rm + CAF (MD: -1.77 mm).

249 ce in KTW gain between ADMG + CAF and SCTG + CAF.

250 mel matrix derivative (EMD) + CAF and SCTG + CAF.

251 zed tissue width (KTW) were found for SCTG + CAF when compared to EMD + CAF (MD: -1.06 mm), and SCTG

252 SCTG, CAF alone or associated with another biomaterial may be

253 signaling alter CAFs, producing a secretory CAF phenotype with low fibrogenic features; and increase

254 oncogenic Kras is associated with secretory CAFs and that CXCR2 inhibition promotes activation of fi

255 reveal a strong correlation between stromal CAF content and MYC protein level in the neoplastic comp

256 there has been a shift in the field to study CAF subpopulations and the emergent functions of these s

257 tical for maintaining the immune-suppressive CAF phenotype in tumors.

258 The suitability of targeting CAFs therapeutically is also discussed.

259 These findings demonstrate that CAF-mediated immunotherapy resistance can be effectively

260 tic signaling by testing the hypothesis that CAF-generated mechanical forces lead to activin A releas

261 We show for the first time that CAF state influences patient outcomes and that this is m

262 We also demonstrate that CAFs educated by null p53 cancer cells may be reprogramm

263 These studies establish that CAFs are efficient delivery vehicles for saRNA both for

264 accine), alphaPD-1, and MC38] and found that CAFs broadly suppressed response by specifically excludi

265 We show here that CAFs and other mesenchymal cells rely much more on gluta

266 We report that CAFs from skin squamous cell carcinomas (SCCs) display c

267 Several studies have recently reported that CAFs are more heterogenous and plastic than was previous

268 ractions on a microfluidic chip reveals that CAFs promote invasion by enhancing expression of GPNMB i

269 Here we show that CAFs regulate malignant cell metabolism through pathways

270 ents of tumor organoids and CAFs showed that CAFs shape the epithelial-to-mesenchymal phenotype and c

271 pport T lymphocyte activity, suggesting that CAFs may be reprogrammable to an immunosupportive state.

272 The CAF and CAF + CM groups showed a superior epithelial len

273 with a netrin-1-mAb (Net1-mAb) abrogated the CAF-mediated increase of cancer stemness both in cocultu

274 his tumor-preferential activity enhances the CAF-reprogramming effects of ARBs while eliminating bloo

275 ing to an increase in drug resistance in the CAF co-culture and the 3D spheroids.

276 progression, and molecular mediators of the CAF "state." Here, we identify a novel cell surface pan-

277 mechanisms regulating the acquisition of the CAF phenotype are not well understood.

278 TGFbeta1 inhibition, a key regulator of the CAF phenotype.

279 Hypoxia induced pronounced remodeling of the CAF proteome, including proteins that have not been prev

280 ng that it acts as a master regulator of the CAF state.

281 otein subunit vaccines; here we optimize the CAFs for delivery of saRNA in vivo and observe the immun

282 the oncogenic Kras-CXCR2 axis regulates the CAFs function in PDAC and contributes to CAFs heterogene

283 mmed by either GOF mutant p53 cells or their CAFs.

284 Importantly, this CAF phenotype determines tumor differentiation and disru

285 on during de novo differentiation of MSCs to CAF.

286 the CAFs function in PDAC and contributes to CAFs heterogeneity.

287 The action of DDR2 in tumor CAFs is thus critical for remodeling collagen fibers at

288 egrin alpha11-positive subset of pro-tumoral CAFs that exploits PDGFRbeta/JNK signalling axis to prom

289 transcription factor is critical for tuning CAF activation, allowing a dynamic switch between a dorm

290 Understanding CAF states in more detail could lead to better patient s

291 dex, defined as the ratio of Access-to-Watch CAF standard units.

292 sites shows marked nucleosome depletion when CAF-1 function is reduced.

293 s greater association with target sites when CAF-1 is depleted and misregulation of target gene expre

294 on, we generated a PDAC mouse model in which CAF plasticity is modulated by genetic depletion of the

295 s expanded by chronic UVA exposure, to which CAFs are resistant.

296 he VEX-complex controls VSG-exclusion, while CAF-1 sustains VEX-complex inheritance in association wi

297 DBS and DE associated with CAF presented satisfactory clinical outcomes.

298 ctors, including the enzymes associated with CAF-1.

299 Tumor models of human PCa epithelia with CAF expanded similarly in mice in the presence or absenc

300 Co-culture of neoplastic cells with CAFs led to increased invasiveness that was abrogated by

301 MOMP-encoding saRNA complexed with CAFs resulted in both MOMP-specific cellular and humoral