ライフサイエンスコーパス: tumor hypoxia

1 r for noninvasive identification of regional tumor hypoxia.

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

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

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

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

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

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

8 ng existing and future exogenous markers for tumor hypoxia.

9 et for anticancer drug discovery directed at tumor hypoxia.

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

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

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

13 and pimonidazole, two extrinsic markers for tumor hypoxia.

14 idated their use as endogenous indicators of tumor hypoxia.

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

16 proteins will provide a surrogate measure of tumor hypoxia.

17 sizing the need for noninvasive detection of tumor hypoxia.

18 llent radiotracer for noninvasive imaging of tumor hypoxia.

19 etanidazole are being explored as probes for tumor hypoxia.

20 this apoptosis is predominant in regions of tumor hypoxia.

21 apeutics that simultaneously target TAMs and tumor hypoxia.

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

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

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

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

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

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

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

29 te the magnitude and spatial distribution of tumor hypoxia.

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

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

32 nitrogen mustard prodrug designed to target tumor hypoxia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Tumor hypoxia and perfusion are independent prognostic i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 Tumor hypoxia confers chemotherapy resistance.

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

78 Tumor hypoxia contributes resistance to chemo- and radio

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

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

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

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

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

84 Tumor hypoxia drives metastatic progression, drug resist

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

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

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

88 Tumor hypoxia hampers the efficacy of radiotherapy becau

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

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

91 Tumor hypoxia has been identified as a significant step

92 Since tumor hypoxia has been proposed to increase tumor aggres

93 Tumor hypoxia has long been associated with resistance t

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

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

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

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

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

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

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

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

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

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

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

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

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

107 In all tumors, hypoxia increased markedly after either radiatio

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

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

110 Tumor hypoxia indicates a poor prognosis.

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

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

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

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

115 Tumor hypoxia is a known adverse prognostic factor, and

116 Tumor hypoxia is a persistent obstacle for traditional t

117 Tumor hypoxia is a spatially and temporally heterogeneou

118 Tumor hypoxia is a therapeutic concern since it can redu

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

120 Tumor hypoxia is an established facilitator of survival

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

122 Tumor hypoxia is an inherent impediment to cancer treatm

123 Tumor hypoxia is associated clinically with therapeutic

124 Tumor hypoxia is associated with impaired efficacy of ca

125 Tumor hypoxia is associated with low rates of cell proli

126 Tumor hypoxia is associated with poor patient survival a

127 Tumor hypoxia is associated with resistance to antiangio

128 Although tumor hypoxia is associated with tumor aggressiveness an

129 Tumor hypoxia is central to the pathogenesis of metastas

130 Tumor hypoxia is commonly observed in primary solid mali

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

132 Tumor hypoxia is important in the development and treatm

133 Tumor hypoxia is known to activate angiogenesis, anaerob

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

135 Tumor hypoxia is often associated with resistance to che

136 Tumor hypoxia is often linked to decreased survival in p

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

138 Because tumor hypoxia is related to aggressive tumor behavior an

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

140 In tumors, hypoxia is associated with aggressive disease co

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

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

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

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

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

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

147 Tumor hypoxia modifies the efficacy of conventional anti

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

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

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

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

152 Tumor hypoxia often directly correlates with aggressive

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

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

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

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

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

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

159 Tumor hypoxia presents an obstacle to the effectiveness

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

161 Tumor hypoxia provides a key difference between healthy

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

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

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

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

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

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

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

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

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

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

172 1 (Gal-1) and specific target N-glycans link tumor hypoxia to neovascularization as part of the patho

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

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

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

176 Tumor hypoxia was found to mechanistically induce BIRC3

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

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

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

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

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

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

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

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

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

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

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

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

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