ライフサイエンスコーパス: CAF

1 CAF-derived WNT2 activated canonical signaling in adenom

2 CAF-induced gene expression signatures predicted clinica

3 CAFs align the Fn matrix by increasing nonmuscle myosin

4 CAFs are thought to be more mechanically active but how

5 CAFs subsequently secrete factors that promote expansion

6 CAFs support multiple aspects of cancer progression, inc

7 Chromatin assembly factor 1 (CAF-1) deposits histones during DNA synthesis.

8 stone chaperone Chromatin Assembly Factor 1 (CAF-1) deposits tetrameric (H3/H4)2 histones onto newly-

9 Chromatin assembly factor 1 (CAF-1) is a H3-H4 histone chaperone that associates with

10 Chromatin assembly factor 1 (CAF-1) is a histone H3-H4 chaperone that deposits newly

11 Chromatin assembly factor 1 (CAF-1) is the histone chaperone responsible for histone

12 ysfunctional in chromatin assembly factor-1 (CAF-1) (fas1 and fas2 mutants), which are known to have

13 Used as a probe to identify Thy-1(+) CAF-enriched tumors in a compendium of 1,586 lung adenoc

14 sence of Thy-1(+) CAFs, we isolated Thy-1(+) CAFs and normal lung fibroblasts (LFs) from the lungs of

15 man lung adenocarcinomas containing Thy-1(+) CAFs have a worse prognosis.

16 We first examined the location of Thy-1(+) CAFs within human lung adenocarcinomas.

17 cancer database for the presence of Thy-1(+) CAFs, we isolated Thy-1(+) CAFs and normal lung fibrobla

18 ass I/II GRs were treated with CAF (n = 17), CAF + CM (n = 17), CAF + EMD (n = 17), and CAF + CM + EM

19 reated with CAF (n = 17), CAF + CM (n = 17), CAF + EMD (n = 17), and CAF + CM + EMD (n = 17).

20 mly assigned to receive either CAF (n = 17); CAF + CM (n = 17); CAF + EMD (n = 17), or CAF + CM + EMD

21 eive either CAF (n = 17); CAF + CM (n = 17); CAF + EMD (n = 17), or CAF + CM + EMD (n = 17).

22 ignificantly superior to CAF alone (23.53%); CAF + CM (52.94%), and CAF + CM + EMD (51.47%) (P <0.05)

23 and alpha-smooth muscle actin (alphaSMA), a CAF marker, were located on the tumor periphery surround

24 utcomes in single-tooth defects treated by a CAF procedure.

25 The resulting cells exhibited a CAF-like phenotype, suggesting that they had differentia

26 We identified a CAF subpopulation with elevated expression of alpha-smoo

27 ssociated human fibroblasts, we identified a CAF/D-ECM phenotype that correlates with improved patien

28 Thus, Thy-1 marks a CAF population that adversely impacts clinical outcome i

29 F1/IGF1R signaling initiated by RT-activated CAF worsens colorectal cancer progression, establishing

30 ds, and demonstrated that organoid-activated CAFs produced desmoplastic stroma.

31 Subsequently, RT-activated CAFs promoted survival of colorectal cancer cells, as we

32 Mean RC after CAF + CMX amounted to 89.9% after 6 months and 91.7% aft

33 Although CAFs are abundantly present, the effects of RT to CAF an

34 tient samples, we demonstrated that although CAFs promoted prostate cancer growth, matrix metalloprot

35 3.9] to 7.7 [95% CI, 5.7-10.3]; P < .05) and CAF (range of AORs, 1.7 [95% CI, 1.0-2.9] to 6.3 [95% CI

36 , CAF + CM (n = 17), CAF + EMD (n = 17), and CAF + CM + EMD (n = 17).

37 o CAF alone (23.53%); CAF + CM (52.94%), and CAF + CM + EMD (51.47%) (P <0.05).

38 Groups CAF and CAF+PERIO were exposed to a high-fat, hypercaloric diet.

39 was significant for CAF + CM, CAF + EMD, and CAF + CM + EMD (P <0.05).

40 th GRs treated with CAF + CM, CAF + EMD, and CAF + CM + EMD.

41 to investigate interactions between MMR and CAF-1- and ASF1A-H3-H4-dependent histone (H3-H4)2 tetram

42 mispair-containing DNA by the MMR system and CAF-1-dependent packaging of the newly replicated DNA in

43 MP-3 expression in prostate cancer cells and CAFs, but through different regulatory mechanisms.

44 nvestigate the interactions between CSCs and CAFs in mammary gland tumors driven by combined activati

45 tween various microenvironmental factors and CAFs in the CSC niche.

46 tumor-promoting factors by HNSCC-associated CAFs may explain their role in malignant development.

47 autophagy is upregulated in HNSCC-associated CAFs, where it is responsible for key pathogenic contrib

48 s study, we evaluated the cross-talk between CAF and TEC isolated from tumors generated in a mouse mo

49 facilitated HNSCC progression after blocking CAF autophagy.

50 ween 6-month and 3-year RC outcomes for both CAF procedures.

51 In both CAFs and normal fibroblasts, we found that YAP-TEAD acti

52 olecular mechanism for histone deposition by CAF-1, a reaction that has remained elusive for other hi

53 l )-dependent MMR reactions is suppressed by CAF-1- and ASF1A-H3-H4-dependent deposition of the histo

54 /II recession defects, surgically treated by CAF.

55 , we show that fibronectin (Fn) assembled by CAFs mediates CAF-cancer cell association and directiona

56 oma of cancer tissues and produced mainly by CAFs.

57 The remodeling of the stromal matrix by CAFs has been shown to increase tumor rigidity to indire

58 bsence of FN, contractility of the matrix by CAFs is preserved, but their ability to induce invasion

59 Standard and cafeteria (CAF) diet fed rats, a robust model of metabolic syndrome

60 presence of paracetamol (PAR) and caffeine (CAF).

61 ularization in the presence of breast cancer CAFs compared to normal breast fibroblasts.

62 Mutants in the H3.1 chaperone CAF-1 (fas1-4) maintain a pattern similar to that of wil

63 after 6 months was significant for CAF + CM, CAF + EMD, and CAF + CM + EMD (P <0.05).

64 of patients with GRs treated with CAF + CM, CAF + EMD, and CAF + CM + EMD.

65 years changed from 89.5% to 77.6% for CMX + CAF test sites and 97.5% to 95.5% for CTG + CAF control

66 sults reported by other investigators, CMX + CAF appears to present a viable and long-term alternativ

67 s greater for CTG + CAF (0.26 mm) than CMX + CAF (-0.21 mm).

68 ure at both 6 months and 5 years, with CMX + CAF sites tending to be "equally firm" and CTG + CAF sit

69 ain that forms the melanosomal amyloid core (CAF).

70 sites tending to be "equally firm" and CTG + CAF sites "more firm." Patient satisfaction was high, wi

71 grafts with coronally advanced flaps (CTG + CAF) have been deemed the gold standard for recession de

72 om 6 months to 5 years was greater for CTG + CAF (0.26 mm) than CMX + CAF (-0.21 mm).

73 CAF test sites and 97.5% to 95.5% for CTG + CAF control sites.

74 d long-term alternative to traditional CTG + CAF therapy.

75 ent received EMD+CAF for three teeth and CTG+CAF for one tooth for root coverage.

76 d inserting periodontal ligament fibers, CTG+CAF repairs through a long epithelial junction and conne

77 None of the three teeth treated with CTG+CAF showed periodontal regeneration.

78 te that exosomes secreted by patient-derived CAFs can strikingly reprogram the metabolic machinery fo

79 Coinjection of patient-derived CAFs from bone metastases led to de novo HTR tumors, whi

80 These cells (designated CAF-MSCs) enhanced in vitro neuroblastoma cell prolifera

81 entially expressed lncRNAs in distinguishing CAFs from NOFs were assessed using multiple multivariate

82 GRs were randomly assigned to receive either CAF (n = 17); CAF + CM (n = 17); CAF + EMD (n = 17), or

83 EMD+CAF continues to show histologic evidence of periodontal

84 Class I and II GR, each patient received EMD+CAF for three teeth and CTG+CAF for one tooth for root c

85 Seven of the nine teeth treated with EMD+CAF demonstrated varying degrees of periodontal regenera

86 resorption and ankylosis was noted with EMD+CAF.

87 Suicide-engineered CAFs were highly sensitive to apoptosis induction in vit

88 chemically induced skin tumors with enhanced CAF activation.

89 Finally, treatment of gemcitabine-exposed CAFs with an inhibitor of exosome release, GW4869, signi

90 population of alphaFAP- and FSP-1-expressing CAFs that share phenotypic and functional characteristic

91 in human MGMT-deficient cell-free extracts, CAF-1-dependent packaging of irreparable O(6)-mG-T mispa

92 Here we show that chromatin assembly factor (CAF)-1 subunit A (CHAF1A), the p150 subunit of the histo

93 repressor (CCR)4 and CCR4-associated factor (CAF)1 in the CCR4-NOT complex function in mRNA poly(A) t

94 Hic-5(-/-);PyMT tumor stroma contains fewer CAFs and exhibits reduced ECM deposition.

95 ctivation to a cancer-associated fibroblast (CAF) phenotype has been implicated in promoting primary

96 ies identified cancer-associated fibroblast (CAF)-derived EVs (from patients and xenograft models) la

97 rentiate into cancer-associated fibroblasts (CAF) and promote tumor progression.

98 rated that carcinoma-associated fibroblasts (CAF) are major sources of chemokines that recruit granul

99 suggest that cancer-associated fibroblasts (CAF) drive progression of this disease.

100 Cancer-associated fibroblasts (CAF) have been shown to support and regulate CSC functio

101 Cancer-associated fibroblasts (CAF) have been suggested to originate from mesenchymal s

102 Notably, cancer-associated fibroblasts (CAF) isolated from patient-derived tumors expressed mark

103 derived from cancer-associated fibroblasts (CAF) transfer miR-221 to promote hormonal therapy resist

104 410 cells and cancer-associated fibroblasts (CAF) were investigated.

105 lls to obtain cancer-associated fibroblasts (CAF)-like features via induction of tumor-derived Wnt7a.

106 contact with cancer-associated fibroblasts (CAF).

107 activation of cancer-associated fibroblasts (CAF).

108 ma containing cancer-associated fibroblasts (CAF).

109 activated as cancer-associated-fibroblasts (CAF) that stimulate oncogenic signaling in TEC.

110 ssociated adipocytes (CAAs) and fibroblasts (CAFs) than in those from ovarian cancer cells.

111 a key role of cancer-associated fibroblasts (CAFs) and fibrosis in its tumor microenvironment (TME).

112 restricted to cancer-associated fibroblasts (CAFs) and required physiopathologic culture conditions t

113 ass including cancer-associated fibroblasts (CAFs) and self-sustaining extracellular matrix (D-ECM),

114 Cancer-associated fibroblasts (CAFs) are a major cancer-promoting component in the tumo

115 Cancer-associated fibroblasts (CAFs) are a major cellular component of tumor microenvir

116 Cancer-associated fibroblasts (CAFs) are important for tumor initiation and promotion.

117 Cancer-associated fibroblasts (CAFs) are major components of the carcinoma microenviron

118 Cancer-associated fibroblasts (CAFs) are one of the most prominent cell types in the st

119 Cancer-associated fibroblasts (CAFs) are the most abundant cells of the tumor stroma.

120 The role of cancer-associated fibroblasts (CAFs) as regulators of tumor progression, specifically v

121 We identified cancer-associated fibroblasts (CAFs) as the main source of WNT2.

122 Cancer-associated fibroblasts (CAFs) comprise the majority of the tumor bulk of pancrea

123 nism by which cancer-associated fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly

124 Cancer-associated fibroblasts (CAFs) contribute to the poor prognosis of ovarian cancer

125 cer cells and cancer-associated fibroblasts (CAFs) in head and neck cancer (HNC), thereby promoting t

126 Cancer-associated fibroblasts (CAFs) regulate diverse intratumoral biological programs

127 rentiate into cancer-associated fibroblasts (CAFs) that produce desmoplastic stroma, thereby modulati

128 confirmed in cancer-associated fibroblasts (CAFs) when co-cultured with the tumor cells.

129 , a marker of cancer-associated fibroblasts (CAFs), and this effect was blocked by anakinra.

130 ely termed carcinoma-associated fibroblasts (CAFs), are key players in the multicellular, stromal-dep

131 l, can affect cancer-associated fibroblasts (CAFs), which are a key component of tumor microenvironme

132 ry normal and cancer-associated fibroblasts (CAFs).

133 t subtypes of cancer-associated fibroblasts (CAFs).

134 activated in cancer-associated fibroblasts (CAFs).

135 ressed in the cancer-associated fibroblasts (CAFs).

136 state cancer-associated stromal fibroblasts (CAFs) derived from a coculture cell model and clinical p

137 Compared with normal fibroblasts, CAFs produce an Fn-rich extracellular matrix with anisot

138 recession (GR) by a coronally advanced flap (CAF) combined with CM and/or EMD.

139 combination with a coronally advanced flap (CAF) on CDH, esthetics, and oral health-related quality

140 ects treated with a coronally advanced flap (CAF) procedure.

141 ot coverage (RC) by coronally advanced flap (CAF) procedures in localized gingival recessions.

142 grafts (CTGs) and coronally advanced flaps (CAFs) do not regenerate periodontal attachment apparatus

143 e with 61%/61% for CAF + CMX and 39%/39% for CAF after 6 months/3 years, respectively.

144 Likewise, CRC was stable with 61%/61% for CAF + CMX and 39%/39% for CAF after 6 months/3 years, re

145 Complete root coverage (CRC) for CAF + EMD was 70.59%, significantly superior to CAF alon

146 y reveal interactions that are essential for CAF-1 function in budding yeast, and importantly indicat

147 an PDA tissue, providing direct evidence for CAF heterogeneity in PDA tumor biology with implications

148 required in addition to the YAP pathway for CAF contractile and proinvasive properties.

149 th on QoL after 6 months was significant for CAF + CM, CAF + EMD, and CAF + CM + EMD (P <0.05).

150 Corresponding values for CAF were 83.7% versus 82.8% (Pearson's correlation: 0.94

151 three-dimensional covalent amide frameworks (CAFs) by devitrification of amorphous polyamide network

152 Further, CAFs exposed to gemcitabine significantly increase the r

153 Groups CAF and CAF+PERIO were exposed to a high-fat, hypercalor

154 promoted the biogenesis of onco-miR-221(hi) CAF microvesicles and established stromal CSC niches in

155 However, how CAF-1 functions in this process is not yet well understo

156 Here, we developed an engineered human CAF cell line with an inducible suicide gene to enable s

157 The p150 subunit of human CAF-1 contains an N-terminal domain (p150N) that is disp

158 ensitive cancer cells, both murine and human CAFs promoted de novo HT resistance via the generation o

159 Murine and human CAFs were enriched in HTR tumors expressing high levels

160 ogression has been ill-defined because human CAFs lack a unique marker needed for a cell-specific, pr

161 nable selective in vivo elimination of human CAFs at different stages of xenograft tumor development,

162 The dynamic role of human CAFs in cancer progression has been ill-defined because

163 riodontitis (PERIO), obesity/hyperlipidemia (CAF), and obesity/hyperlipidemia plus periodontitis (CAF

164 When degradation is impaired, CAFs retain the capacity to induce invasion in an FN-dep

165 brogated the effect of co-culture on Ccl5 in CAF.

166 granulocyte-specific chemokine expression in CAF, which limited migration of these cells to tumors.

167 The systematic rDNA loss in CAF-1 mutants leads to the decreased variability of the

168 y be useful to predict long-term outcomes in CAF procedures with or without additional use of CMX.

169 gulation of the TGFbeta signaling pathway in CAF, resulting in an apparent reversal of their activate

170 this hypothesis, we observed a reduction in CAF-facilitated HNSCC progression after blocking CAF aut

171 n critical function of the middle subunit in CAF-1.

172 Results showed that in CAF administered rats the maximum time of plasma flavano

173 In CAFs, expression of direct MRTF-SRF genomic targets is a

174 r the transcriptional repression of MMP-3 in CAFs.

175 Depletion of ANXA6 in CAFs impaired complex formation and subsequently impaire

176 cancer that are differentially expressed in CAFs compared to NOFs and are predicted to contribute to

177 re identified as differentially expressed in CAFs versus NOFs.

178 odel, we have identified Hic-5 expression in CAFs as a key requirement for deposition and remodeling

179 rix metalloproteinase-3 (MMP-3) was lower in CAFs but elevated in prostate cancer cells relative to t

180 ular that triggers the induction of POSTN in CAFs.

181 e in tumour cells, DNA mutations are rare in CAFs, raising the likelihood of other mechanisms that re

182 tified FZD8 as the putative WNT2 receptor in CAFs.

183 ndings suggest that approaches to inactivate CAF and prevent tumor-stroma cross-talk may offer a viab

184 improved patient outcomes, and that includes CAFs enriched in plasma membrane-localized, active alpha

185 ated desmoplasia, suggesting that individual CAF/D-ECM protein constituents have distinguishable tumo

186 The mechanism by which CNT-induced CAF-like cells promote tumor growth involved the acquisi

187 led and its COOH-functionalized form induced CAF-like cells, which are non-tumorigenic in animals, bu

188 ggressive breast tumour cells, which induces CAF conversion.

189 echanically stimulate mechanically-inhibited CAFs showed partial rescue of vascularization.

190 We have found that MutSalpha inhibits CAF-1- and ASF1A-H3-H4-dependent packaging of a DNA mism

191 o paracrine signals emerging from irradiated CAF.

192 Because Thy-1 (CD90) marks CAFs that promote tumor cell invasion in a murine model

193 fibronectin (Fn) assembled by CAFs mediates CAF-cancer cell association and directional migration.

194 Ecuador (INI10), but not the commercial mix (CAF), and were directly associated with their antioxidan

195 Depletion of murine CAFs from PDX restored sensitivity to HT, with a concurr

196 glandin E2 The capability of human or murine CAFs to promote tumor invasion is dependent on Snail1 ex

197 rmed global proteomic analysis on the murine CAFs and LFs, which identified 425 proteins that were di

198 functional contributions of myofibroblasts, CAFs, and fibrosis to the development of HCC and CCA in

199 d in eukaryotic cells whereby the ability of CAF-1 to bind DNA is important for its association with

200 arge subunit, Cac1 organizes the assembly of CAF-1.

201 F3 converges with CSL in negative control of CAF activation with epigenetic changes amenable to cance

202 h exogenous PEDF decreased the expression of CAF markers and restored PEDF expression.

203 to the generation of CAFs, identification of CAF-specific biomarkers predictive of disease outcome, a

204 Our data highlight the importance of CAF-endothelial cell crosstalk signaling in cancer chemo

205 uced carcinogenesis through the induction of CAF-like cells that support CSCs and drive tumor formati

206 nd metastasis occurrence, while injection of CAF-derived ANXA6+ EVs enhanced tumorigenesis.

207 ls of alpha-smooth muscle actin, a marker of CAF, compared with MSC cultured on a soft matrix.

208 Reciprocally, increased production of CAF-induced CXCL12, IL6 and VEGFA within tumor microenvi

209 We evaluated the damage responses of CAF to RT and investigated changes in colorectal cancer

210 elial cells, signifying an important role of CAF exosomes in chemotherapeutic drug resistance.

211 r effects, indicating the functional role of CAF-like cells and podoplanin in CNT tumorigenic process

212 s dependent on tumor cell-mediated uptake of CAF-derived ANXA6+ EVs carrying the ANXA6/LRP1/TSP1 comp

213 ansductive pathways abrogated the ability of CAFs to deform the matrix and suppressed vascularization

214 ia tumor-derived Wnt7a-induced activation of CAFs.

215 demonstrate enhanced mechanical activity of CAFs may play a crucial and previously unappreciated rol

216 hesized that enhanced mechanical activity of CAFs, as regulated by the Rho/ROCK pathway, contributes

217 we observed that the selective apoptosis of CAFs at these early timepoints did not affect primary tu

218 on novel insights into the contributions of CAFs to disease progression, emergent events leading to

219 emergent events leading to the generation of CAFs, identification of CAF-specific biomarkers predicti

220 n-alphavbeta3 expression as new hallmarks of CAFs that promote tumor invasion.

221 Co-implantation of CAFs and tumor cells with either intact TGF-beta1 expres

222 ute to the metastasis-promoting phenotype of CAFs.

223 tribute to the tumour-promoting phenotype of CAFs.

224 ng-standing recognition of the prominence of CAFs in PDAC, the effect of chemotherapy on CAFs and how

225 e present study was to evaluate the roles of CAFs in modulating tumor vasculature, chemoresistance, a

226 m cells (CSCs) are one of the key sources of CAFs in the tumor niche.

227 d revealed another distinct subpopulation of CAFs, located more distantly from neoplastic cells, whic

228 rmly carry out these tasks or if subtypes of CAFs with distinct phenotypes in PDA exist.

229 Treatment of CAFs but not prostate cancer cells with hydrogen peroxid

230 tion-independent histone variant H3.3 and on CAF-1 that is specific to the replication-dependent cano

231 to migrate efficiently and directionally on CAF-derived matrices.

232 s showed that an expression of podoplanin on CAF-like cells is essential for their effects, indicatin

233 CAFs in PDAC, the effect of chemotherapy on CAFs and how they may contribute to drug resistance in n

234 ); CAF + CM (n = 17); CAF + EMD (n = 17), or CAF + CM + EMD (n = 17).

235 a split-mouth design with CAF procedures or CAF + xenogeneic collagen matrix (CMX).

236 eveal that miR21 is transferred from CAAs or CAFs to the cancer cells, where it suppresses ovarian ca

237 RNA expression from 67 ovarian CAF samples and 10 normal ovarian fibroblast (NOF) sampl

238 Treatment of patient CAF and TGFbeta-treated normal fibroblasts with exogenou

239 d obesity/hyperlipidemia plus periodontitis (CAF+PERIO).

240 pressive functions in fibroblasts to prevent CAF conversion and illustrate the mechanisms by which me

241 e data point to a new type of protumorigenic CAF in the tumor microenvironment of neuroblastoma and t

242 Isolated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exh

243 ith the Hedgehog inhibitor vismodegib reduce CAF and CSC expansion, resulting in an overall delay of

244 rete the Hedgehog ligand SHH, which regulate CAFs via paracrine activation of Hedgehog signaling.

245 naling module that synergistically regulates CAFs and CSCs.

246 f rDNA copies, and plant lines with restored CAF-1 function (segregated from a fas1xfas2 genetic back

247 t tumor-secreted IL-1beta generates skeletal CAFs and conditions the surrounding bone microenvironmen

248 understand the mechanism of the tri-subunit CAF-1 complex in this process, we investigated the prote

249 loss on global gene expression and suppress CAF tumor-promoting properties in an in vivo model of sq

250 nal repressor and Notch mediator, suppresses CAF activation.

251 Selection of timepoints for targeted CAF apoptosis in vivo during the progression of a human

252 Targeting CAFs with Hedgehog inhibitors may offer a novel therapeu

253 We determined that CAF-derived microvesicles horizontally transferred miR-2

254 We find that CAF-derived exosomes (CDEs) inhibit mitochondrial oxidat

255 We found that CAF-1 suppresses the activity of the MMR system in the c

256 Our experiments have also revealed that CAF-1- and ASF1A-H3-H4-dependent deposition of the histo

257 These data suggest that CAF-1- and ASF1A-H3-H4-dependent deposition of the histo

258 Taken together, these findings suggest that CAF-1-dependent incorporation of irreparable O(6)-mG-T m

259 These findings suggest that CAF-tumor cell crosstalk supported by ANXA6+ EVs is pred

260 r endothelial growth factor (VEGF), and that CAFs generated significantly larger deformations in 3D g

261 We found that CAFs are intrinsically resistant to gemcitabine, the che

262 Here, we found that CAFs upregulated the lipoma-preferred partner (LPP) gene

263 We now show that CAFs assemble fibronectin (FN) and trigger invasion main

264 Here, we show that CAFs exposed to chemotherapy have an active role in regu

265 Further studies showed that CAFs regulate endothelial LPP via a calcium-dependent si

266 Forces Mental Health Survey (CFMHS) for the CAF (8161 respondents; response rate, 79.8%) and the 201

267 nes were found to be upregulated only in the CAF subpopulation of tumor samples.

268 lipidemia significantly increased ABL in the CAF+PERIO group compared to the PERIO group (53.60 +/- 3

269 Instead, the CAF-1(chromatin assembly factor I) subunit Cac2 level de

270 Here we investigate the CAF-1*H3-H4 binding mode and the mechanism of nucleosome

271 een the yeast CAF-1 subunits, and mapped the CAF-1 domains responsible for H3-H4 binding.

272 et informs the first structural model of the CAF and provides insights into how the melanosomal amylo

273 in 3 (CLIC3) is an abundant component of the CAF secretome.

274 the protein-protein interactions within the CAF-1-H3/H4 architecture using biophysical and biochemic

275 1 subunit functions as a scaffold within the CAF-1-H3/H4 complex.

276 hesized that CSCs could be the source of the CAFs that support tumor maintenance and survival.

277 promote or inhibit tumorigenesis, but those CAF populations that negatively impact the clinical outc

278 nal network was constructed to predict those CAF-specific lncRNAs involved in metastasis.

279 nvironment induces differentiation of MSC to CAF, triggering enhanced proliferation and survival of m

280 are abundantly present, the effects of RT to CAF and its impact on cancer cells are unknown.

281 RT to CAF induced DNA damage, p53 activation, cell-cycle arres

282 + EMD was 70.59%, significantly superior to CAF alone (23.53%); CAF + CM (52.94%), and CAF + CM + EM

283 The three approaches are superior to CAF alone for root coverage.

284 roximity of proliferating (Ki67(+)) cells to CAFs impacting therapeutic responses.

285 nsable for D-ECM-induced naive fibroblast-to-CAF activation, which depends on alphavbeta5-integrin re

286 This drives the formation of a transient CAF-1*histone*DNA intermediate containing two CAF-1 comp

287 exposed to media conditioned by drug-treated CAFs exhibited a decrease in oncogenic signaling, as man

288 AF-1*histone*DNA intermediate containing two CAF-1 complexes, each associated with one H3-H4 dimer.

289 However, it is not clear whether CAFs remodel the matrix by other means, such as degradat

290 However, it is unknown whether CAFs uniformly carry out these tasks or if subtypes of C

291 ctively, we present a new mechanism by which CAFs organize the Fn matrix and promote directional canc

292 However, the mechanisms by which CAFs regulate cancer cell migration are poorly understoo

293 ad been treated in a split-mouth design with CAF procedures or CAF + xenogeneic collagen matrix (CMX)

294 eated metabolically dormant populations with CAF-derived mtDNA(hi) EVs promoted an escape from metabo

295 ngle Miller Class I/II GRs were treated with CAF (n = 17), CAF + CM (n = 17), CAF + EMD (n = 17), and

296 tisfaction of patients with GRs treated with CAF + CM, CAF + EMD, and CAF + CM + EMD.

297 al protumorigenic phenotypes associated with CAFs.

298 lts define direct structural roles for yeast CAF-1 subunits and uncover a previously unknown critical

299 We show that yeast CAF-1 binding to a H3-H4 dimer activates the Cac1 winged

300 in the direct interaction between the yeast CAF-1 subunits, and mapped the CAF-1 domains responsible