ライフサイエンスコーパス: microenvironmental

1 The microenvironmental abnormalities are likely a consequenc

2 Our findings thus demonstrate that microenvironmental alteration by CSF-1R blockade renders

3 Although microenvironmental alterations have been described in wo

4 tocyte/fibroblast phenotype while pathologic microenvironmental alterations may be permissive for inc

5 hese DCs function in part to orchestrate the microenvironmental alterations required for successful i

6 m to acutely sense and decisively respond to microenvironmental alterations.

7 n driven by specific genetic, epigenetic, or microenvironmental alterations.

8 ges from the HSPCs as a result of MM-related microenvironmental alterations.

9 tic changes and in neighboring cells through microenvironmental alterations.

10 ally imprinted and modulated by local tissue microenvironmental and inflammatory cues.

11 e biologic behavior is the synthesis of both microenvironmental and intrinsic cues.

12 at sites of metastasis in response to tumour microenvironmental and metastasis site-specific cues?

13 st organ of the mammalian body (skin) at the microenvironmental and molecular level.

14 to adequately represent the complex in-vivo microenvironmental and phenotypic characteristics of the

15 Moreover, metastasis is regulated by microenvironmental and systemic processes, such as immun

16 to this combination we analysed the genetic, microenvironmental, and immune factors in tumours derive

17 ing tumor angiogenesis, serving as intrinsic microenvironmental barriers to tumorigenesis.

18 s strategy offers unique insights into tumor microenvironmental biochemistry and should facilitate co

19 ect, indicating that targeting a bone marrow microenvironmental cell can lead to a delay in MM tumor

20 n showed better inhibition of adhesion to BM microenvironmental cells and inhibition of homing in viv

21 s MM-cell proliferation in coculture with BM microenvironmental cells and the development of drug res

22 Microenvironmental cells of likely importance include fo

23 so contribute to WM proliferation through BM microenvironmental cells.

24 Marrow microenvironmental cellular components of the NHD13 BMME

25 tumor models that recapitulate size-induced microenvironmental changes and, consequently, natural tu

26 r data indicate that epithelial induction of microenvironmental changes can play a significant role i

27 mous with human Treg activation and indicate microenvironmental changes conducive to transformation i

28 MSC production of VEGF and IL-10, suggesting microenvironmental changes from pFUS also increased pote

29 cting against the BBB disruption and related microenvironmental changes in the hippocampus.

30 ac pathological conditions such as ischemia, microenvironmental changes instruct a series of cellular

31 Our results show that microenvironmental changes, such as hypoxia, can affect

32 mor models faithfully represent size-induced microenvironmental changes, such as hypoxic gradients, c

33 nstrate that the nucleodyes are sensitive to microenvironmental changes.

34 nsitivity suggests that therapies matched to microenvironmental characteristics will be more efficaci

35 illustrate a central role for disruption of microenvironmental communication in cancer progression.

36 ggressive experimental tumors has a critical microenvironmental component that involves specific regu

37 oth at initial diagnosis and at relapse) and microenvironmental components as assessed by immunohisto

38 ther work should address the requirement for microenvironmental components such as immune or mesenchy

39 continuum part of the OLHDC model describes microenvironmental components such as matrix-degrading e

40 r treating tumors via selective targeting of microenvironmental components.

41 analysis enables objective quantification of microenvironmental composition of ovarian tumours.

42 are diverse in their genetic, metabolic and microenvironmental compositions, accounting for their ph

43 ent signaling and is activated by hypoxia, a microenvironmental condition that promotes cellular inva

44 l and mechanical properties to determine the microenvironmental conditions (microstructure, degradati

45 e used by PMEIs to inhibit PMEs in different microenvironmental conditions and paving the way to iden

46 Indeed, a number of studies have found that microenvironmental conditions can selectively modify uni

47 Altered microenvironmental conditions in lymphoid tissues leadin

48 adaptive landscape model, hypoxic and acidic microenvironmental conditions reduce the fitness of canc

49 tissues, those with viral infection or other microenvironmental conditions that might promote fusion.

50 tissues, those with viral infection or other microenvironmental conditions that might promote fusion.

51 , thus mTORC1 signaling remains active under microenvironmental conditions that potentially promote e

52 tworks support metabolic activity and define microenvironmental conditions within tissues in health a

53 Hostile microenvironmental conditions within tumor masses, such

54 stem from an increased resistance to adverse microenvironmental conditions, accumulating evidence ind

55 culture systems in terms of high control of microenvironmental conditions, including accurate pertur

56 Microenvironmental conditions, including hypoxia, drive

57 conserved mechanism of adaptation to adverse microenvironmental conditions, including limited nutrien

58 g tumourigenesis, depending on cell type and microenvironmental conditions.

59 ch facilitates tumor survival under changing microenvironmental conditions.

60 cally antagonistic cell types is dictated by microenvironmental conditions.

61 d for diagnostic approaches addressing these microenvironmental contents-approaches enabling a sensit

62 ypic system that recreates the molecular and microenvironmental context in which squamous carcinogene

63 ne responses in the skin by interpreting the microenvironmental context in which they encounter forei

64 In the appropriate genetic and microenvironmental context, acute deregulation of SOX2 d

65 iferation of breast cancer cells in specific microenvironmental contexts that require ERK1/2 signalin

66 umor biology by focusing through the lens of microenvironmental contributions, namely inflammation, a

67 ounding normal cells as active and essential microenvironmental contributors to early tumour growth t

68 omimetic systems for dynamic multiparametric microenvironmental control of emergent and integrated ce

69 nd/or temporal resolution and limitations on microenvironmental control.

70 how that substrate stiffness is an important microenvironmental cue, to which mouse hippocampal neuro

71 al impairment of HSPCs depends on MM-related microenvironmental cues and is reversible.

72 or assessing cell quality and the effects of microenvironmental cues and manufacturing processes on c

73 of differentiation and plasticity, including microenvironmental cues and molecular mediators, such as

74 These features are controlled through key microenvironmental cues and regulatory pathways, such as

75 o show that NK cell-intrinsic properties and microenvironmental cues are involved in this process, in

76 bit high phenotypic diversity and respond to microenvironmental cues by altering their functional pro

77 helial cells is their capacity to respond to microenvironmental cues by undergoing epithelial-mesench

78 mechanisms on tumor cell function, including microenvironmental cues controlling the movement of tumo

79 successfully demonstrated the importance of microenvironmental cues for proteolytic activity and als

80 Specific microenvironmental cues from tissues are likely to deter

81 equence of prior therapeutic intervention or microenvironmental cues has significant implications for

82 Whether different microenvironmental cues impose invasive or therapy-resis

83 This capability of platelets to mechanosense microenvironmental cues in a growing thrombus or hemosta

84 oles during metastasis; however, the role of microenvironmental cues in the regulation of miRNAs in m

85 ed macrophages (TAM) are exposed to multiple microenvironmental cues in tumors, which collaborate to

86 in distinct patterns, possibly determined by microenvironmental cues including chemokines, structural

87 ation in tumor predisposition is dictated by microenvironmental cues rather than intrinsic difference

88 toll-like receptor 3, together with external microenvironmental cues that drive endothelial cell (EC)

89 PHD3 restrains tumour growth in response to microenvironmental cues through the control of EGFR.

90 However, how platelets transduce microenvironmental cues to mediate contraction and alter

91 This process is tightly controlled by microenvironmental cues, although a few endogenous facto

92 In response to microenvironmental cues, embryonic cells form adhesive s

93 Here we show that microenvironmental cues, including inflammation-mediated

94 d MM cancer stem cells within the context of microenvironmental cues, providing preclinical support f

95 in their ability to model the full range of microenvironmental cues, such as ones elicited by 3D cel

96 These microenvironmental cues, which include hypoxia, also reg

97 ly change their direction according to other microenvironmental cues, which is important for both nor

98 rol various signaling pathways downstream of microenvironmental cues.

99 lastic cells whose functions are governed by microenvironmental cues.

100 ribution of NK cell-intrinsic properties and microenvironmental cues.

101 election at advanced ages in the presence of microenvironmental decline.

102 homeostasis in mammary tissue, resulting in microenvironmental defects similar to those observed at

103 to a more complex mix of cell-intrinsic and microenvironmental defects.

104 Hypoxia (low O2) is a fundamental microenvironmental determinant of bone marrow (BM) patho

105 ditions of adipose tissue wasting and review microenvironmental determinants of adipocyte (dys)functi

106 melanoma metastases in patients, suggesting microenvironmental differences in immune homing receptor

107 those in rods, possibly due to structural or microenvironmental differences in the two cell types.

108 but little is known about the roles of local microenvironmental differences in three-dimensional (3D)

109 at were enriched in grade 3 tumors with high microenvironmental diversity that also substratified pat

110 te the signals a cell receives from specific microenvironmental domains.

111 model has been developed by considering the microenvironmental dynamics of the pesticide in conjunct

112 Yet, how such microenvironmental effects are integrated with direct th

113 cytes is now firmly established, but how the microenvironmental effects of UV radiation influence mel

114 ment and progression via cell autonomous and microenvironmental effects.

115 eased VLA-4 expression in host hematopoietic microenvironmental elements.

116 dence that oncogenic BRAF contributes to the microenvironmental escape of melanocytes through the dow

117 Microenvironmental expansion of hematopoietic stem cells

118 A microenvironmental exposure model was used to estimate t

119 ated from birth to 11 years of age through a microenvironmental exposure model.

120 ns predicted that small perturbations of the microenvironmental extracellular pH (pHe) could invert t

121 ting that intratumoral hypoxia is a critical microenvironmental factor driving cancer progression.

122 Hypoxia is an important microenvironmental factor influencing atherosclerosis pr

123 We identified CCN1 as a microenvironmental factor produced by mesenchymal cells

124 consistent with a role of HIV as a critical microenvironmental factor promoting lymphoma development

125 Hypoxia is a potent microenvironmental factor promoting metastatic progressi

126 ut the response of NP cells to this aberrant microenvironmental factor remains to be fully characteri

127 (+) BM-MSCs in the hypoxic niche, a critical microenvironmental factor that is well known to induce t

128 Hypoxia is a potent microenvironmental factor that promotes tumor metastasis

129 ncreasingly being recognized as an important microenvironmental factor that suppresses antitumor immu

130 Here, we show that the same microenvironmental factor, IL-6, can both promote and pr

131 tor of semaphorin 3F (SEMA3F), a suppressive microenvironmental factor.

132 s into the dynamic interplay between various microenvironmental factors and CAFs in the CSC niche.

133 ta provide a key illustrative example of how microenvironmental factors and cell lineage drive the ge

134 , CLL cells rapidly undergo apoptosis unless microenvironmental factors are provided that support the

135 signals, epigenetic modifications and other microenvironmental factors can substantially and, in som

136 c lymphocytic leukemia (CLL) cells depend on microenvironmental factors for proliferation and surviva

137 plain the zonal pattern suggesting a role of microenvironmental factors in shaping functional ITH.

138 nutrient and oxygen availability, and other microenvironmental factors influence fuel choice.

139 Furthermore, modulation of uptake by microenvironmental factors is largely unstudied.

140 tivation of tumor suppressors and inhibitory microenvironmental factors is necessary for breast cance

141 We screened for microenvironmental factors leading to phenotype switchin

142 n survival cues following targeting of tumor microenvironmental factors may play an important role in

143 cell receptor (BCR)-triggered signals, other microenvironmental factors might well be involved.

144 ties and discuss stem cell tools to identify microenvironmental factors of importance to the developm

145 be the convergence of genetic, metabolic and microenvironmental factors on mechanisms of epigenetic d

146 t our approach could speed the dissection of microenvironmental factors responsible for driving steat

147 Solid tumours are exposed to microenvironmental factors such as hypoxia that normally

148 condary sites, and is strongly influenced by microenvironmental factors such as hypoxia.

149 that integrate many of the (epi-)genetic and microenvironmental factors that contribute to colorectal

150 S/mTOR signal transduction pathway and alter microenvironmental factors that contribute to tumor prog

151 However, our understanding of microenvironmental factors that modulate the process of

152 Of microenvironmental factors that senescent fibroblasts pr

153 To identify microenvironmental factors underlying the resistance of

154 pregulated under hypoxic conditions or other microenvironmental factors), this work calls for a more

155 currently undefined interactions with other microenvironmental factors, including extracellular matr

156 EMT is induced by microenvironmental factors, including TGF-beta and Wnt a

157 ion of differentiated hematopoietic cells by microenvironmental factors, including those generated du

158 ganization events are precisely modulated by microenvironmental factors, which are known to strongly

159 nd tumor metabolism and its interaction with microenvironmental factors.

160 nd was independent of prognostic markers and microenvironmental factors.

161 ke normal stem cells (NSCs), are affected by microenvironmental factors.

162 interventions, heterocellular components and microenvironmental factors.

163 observations suggest that a tissue-specific microenvironmental feature cooperates with oncogenic mut

164 unologic factors and identification of tumor/microenvironmental features correlating with distant met

165 rectly reconstitute the histomorphologic and microenvironmental features of primary MPNST-like melano

166 oes not depend on the space dimension or the microenvironmental geometry.

167 issue of Blood, Jitschin et al demonstrate a microenvironmental glycolytic shift in chronic lymphocyt

168 apitulate the original tumor architecture or microenvironmental gradients and are not designed to ret

169 We developed a quantitative measure of microenvironmental heterogeneity along three spatial dim

170 We propose a clinically relevant role of microenvironmental heterogeneity for advanced breast tum

171 We aimed to assess the degree of microenvironmental heterogeneity in breast cancer and co

172 s, we uncovered a striking link between high microenvironmental heterogeneity measured by EDI and a p

173 r understanding the synergistic interplay of microenvironmental heterogeneity with genomic alteration

174 e first study to couple unbiased measures of microenvironmental heterogeneity with genomic alteration

175 xhibit considerable genetic, pathologic, and microenvironmental heterogeneity.

176 cytes and stromal cells to maintain lymphoid microenvironmental homeostasis.

177 s had no increase in signals associated with microenvironmental HSC support, and the spindle-shaped o

178 on, via localized O2 depletion, resulting in microenvironmental hypoxia and effective inflammatory re

179 enduring activity is abrogated by different microenvironmental immunosuppressive DCs.

180 We aimed to test combined genomic and microenvironmental indices in prostate cancer to improve

181 Here we discuss recent findings of host-microenvironmental induced fungal cell wall changes, inc

182 Thus, a mechanism is presented for microenvironmental influence on tumour growth.

183 ltaneously cultured to explore new facets of microenvironmental influences and CSC biology.

184 zed that epigenetic modifications induced by microenvironmental influences of cytokines can reveal th

185 ioma), and other mechanisms must account for microenvironmental influences on central nervous system

186 pportunities to investigate species-specific microenvironmental influences on normal and malignant he

187 al common processes-reflecting in part tumor microenvironmental influences-driving cellular behavior

188 segregation and myelin extent is limited by microenvironmental inhibition.

189 ates muTSA as a platform for studying tumour microenvironmental interactions and cancer field effects

190 he recently discovered intrinsic mechanisms, microenvironmental interactions and communication with s

191 The dependency of HRS cells on microenvironmental interactions and deregulated signalin

192 Microenvironmental interactions are crucial for the surv

193 These findings indicate that microenvironmental interactions are key regulators of AM

194 mmunologic function is not only modulated by microenvironmental interactions but is also a feature of

195 Predicting the effects of microenvironmental interactions on the electronic struct

196 gy and therapy, with a focus on genetics and microenvironmental interactions, which contribute to dis

197 on in the context of chemokine signaling and microenvironmental interactions, which may have importan

198 to bone and to increase marrow HSCs through microenvironmental interactions.

199 an with complexity derived from cellular and microenvironmental interactions.

200 ven by the mobilization of immunosuppressive microenvironmental leukocytes, rather than loss of tumor

201 nism of Propionibacterium acidipropionici at microenvironmental levels by analyzing physiological cha

202 ic progenitor cells interacting with splenic microenvironmental ligands/cells is instrumental for the

203 mal cells controls leukocyte recruitment and microenvironmental localization in intestine and in the

204 us, we found that mechanical features of the microenvironmental matrix influence tissue-specific diff

205 ld not be properly accounted for with indoor microenvironmental measurements.

206 hich are anucleate cellular fragments, sense microenvironmental mechanical properties, such as substr

207 roughput investigations of cell-intrinsic or microenvironmental modifiers of metastasis.

208 and in-vehicle exposure was estimated using microenvironmental monitoring data based on field measur

209 ed using subtle morphological differences of microenvironmental myoepithelial cell nuclei without any

210 Specifically, it is unknown whether microenvironmental N-cadherin is required for normal mar

211 host cells, which collectively form a tumor microenvironmental network that either suppresses or pro

212 ogenitor cell lines, helping explain how the microenvironmental niche becomes reprogrammed during inv

213 loited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis.

214 f in vivo bone micrometastases regarding the microenvironmental niche, gene expression profile, metas

215 tion of neuroblasts is controlled by the SVZ microenvironmental niche.

216 insic regulatory signals received from their microenvironmental niche.

217 ed to somatic mutations or to changes in the microenvironmental niche.

218 ally colocalize with PD-L1(+) HRS cells in a microenvironmental niche.

219 eir fate in vivo in the context of a complex microenvironmental "niche" comprised of heterologous cel

220 PS can reconstruct cellular arrangements and microenvironmental niches as dominated by PPARalpha sign

221 propagating cells (CPCs) within preferential microenvironmental niches has a major part in evading th

222 of lymph nodes (LNs) and establish distinct microenvironmental niches to provide key molecules that

223 c leukaemia (CLL) cells access to protective microenvironmental niches within tissues, ultimately res

224 om their site of origin and colonize distant microenvironmental niches.

225 Here we show that HGG growth depends on microenvironmental NLGN3, identify signalling cascades d

226 Transmigrating PMNs rapidly depleted microenvironmental O2 sufficiently to stabilize intestin

227 Microenvironmental oxygen (O(2)) regulates stem cell act

228 OX2) are required for the rapid depletion of microenvironmental oxygen and compensatory responses, re

229 nsport of NPs and its variation due to tumor microenvironmental parameters have been studied includin

230 pectrum of the trityl probe and assess these microenvironmental parameters within a few microseconds.

231 Using real-time analyses of lumenal microenvironmental parameters, in conjunction with hydro

232 ingle-cell analyses suggested distinct tumor microenvironmental patterns, including cell-to-cell inte

233 lly understanding the relative influences of microenvironmental perturbations and simultaneously engi

234 diac differentiation to assess the effect of microenvironmental perturbations on fetal cardiac reprog

235 tronic states of oxyluciferin are altered by microenvironmental perturbations.

236 tablish a proper reference when there are no microenvironmental perturbations.

237 nnate host defences and reveal an additional microenvironmental pressure that selected for a specific

238 ction as a novel and unexpected critical ECM microenvironmental pro-oncogenic regulator of epithelial

239 lls, and kill thereof, are mediated by these microenvironmental properties and affected by the diffus

240 No single microenvironmental property was able to predict the loca

241 Our study reveals a mechanism by a microenvironmental protease that regulates Wnt signaling

242 o-step model of resistance whereby extrinsic microenvironmental proteins FLT3 ligand (FL) and fibrobl

243 gent Notch ligand function and combinatorial microenvironmental regulation in liver progenitor fate s

244 ings also contribute to the understanding of microenvironmental regulation of hESC identity and somat

245 amples and provide improved understanding of microenvironmental regulation of normal and leukemic LTH

246 /niche pairs to advance the understanding of microenvironmental regulation of stem cell function.

247 tants with mislocalized PGCs corroborate the microenvironmental regulation of the cell cycle, except

248 This knowledge of the microenvironmental regulation of the MK lineage could le

249 blish lipid-sensing nuclear receptors in the microenvironmental regulation of tumor progression.

250 esting that Akt dynamics mediates contextual microenvironmental regulation.

251 Extracellular AGR2 (eAGR2) is a microenvironmental regulator of epithelial tissue archit

252 use lines using an in vivo assay to identify microenvironmental regulators of metastatic colonization

253 re than 950 GM mouse lines to identify novel microenvironmental regulators of metastatic colonization

254 Targeted modulation of microenvironmental regulatory pathways may be essential

255 nction of E-cad was inactivated by increased microenvironmental rigidity, and was not recapitulated b

256 lic phenotype of tumor cells is plastic, and microenvironmental selection leads to increased tumor gl

257 e escape mechanism that is subject to strong microenvironmental selection pressures later in tumor ev

258 Here we introduce microenvironmental selective plane illumination microsco

259 HBECs to engage EMT machinery in response to microenvironmental (serum/TGF-beta) or oncogenetic (MYC)

260 t extracellular ATP (eATP) could represent a microenvironmental signal potentially affecting virion r

261 ults show an unexpected link between altered microenvironmental signaling cues such as FGF-2 overexpr

262 tream of regulatory processes that integrate microenvironmental signals and directly implicated in fe

263 Lastly, microenvironmental signals from the microbiome can serve

264 upon microbial activation in the presence of microenvironmental signals including IL-15, and were cap

265 he ability for cells to sense and respond to microenvironmental signals is influenced by their three

266 from infection and involve the processing of microenvironmental signals that determine macrophage cel

267 that venetoclax resistance may be induced by microenvironmental signals that upregulate antiapoptotic

268 al a mechanism by which Sox2 cooperates with microenvironmental signals to malignantly transform epit

269 Such tissue microenvironmental signals together with epigenetic chan

270 In response to microenvironmental signals, macrophages undergo differen

271 eporters that can nonlinearly amplify tumour microenvironmental signals, permitting the identificatio

272 It is known that microenvironmental signals, such as substrate topography

273 uration, enabling them to respond readily to microenvironmental signals, such as TGFbeta.

274 diverse extent and quality of adaptation to microenvironmental signals.

275 a pathologic fibrogenic state in response to microenvironmental signals.

276 resident or inflammatory Mphis, depending on microenvironmental signals.

277 Using a stochastic microenvironmental simulation model, distributions of da

278 ET in HPCs can be accelerated in response to microenvironmental stiffening and can be inhibited by so

279 c lymphocytic leukemia (CLL) cells depend on microenvironmental stimuli for their survival, provided

280 In vivo, however, various microenvironmental stimuli in lymphoid and mucosal tissu

281 quirement for additional mutagenic events or microenvironmental stimuli, including inflammation.

282 riggered by cell autonomous mechanisms or by microenvironmental stimuli.

283 heir polarization state in response to local microenvironmental stimuli.

284 associated with tumorigenesis in response to microenvironmental stimuli; however, the regulatory path

285 Cancers can upregulate autophagy to survive microenvironmental stress and to increase growth and agg

286 ed starvation response, has been hijacked by microenvironmental stress signals in melanoma to drive p

287 ction reveals an miRNA-mediated link between microenvironmental stress, oxidative phosphorylation, RO

288 hway that coordinates cellular adaptation to microenvironmental stresses that include hypoxia, nutrie

289 n tumor progression and response to therapy, microenvironmental (stromal) heterogeneity in TNBC has n

290 stromal cells (BMSCs) are key players in the microenvironmental support of multiple myeloma (MM) cell

291 nnate immunity reveals a potential route for microenvironmental support of tumor cells, mediated via

292 elta) mediates B-cell receptor signaling and microenvironmental support signals that promote the grow

293 F-kappaB signaling apparently independent of microenvironmental support.

294 n preactivated CD8(+) T cells in response to microenvironmental transforming growth factor-beta (TGF-

295 Main processes considered in the model are microenvironmental transport and deposition, volatilizat

296 discuss the implications of these results on microenvironmental transport barriers, and the tumor inv

297 of chemoresistant CSCs is less dependent on microenvironmental tumor structure, while cisplatin show

298 Further, we find that the microenvironmental variable does not strongly affect the

299 eas stem initiation and growth are driven by microenvironmental variables such as light availability

300 The model focuses on key cellular and microenvironmental variables that regulate interactions