ライフサイエンスコーパス: tumor hypoxia

1 sic capability to prevent the progression of tumor hypoxia.

2 sel density yet are hypoperfused, leading to tumor hypoxia.

3 ogical effects of anti-angiogenic agents and tumor hypoxia.

4 cell (CSC) activity resulting from increased tumor hypoxia.

5 nitrogen mustard prodrug designed to target tumor hypoxia.

6 ay be a result of the sustained reduction in tumor hypoxia.

7 window, resulting in the decrease of cycling tumor hypoxia.

8 and MRI) as well as a sustained reduction in tumor hypoxia.

9 y of (18)F-FMISO, rather than a reduction in tumor hypoxia.

10 s and is the preferred method for imaging of tumor hypoxia.

11 l leakiness, resulting in large increases in tumor hypoxia.

12 t mir-210 may serve as an in vivo marker for tumor hypoxia.

13 ng existing and future exogenous markers for tumor hypoxia.

14 et for anticancer drug discovery directed at tumor hypoxia.

15 s a recently developed PET imaging agent for tumor hypoxia.

16 beta-hCG as a secreted reporter protein for tumor hypoxia.

17 and pimonidazole, two extrinsic markers for tumor hypoxia.

18 idated their use as endogenous indicators of tumor hypoxia.

19 were seen, consistent with the induction of tumor hypoxia.

20 proteins will provide a surrogate measure of tumor hypoxia.

21 sizing the need for noninvasive detection of tumor hypoxia.

22 llent radiotracer for noninvasive imaging of tumor hypoxia.

23 etanidazole are being explored as probes for tumor hypoxia.

24 this apoptosis is predominant in regions of tumor hypoxia.

25 OS, MYC and MCL1, and effectively alleviates tumor hypoxia.

26 O(2) nanoeconomizer pHPFON-NO/O(2) to combat tumor hypoxia.

27 T/CT scan was performed to assess changes in tumor hypoxia.

28 ergy CT perfusion according to the degree of tumor hypoxia.

29 overlap with EPR pO(2) images for measuring tumor hypoxia.

30 tanidazole PET/CT scan to determine baseline tumor hypoxia.

31 radiotherapy is significantly restricted by tumor hypoxia.

32 for the visualization and quantification of tumor hypoxia.

33 owever, its efficacy is often compromised by tumor hypoxia.

34 lly through regulating hypoxia signaling and tumor hypoxia.

35 ment effects that were dependent on baseline tumor hypoxia.

36 r for noninvasive identification of regional tumor hypoxia.

37 apeutics that simultaneously target TAMs and tumor hypoxia.

38 global decrease, rather than an increase, in tumor hypoxia.

39 te the magnitude and spatial distribution of tumor hypoxia.

40 y photobleaching, low tumor selectivity, and tumor hypoxia.

41 arabinoside ((18)F-FAZA) is a PET tracer of tumor hypoxia.

42 factor HuR (Hu antigen R) in the context of tumor hypoxia.

43 Tag2 tumors, in parallel to an inhibition of tumor hypoxia.

44 nsity (TBmax) and the spatial extent (HV) of tumor hypoxia.

45 ice), where it was associated with increased tumor hypoxia.

46 hreefold, resulting in a 10-fold increase in tumor hypoxia along with a fourfold increase in hypoxia-

47 Tumor hypoxia, an integral biomarker to guide radiothera

48 nhances the radiotherapy effect, alleviating tumor hypoxia and achieving synergistic anticancer effic

49 The spatial relationship between tumor hypoxia and angiogenesis was assessed by an overla

50 ibuted to the closely interrelated phenomena tumor hypoxia and angiogenesis, although few in vivo dat

51 e potential to act as imaging correlates for tumor hypoxia and angiogenesis.

52 h was, to some extent, due to a reduction of tumor hypoxia and apoptosis.

53 cally as a PET agent both for delineation of tumor hypoxia and as an effective indicator of patient p

54 resence of metastases, particularly in bone, tumor hypoxia and chromosomal instability (CIN).

55 racerebral BM models to further characterize tumor hypoxia and evaluate the potential of Hypoxia-imag

56 Sema3A also reduced tumor hypoxia and halted cancer dissemination induced by

57 Tumor hypoxia and high glutathione (GSH) expression prom

58 Tumor hypoxia and hypoxia-inducible factor 1 (HIF-1) act

59 There was a significant correlation between tumor hypoxia and ICD (P < 0.005) but not MVD (P = 0.41)

60 Emerging evidence suggests a link between tumor hypoxia and immune suppression.

61 model provides a valuable tool for studying tumor hypoxia and in validating existing and future exog

62 rteriovenous (AV) shunting, which results in tumor hypoxia and inadequate delivery of systemic treatm

63 NP formulation before radiotherapy modulated tumor hypoxia and increased radiotherapy efficacy, actin

64 ration to reduce leakage, leading to reduced tumor hypoxia and increased tumor perfusion.

65 tumor microenvironment through reductions in tumor hypoxia and induces sustained treatment synergy.

66 y, CD93 blockade mitigates sunitinib-induced tumor hypoxia and invasiveness, preventing the upregulat

67 that IKKbeta is a novel endogenous marker of tumor hypoxia and may represent a new target for antican

68 icability in monitoring factors that control tumor hypoxia and metabolism and may have future clinica

69 ked functionality, correlating with enhanced tumor hypoxia and necrosis, and reduced tumor growth.

70 by improving vessel stabilization to prevent tumor hypoxia and necrosis.

71 Low-dose GM-CSF uniquely reduced tumor hypoxia and normalized tumor vasculature by increa

72 Tumor hypoxia and perfusion are independent prognostic i

73 ed the utility of multiparametric imaging of tumor hypoxia and perfusion with (18)F-fluoromisonidazol

74 Tumor hypoxia and poor penetration of therapeutics acros

75 ystemic Ang-2 overexpression does not affect tumor hypoxia and proliferation, it significantly inhibi

76 esirable effects, including the induction of tumor hypoxia and reduction of delivery of chemotherapeu

77 as an in vivo predictive assay of individual tumor hypoxia and resultant therapy resistance.

78 Some markers of tumor hypoxia and the level of tumor EGFR expression hav

79 PET to assist the identification of regional tumor hypoxia and to investigate the relationship among

80 a levels can serve as a surrogate marker for tumor hypoxia and treatment outcome in head and neck can

81 evelops, and one major mechanism is elevated tumor hypoxia and upregulated hypoxia-inducible factor-1

82 emission tomography scan was used to measure tumor hypoxia and was repeated 1-2 weeks intratreatment.

83 oxia marker pimonidazole was used to measure tumor hypoxia, and a commercially available antibody was

84 ies showed that OPN expression is induced by tumor hypoxia, and its plasma levels can serve as a surr

85 F transcriptional activity, VEGF production, tumor hypoxia, and tumor angiogenesis.

86 assessment of met-hemoglobin, investigating tumor hypoxia andcancer lymph node metastases are some o

87 ential and the current status of preclinical tumor hypoxia approaches in clinical trials for advanced

88 ric images of K(i) (potentially representing tumor hypoxia) are shown.

89 lignancies, but their efficacy is limited by tumor hypoxia arising from dysfunctional blood vessels.

90 the development of significant gradients in tumor hypoxia as a function of distance to a perfused bl

91 However, PDT-induced tumor hypoxia as a result of oxygen consumption and vasc

92 tumor lines and previous characterization of tumor hypoxia as being primarily diffusion-limited does

93 ted by different mechanisms, among which the tumor hypoxia-associated radiation resistance is a well-

94 method for detection of CA IX as a marker of tumor hypoxia based on a near-infrared (NIR) fluorescent

95 parametric analysis provided information on tumor hypoxia by distinction of the specific tracer rete

96 weeks after starting CRT were evaluated for tumor hypoxia by nuclear medicine physicians.

97 adioactive EF5 for independent assessment of tumor hypoxia by PET and immunohistochemistry methods is

98 (EF5) allows for a comparative assessment of tumor hypoxia by PET and immunohistochemistry; however,

99 and MAOA-downstream genes that promote EMT, tumor hypoxia, cancer cell migration, and invasion.

100 ounteracting undesirable effects of elevated tumor hypoxia caused by bevacizumab.

101 nd HIF-2alpha-dependent transcription during tumor hypoxia caused by the hypoxia associated factor (H

102 BACKGROUND & AIMS: In colorectal tumors, hypoxia causes resistance to therapy and promote

103 Tumor hypoxia, characterized by low oxygen concentration

104 on of tumor initiation and growth, including tumor hypoxia, clonal stem cell selection, and immune ce

105 tive pericyte coverage and increased overall tumor hypoxia (compared with controls).

106 Tumor hypoxia confers chemotherapy resistance.

107 mic contrast-enhanced MRI) did not relate to tumor hypoxia consistently.

108 Tumor hypoxia contributes resistance to chemo- and radio

109 eterogeneity across molecular subtypes, with tumor hypoxia contributing to poor therapeutic outcomes.

110 Background Optoacoustic imaging can assess tumor hypoxia coregistered with US gray-scale images.

111 n feature of solid tumors, and the extent of tumor hypoxia correlates with advanced disease stages an

112 hypoxic tumor environment, and the extent of tumor hypoxia correlates with poor clinical outcome.

113 sensitive fluorescent UnaG reporter to track tumor hypoxia, coupled with single-cell transcriptomics,

114 ional tumor cell death accompanied by severe tumor hypoxia, decreased microvessel density, increased

115 rior pilot results showing that pretreatment tumor hypoxia demonstrated by PET with (60)Cu-labeled di

116 Interestingly, reduced tumor hypoxia did not alter the relative abundance of TA

117 cells, changes in drug metabolism/transport, tumor hypoxia, DNA repair, and the role of microRNAs in

118 This study showed that tumor hypoxia downregulates STING in multiple cancer typ

119 Tumor hypoxia drives metastatic progression, drug resist

120 detailed and more accurate quantification of tumor hypoxia during PDT.

121 ex, for quantitative longitudinal imaging of tumor hypoxia dynamics during radiotherapy.

122 e, quantitative, and longitudinal imaging of tumor hypoxia dynamics following radiotherapy, and demon

123 The nanoprobe was used to image tumor hypoxia dynamics over 7 days during fractionated r

124 Tumor hypoxia dysregulates m(6)A profiles, bridging prio

125 ucing factor, (4) nanoparticles that relieve tumor hypoxia for enhancement of chemotherapy, photodyna

126 clinical need for noninvasive biomarkers of tumor hypoxia for prognostic and predictive studies, rad

127 ) novel role for low-dose GM-CSF in reducing tumor hypoxia for synergy with anti-PD1 and highlight wh

128 d were found to correlate with the degree of tumor hypoxia found in these patients.

129 Tumor hypoxia hampers the efficacy of radiotherapy becau

130 The adverse prognostic impact of tumor hypoxia has been demonstrated in human malignancy.

131 Primary tumor hypoxia has been demonstrated to play a pivotal ro

132 Tumor hypoxia has been identified as a significant step

133 Since tumor hypoxia has been proposed to increase tumor aggres

134 Tumor hypoxia has long been associated with resistance t

135 ongly associated with cervical neoplasia and tumor hypoxia has prognostic significance in human cervi

136 Thus far, targeting tumor hypoxia has remained unsuccessful.

137 t adult brain tumor, and increased levels of tumor hypoxia have been associated with worse clinical o

138 apeutic targeting systems, solely to TAMs or tumor hypoxia, however, novel therapeutics that target b

139 orter substrate (124)I-FIAU, yielded similar tumor hypoxia images for the HT29-9HRE xenograft but not

140 aded nanoparticles as theranostic agents for tumor hypoxia imaging and chemotherapy.

141 re enables serial, noninvasive monitoring of tumor hypoxia in a mouse model by measuring a urinary re

142 GBM cell proliferation, as well as decreased tumor hypoxia in a mouse xenograft model.

143 for evaluation of arteriovenous shunting and tumor hypoxia in glioblastoma.

144 Tumor hypoxia in head-and-neck squamous cell carcinoma (

145 can be used to obtain high-quality images of tumor hypoxia in human cancers.

146 If the patterns of tumor hypoxia in human patients are similar to those obs

147 ed melanoma and underscore the importance of tumor hypoxia in melanoma progression.

148 icantly decreased (18)F-FDG accumulation and tumor hypoxia in microscopic tumors but had little effec

149 g sources" strategy significantly alleviates tumor hypoxia in multiple ways, greatly enhances the eff

150 ion is a potential strategy to relieve solid tumor hypoxia in order to increase the effectiveness of

151 and quantify arteriovenous (AV) shunting and tumor hypoxia in patients with GBM.

152 alize and quantify spatiotemporal changes in tumor hypoxia in response to AVO.

153 Significant difference in tumor hypoxia in response to PDT over time was found bet

154 Given the high significance of tumor hypoxia in therapeutic results, we here discuss a

155 ing and monitoring intrinsic and PDT-induced tumor hypoxia in vivo during PDT is of high interest for

156 The noninvasive assessment of tumor hypoxia in vivo is under active investigation beca

157 In all tumors, hypoxia increased markedly after either radiatio

158 Increased tumor growth was accompanied by tumor hypoxia, increased tumor angiogenesis, and vascula

159 vestigate the relationship among a potential tumor hypoxia index (K(i)), tumor-to-blood ratio (T/B) i

160 Tumor hypoxia indicates a poor prognosis.

161 identify survival mechanisms governed by the tumor hypoxia-induced pH regulator carbonic anhydrase IX

162 preferentially in hypoxic zones of melanoma tumors, hypoxia-induced CCL-2 production in MCs requires

163 Tumor hypoxia induces the up-regulation of a gene progra

164 bitory activity associated with induction of tumor hypoxia-inducible factor 1 alpha expression and ma

165 was significantly inversely associated with tumor hypoxia-inducible factor 1alpha (P < 0.05), tumor

166 In tumors, hypoxia-inducible factor 1alpha (HIF-1alpha) and

167 Tumor hypoxia is a known adverse prognostic factor, and

168 Tumor hypoxia is a persistent obstacle for traditional t

169 Tumor hypoxia is a promising approach to direct dosing o

170 Tumor hypoxia is a spatially and temporally heterogeneou

171 Tumor hypoxia is a therapeutic concern since it can redu

172 One feature of tumor hypoxia is activated expression of carbonic anhydr

173 Tumor hypoxia is an established facilitator of survival

174 Clinical evidence shows that tumor hypoxia is an independent prognostic indicator of

175 Tumor hypoxia is an inherent impediment to cancer treatm

176 Tumor hypoxia is associated clinically with therapeutic

177 Tumor hypoxia is associated with impaired efficacy of ca

178 Tumor hypoxia is associated with low rates of cell proli

179 Tumor hypoxia is associated with poor patient outcomes i

180 Tumor hypoxia is associated with poor patient survival a

181 Tumor hypoxia is associated with resistance to antiangio

182 Although tumor hypoxia is associated with tumor aggressiveness an

183 Tumor hypoxia is central to the pathogenesis of metastas

184 Tumor hypoxia is commonly observed in primary solid mali

185 The importance of RRM2B in the response to tumor hypoxia is further illustrated by correlation of i

186 Tumor hypoxia is important in the development and treatm

187 Tumor hypoxia is known to activate angiogenesis, anaerob

188 However, the role of PGE(2) in tumor hypoxia is not well understood.

189 Tumor hypoxia is often associated with resistance to che

190 Tumor hypoxia is often linked to decreased survival in p

191 As a result, tumor hypoxia is reduced after HT, suggesting that these

192 Because tumor hypoxia is related to aggressive tumor behavior an

193 In solid tumors, hypoxia is a common feature and an indicator of

194 In tumors, hypoxia is associated with aggressive disease co

195 t model to calculate surrogate biomarkers of tumor hypoxia (k3), perfusion (K1), and (18)F-FMISO dist

196 Tumor hypoxia leads to increased therapy resistance and

197 Tumor hypoxia leads to radioresistance and markedly wors

198 Tumor hypoxia levels range from mild to severe and have

199 Reducing T cell-intrinsic ROS and lowering tumor hypoxia limited T cell exhaustion, synergizing wit

200 ver, it is subject to limitations, including tumor hypoxia, low tumor targeting, off-target phototoxi

201 chemotherapeutic agents but also aggravates tumor hypoxia, making the tumor cells further resistant

202 As the result of genetic alterations and tumor hypoxia, many cancer cells avidly take up glucose

203 positively correlated with expression of the tumor hypoxia marker CA-IX, and is robustly induced in E

204 Overall, this work establishes that tumor hypoxia may drive aggressive molecular features ac

205 r, and they suggest a novel pathway by which tumor hypoxia may influence cell survival and DNA repair

206 The relationship was also examined of tumor hypoxia, measured using an Eppendorf needle electr

207 Efficient investigations into tumor hypoxia mechanisms have been hindered by the lack

208 Tumor hypoxia modifies the efficacy of conventional anti

209 omplex 1 (PI3K/Akt/TORC1) pathway as well as tumor hypoxia/necrosis.

210 Recent clinical data indicate that tumor hypoxia negatively affects the treatment outcome o

211 hat the Oxy-R fraction accurately quantifies tumor hypoxia noninvasively and is immediately translata

212 azole dynamic PET (dPET) is used to identify tumor hypoxia noninvasively.

213 Tumor hypoxia often directly correlates with aggressive

214 Tumor hypoxia on 18F-fluoromisonidazole (FMISO) positron

215 fferences across patients, and the impact of tumor hypoxia on response to RPT.

216 ogical effects of anti-angiogenic agents and tumor hypoxia.Oncogene advance online publication, 17 De

217 y be reduced by the presence of pre-existing tumor hypoxia or by oxygen depletion during the therapy.

218 During unfavorable conditions (e.g. tumor hypoxia or viral infection), canonical, cap-depend

219 ent of microenvironment parameters including tumor hypoxia, perfusion and proliferation, as well as t

220 ata necessary to generate parametric maps of tumor hypoxia, perfusion, and radiotracer distribution v

221 on vascular composition with consequences to tumor hypoxia, photosensitizer uptake, and PDT response

222 aphy and compared with histologic markers of tumor hypoxia (pimonidazole, carbonic anydrase 9 [CA9])

223 Upon relief of tumor hypoxia, PMNs were recruited less intensely to the

224 Tumor hypoxia presents an obstacle to the effectiveness

225 extent and duration of anemia and associated tumor hypoxia, protected the bone marrow cells and preve

226 Tumor hypoxia provides a key difference between healthy

227 Together, our findings suggest that primary tumor hypoxia provides cytokines and growth factors capa

228 esolution of (18)F-misonidazole PET-detected tumor hypoxia quantified by (18)F-misonidazole dynamics

229 -response relationship between the extent of tumor hypoxia quantified by dynamic (18)F-fluoromisonida

230 However, to what extent tumor hypoxia regulates the TAM phenotype in vivo is unk

231 t metastasis, but the molecular hallmarks of tumor hypoxia remain poorly defined.

232 effect of antiangiogenic therapy on cycling tumor hypoxia remains unknown.

233 Tumor hypoxia renders treatments ineffective that are di

234 data validate a novel strategy to target the tumor hypoxia response through coordinated inhibition of

235 amage repair, and increased understanding of tumor hypoxia responses are pointing to new therapeutic

236 We demonstrate that in ES, tumor hypoxia selectively exacerbates bone metastasis.

237 s strongly suggest that the BRCA1 status and tumor hypoxia should be considered as potentially import

238 fluence rate conditions, confirming regional tumor hypoxia shown by 2-(2-nitroimidazol-1[H]-yl)-N-(3,

239 luences tumor biology is important; to study tumor hypoxia, simple and robust quantification of tissu

240 ature tumor blood vessels and exacerbate the tumor hypoxia state.

241 of the proangiogenic signaling generated by tumor hypoxia still remains as an important unmet need.

242 oxia-inducible factor-1alpha (HIF-1alpha) by tumor hypoxia strongly activates secretion of the sonic

243 issue of Cancer Research, paves the way for tumor hypoxia studies using an intrinsic optical contras

244 To date, only a few molecular key players in tumor hypoxia, such as hypoxia-inducible factor-1 (HIF-1

245 azole data provides better discrimination of tumor hypoxia than methods based on a simple tissue-to-p

246 Tumor hypoxia, the "Achilles' heel" of current cancer th

247 hotodynamic therapy (PDT) inevitably induces tumor hypoxia, thereby weakening the PDT effect.

248 Relieving tumor hypoxia thus greatly improved net PMN-dependent tu

249 ide more-effective strategies for overcoming tumor hypoxia, thus leading to an ideal treatment effica

250 CD39 is induced on tT(ex) cells by tumor hypoxia, thus mitigation of hypoxia limits tT(ex)

251 a et al. present compelling evidence linking tumor hypoxia to acquired resistance mechanisms in non-s

252 substitutes in hemorrhage but also alleviate tumor hypoxia to enhance radiotherapy, photodynamic ther

253 1 (Gal-1) and specific target N-glycans link tumor hypoxia to neovascularization as part of the patho

254 -independent mechanisms that serve to couple tumor hypoxia to pathological angiogenesis, our findings

255 prohibited desmosome integrity and enhanced tumor hypoxia tolerance.

256 In solid tumors, hypoxia triggers an aberrant vasculogenesis, enh

257 tion on non-small cell lung cancer xenograft tumor hypoxia using PET imaging with the hypoxia tracer

258 application, oxygen-guided dose painting of tumor hypoxia, using actual mouse data.

259 for their maximum values (volume of maximal tumor hypoxia vs. relative CBV: r = 0.61, P = 0.002) and

260 a (FaDu), APT MRI showed that a reduction in tumor hypoxia was associated with a shift in tumor pH.

261 Tumor hypoxia was found to mechanistically induce BIRC3

262 rounding liver than in localized tumors, and tumor hypoxia was uniquely associated with prognosis of

263 ous carbonic anhydrase (mCA) IX, a marker of tumor hypoxia, was assessed in tumor specimens.

264 role of MAPKs in the regulation of c-jun by tumor hypoxia, we focused on the activation SAPK/JNKs in

265 Increasing levels of tumor hypoxia were also correlated with diminished metab

266 h dual anti-HER2/EGFR demonstrated decreased tumor hypoxia, when compared to single agent therapies.

267 in hand, we tested the reducing potential of tumor hypoxia, where an oxygen-dependent bioreduction wa

268 We hypothesized that PTEN loss and tumor hypoxia, which characterize glioblastoma but not l

269 vir decreases HIF-1alpha/VEGF expression and tumor hypoxia, which could play a role in its in vivo ra

270 xt is critical because it is associated with tumor hypoxia, which in turn is linked to drug resistanc

271 Sorafenib intensifies tumor hypoxia, which increases stromal-derived factor 1

272 n is also associated with the development of tumor hypoxia, which is mechanistically linked to the ac

273 rgence of drug resistance in solid tumors is tumor hypoxia, which leads to the formation of localized

274 ystem (Au@Rh-ICG-CM) is developed to address tumor hypoxia while achieving high PDT efficacy.

275 Hence, strategies aimed at alleviating tumor hypoxia while improving perfusion may enhance the

276 ation with fluorothymidine and evaluation of tumor hypoxia with agents such as fluoromisonidazole.

277 sintegrity under hypoxic conditions, linking tumor hypoxia with downstream processes driving cancer p

278 c modeling on a voxelwise basis can identify tumor hypoxia with improved accuracy over simple tumor-t

279 Both PET and SPECT could be used to image tumor hypoxia with markers labeled with (64)Cu and (67)C

280 Given the association of tumor hypoxia with more aggressive tumor phenotypes, the

281 Therefore, imaging ITPP-modulated tumor hypoxia with PAI was related to ICB treatment resp

282 nstrating significant, dynamic modulation of tumor hypoxia with the heme-targeting drug treatments cr

283 idazole demonstrated a significant change in tumor hypoxia, with a mean intratumoral reduction in (18

284 Ang-2 overexpression transiently exacerbates tumor hypoxia without affecting ATP levels.