ライフサイエンスコーパス: tumor-induced

1 The COX-2(+) tumor induced a greater number of Tr1 than COX-2(-) tumo

2 In contrast, tumor-induced activation of p56(lck) in lytic TIL is sus

3 tion assays in C2C12 myotubes indicated that tumor-induced activation of the p38beta isoform is suffi

4 um lipid nanoparticles were able to identify tumor-induced alterations in contrast agent drainage int

5 elanoma footpad tumors were imaged to assess tumor-induced alterations in lymph drainage through tumo

6 uncated MYBL1 transcripts identified in this tumor induced anchorage-independent growth in 3T3 cells

7 Both tumor-induced and G-CSF-induced MDSCs effectively suppre

8 Using superantigen- and tumor-induced anergy models, we found that Egr2 is neces

9 ay provide new insights on the mechanisms of tumor-induced anergy/tolerance and may help explain why

10 ture vasculature (von Willebrand Factor) and tumor induced angiogenesis (by means of Endoglin express

11 hibitors as a strategy to block or attenuate tumor-induced angiogenesis and inhibition of primary and

12 ne (LY294002) exert significant control over tumor-induced angiogenesis and tumor growth in vivo.

13 signaling plays important roles in both the tumor-induced angiogenesis and tumorigenesis through the

14 CAGE mediated tumor-induced angiogenesis and was necessary for VEGF-pr

15 inuum model of multispecies tumor growth and tumor-induced angiogenesis in two and three dimensions.

16 Berberine also reduced tumor-induced angiogenesis in vitro and in vivo.

17 Understanding tumor-induced angiogenesis is a challenging problem with

18 Additionally, tumor-induced angiogenesis was decreased in in vitro exp

19 ill investigate multispecies tumor invasion, tumor-induced angiogenesis, and focus on the morphologic

20 VEGF is crucial in the process of tumor-induced angiogenesis, and recent experiments stron

21 s that exacerbate invasive behavior, promote tumor-induced angiogenesis, and recruit protumoral bone

22 main blocked anthrax intoxication, inhibited tumor-induced angiogenesis, displayed broad antitumor ac

23 uggest that host deficiency in Cav-2 impairs tumor-induced angiogenesis, leading to compromised tumor

24 within host tissue reduced tumor growth and tumor-induced angiogenesis, leading to improved survival

25 tral in diverse human pathologies, including tumor-induced angiogenesis, ocular diseases, and septic

26 Cancer invasion and metastasis depend on tumor-induced angiogenesis, the means by which cancer ce

27 the prominent role of extracellular FGF2 in tumor-induced angiogenesis, we will discuss possibilitie

28 ses (MMPs) have been shown to be involved in tumor-induced angiogenesis.

29 av-2 may promote tumor growth via supporting tumor-induced angiogenesis.

30 ing interest in molecular imaging markers of tumor-induced angiogenesis.

31 environment for the tumor, particularly for tumor-induced angiogenesis.

32 miR-200b exerted a negative regulation on tumor-induced angiogenesis.

33 and regression during both developmental and tumor-induced angiogenesis.

34 gen with a central role in specific steps of tumor-induced angiogenesis.

35 mportant roles in human tumor metastasis and tumor-induced angiogenesis.

36 essor function for P14ARF as an inhibitor of tumor-induced angiogenesis.

37 ma3E acts as a potent inhibitor of adult and tumor-induced angiogenesis.

38 al and biomechanical mechanisms that control tumor-induced angiogenesis.

39 work describes the first cell-based model of tumor-induced angiogenesis.

40 ane type 1-matrix metalloproteinase controls tumor-induced angiogenesis.

41 apeutic for the treatment of PC by targeting tumor-induced angiogenesis.

42 togen promoting both tumor cell survival and tumor-induced angiogenesis.

43 ctor 2 (FGF2) is a key signaling molecule in tumor-induced angiogenesis.

44 Furthermore, IL-7 decreased the tumor-induced apoptosis of T cells with subsequent decre

45 tepimine), protected the CD4(+) T cells from tumor-induced apoptosis.

46 ng PD-L1 signaling abolished conversion in a tumor-induced aTreg conversion model.

47 y modulates various persistent and transient tumor-induced behavioral and immune changes.

48 We show that the tumor-induced bone derives partly from tumor-associated

49 early treatment with an NGF antibody reduced tumor-induced bone destruction, delayed time to bone fra

50 PTHrP inhibition can prevent tumor-induced bone destruction, whereas Gli2 overexpress

51 ng Hh-independent Gli2 activity will inhibit tumor-induced bone destruction.

52 Further, platelet depletion prevented tumor-induced bone formation, highlighting the importanc

53 rve the integrity and use, delay the time to tumor-induced bone fracture, and maintain body weight.

54 on of pitavastatin's therapeutic efficacy in tumor-induced bone loss, as well as VOC-based diagnosis

55 as a drug candidate for inhibiting tumor and tumor-induced bone loss.

56 d for progression within bone and determines tumor-induced bone tissue transformation.

57 tome analysis of the conditioned medium from tumor-induced bone to identify proteins (termed "osteocr

58 Tumor-induced bone was reduced in trigenic mice (Tie2(cr

59 mportant resistance mechanism initiated from tumor-induced bone.

60 ctive therapeutic target for preventing skin tumor induced by aberrant Pten signaling.

61 ar carcinoma (HCC) is the main type of liver tumor induced by kras(V12) expression.

62 the radiotracer in the necrotic zone of the tumor induced by photothermal ablation therapy.

63 weakened, but did not abrogate, formation of tumors induced by a control oncogene (HRAS/G12V).

64 erexpressing Bmx in epidermal keratinocytes, tumors induced by a two-stage chemical skin carcinogenes

65 AR4-2J tumors and A431(CCKR+) tumors (i.e., tumors induced by A431 cells transfected to stably expre

66 In contrast, removal of cilia accelerated tumors induced by activated Gli2, a transcriptional effe

67 At the molecular level, liver tumors induced by AKT/c-Met display activation of AKT/mT

68 Ciliary ablation strongly inhibited BCC-like tumors induced by an activated form of Smoothened.

69 efine the cross-species genomic landscape of tumors induced by an important compendium of agents with

70 ned 2 months postcastration, suggesting that tumors induced by Apc loss of function are capable of gr

71 d overexpression of RAC1 protein occurred in tumors induced by arsenic plus TPA compared with TPA alo

72 ly increased the incidence and size of colon tumors induced by azoxymethane (AOM)/dextran sulfate sod

73 Tumors induced by CCND1/c-Met had a longer latency perio

74 enetic ablation of Chk1 in the mouse skin on tumors induced by chemical carcinogens.

75 Prevention of tumors induced by environmental carcinogens has not been

76 Interestingly, the tumors induced by GDNF stimulation contain enteric neuro

77 to detect 0.2-0.3 pH unit changes in vivo in tumors induced by i.p. injection of glucose.

78 We analyzed tumors induced by K-RAS and AKT and compared them to oli

79 a(2)-microglobulin are highly susceptible to tumors induced by mouse polyoma virus (PyV), but CD8-def

80 the VP1 capsid protein shifts the profile of tumors induced by MPyV from an epithelial to a mesenchym

81 ort that eliminating HSF1 protects mice from tumors induced by mutations of the RAS oncogene or a hot

82 These results suggest that tumors induced by MYC remain addicted to overexpression

83 roliferative arrest in benign or early-stage tumors induced by oncoproteins, chromosomal instability,

84 t of the TGF-beta signaling pathway on liver tumors induced by phosphatase and tensin homolog (Pten)

85 In addition, mammary gland tumors induced by polyomavirus middle T antigen in JNK2(

86 (-1) per os, Pz-1 abrogated the formation of tumors induced by RET-mutant fibroblasts and blocked the

87 mg/kg/day) completely prevented formation of tumors induced by RET/C634Y-transformed cells, while it

88 e-wide mRNA expression profiling data for 97 tumors induced by retroviral insertional mutagenesis.

89 Nevertheless, tumors induced by silencing both Smads 2 and 3 were larg

90 monstrate here that the development of mouse tumors induced by the concomitant application of a carci

91 ressed in mouse mammary glands, we show that tumors induced by the cooperative actions of two oncogen

92 Prostate tumors induced by the deletion of Apc have elevated leve

93 2 expression levels were elevated in mammary tumors induced by the Neu (ErbB-2) oncogene, homozygous

94 nt distinct from those mechanisms that cause tumors induced by the rare inheritance of a mutant adeno

95 s through the inhibition of the formation of tumors induced by tobacco carcinogens.

96 rotein is markedly elevated in mouse mammary tumors induced by transgenic ErbB2 overexpression.

97 at ErbB2-induced tumors in mice or xenograft tumors induced by transplantation of HER2-amplified BC c

98 ly unsuspected molecular heterogeneity among tumors induced by truncating Apc mutations.

99 immune responses and capable of controlling tumors induced by type 16 human papilloma virus (HPV-16)

100 o Spdef(dox-intestine) mice with established tumors, induced by the combination of AOM and DSS or by

101 lture, immune cells seemed to be involved in tumor-induced bystander effects in animals because CCL2-

102 ological blockade of Nox4 activity abrogated tumor-induced cachexia in mice.

103 es both end-stage metastatic progression and tumor-induced cachexia in tumor-bearing mice.

104 how these drugs affected the development of tumor-induced cardiac atrophy and function.

105 e measures of existing (CD31-expressing) and tumor-induced (CD105-expressing) vessels, in pretreatmen

106 ulation of IFN regulatory factor 8 levels in tumor-induced CD11b(+)Gr-1(+) cells can significantly ab

107 Overall, our data indicate that 1) tumor-induced CD11b(+)Gr-1(+) cells from both cancer mod

108 owever, the protumorigenic behavior of these tumor-induced CD11b(+)Gr-1(+) cells was significantly di

109 Despite limited differences in phenotype, tumor-induced CD11b(+)Gr-1(+) cells were found to produc

110 ng type-1 antitumor immune responses, impair tumor-induced CD4(+)CD25(+)FoxP3(+) regulatory T lymphoc

111 By illustrating the dependence of tumor-induced CD4+ T-cell anergy on NFAT1, our findings

112 ings demonstrate the primary role of Chop in tumor-induced CD8(+) T cell dysfunction and the therapeu

113 ficacy against pancreatic cancer by breaking tumor-induced CD8(+) T cell suppression.

114 oduce differential immune responses and that tumor-induced central pro-inflammatory cytokine producti

115 , studies of bone metastasis have shown that tumor-induced changes in bone remodeling are likely medi

116 nd metastasis, but little is known about how tumor-induced changes in the microenvironment affect ben

117 Thus, tumor-induced chemokine production in hypoxic TAMs and c

118 In the first but not two latter models, tumors induced CTL hyporesponsiveness to tumor-unrelated

119 rs may exacerbate the deleterious effects of tumor-induced cytokines on affective states.

120 fect on neurons that shielded the brain from tumor-induced damage, as indicated by a relative 3.5-fol

121 litaxel-mediated activation of TLR4-positive tumors induced de novo generation of deep intratumoral l

122 apter protein MyD88, were not protected from tumor-induced decreases in wheel running, despite attenu

123 Shp-1 activity in lytic TIL in vitro blocks tumor-induced defective TIL cytolysis.

124 ue of Cancer Cell, Katlinski et al. describe tumor-induced degradation of type I interferon receptor

125 Thus, our results suggest that tumor-induced dysregulation of endocytic activity of DC

126 Thus, tumor-induced EC-to-OSB conversion is one mechanism that

127 Brain tumor growth and tumor-induced edema result in increased intracranial pre

128 We hypothesize that prevention of tumor-induced effector cell dysfunction is a major mecha

129 extracellular traps (NET) were implicated in tumor-induced effects on distant organs unaffected by th

130 Further, tumor-induced elevation of circulating TNFalpha and inte

131 ammation and coagulation, the involvement of tumor-induced endothelium activation and the subsequent

132 ht loss in cancer patients that results from tumor-induced energy wasting, is a serious problem that

133 Tumor-induced expression of PD-L1 was limited to F4/80(+

134 Thus, our data show that tumor-induced Foxp3(+)CD4(+) T cells can be reprogrammed

135 erexpression in vivo selectively constrained tumor-induced GP expansion.

136 ase 1 (SphK1) in producing S1P and mediating tumor-induced hemangiogenesis and lymphangiogenesis in a

137 mechanisms of differential MEK activation in tumor-induced host wasting.

138 TIL infiltrate, decreased susceptibility to tumor-induced hypofunction, and attenuation of IR expres

139 regation, tumor clearance from the blood, or tumor-induced immune cell activation and recruitment.

140 Tumor-induced immune defects can weaken host immune resp

141 mely tumor site immune modulation, targeting tumor-induced immune defects, and repairing ongoing (rat

142 ch is involved in both tumor progression and tumor-induced immune dysfunction.

143 providing a previously unexplored aspect of tumor-induced immune escape and a basis for biomarker de

144 minimal residual disease and, thus, minimize tumor-induced immune evasion.

145 tolerance represents one major mechanism of tumor-induced immune evasion.

146 MTEX emerge as the major mechanism of tumor-induced immune suppression and as an underestimate

147 itumor effect was associated with attenuated tumor-induced immune suppression and substantially reduc

148 Tumor-induced immune suppression can permit tumor cells

149 ed suppressor cells are a major mechanism of tumor-induced immune suppression in cancer.

150 Tumor-induced immune suppression involves the accumulati

151 ased therapy and simultaneously reducing the tumor-induced immune suppression is well-tolerated and s

152 ve in effector phase function, demonstrating tumor-induced immune suppression that likely underlies t

153 immunomodulatory role for Dkk1 in regulating tumor-induced immune suppression via targeting beta-cate

154 mor-derived exosomes (TEX) are harbingers of tumor-induced immune suppression: they carry immunosuppr

155 The molecular mechanisms underlying tumor-induced immune tolerance are largely unknown.

156 yme in the kynurenine pathway which augments tumor-induced immune tolerance.

157 This is primarily due to the presence of tumor-induced immune-suppressive mechanisms as well as t

158 ) D2F2/E2 tumor enabled the functionality of tumor-induced immunity, but secondary tumors were refrac

159 B3) in MDSC differentiation, and its role in tumor-induced immunity.

160 cell growth and survival but also facilitate tumor-induced immunomodulation and eventual metastasis.

161 rming growth factor-beta (TGF-beta) promotes tumor-induced immunosuppression and contributes to resis

162 une responses, and strategies for overcoming tumor-induced immunosuppression are reviewed.

163 Newer trials are addressing the problem of tumor-induced immunosuppression by the use of antibodies

164 Tumor-induced immunosuppression is a common obstacle for

165 thal epithelial tumors may require targeting tumor-induced immunosuppression on an individualized bas

166 Tumor-induced immunosuppression plays a key role in tumo

167 Tumor-induced immunosuppression remains one of the major

168 ity with the inhibition of the mechanisms of tumor-induced immunosuppression represent a key objectiv

169 However, much of our knowledge on tumor-induced immunosuppression was acquired using tumor

170 ressor cells (MDSCs) play a critical role in tumor-induced immunosuppression, we investigated their r

171 y useful for immunotherapy in the setting of tumor-induced immunosuppression.

172 relevant immunotherapies requires reversing tumor-induced immunosuppression.

173 n for their clinical potential in overcoming tumor-induced immunosuppression.

174 Recent findings show a tumor-induced immunosuppressive mechanism, whereby tumor

175 gely unsuccessful to date, partly because of tumor-induced immunosuppressive mechanisms, including ad

176 nt for the distinguishing characteristics of tumor-induced immunosuppressive neutrophils.

177 rizes recent findings that are in support of tumor-induced immunosurveillance in regulating metastati

178 In this review, we discuss tumor-induced impairment of CTLs and experimental treatm

179 In addition to tumor-induced impairment of pleural fluid drainage, pert

180 We found that tumors induced in Rras(-/-) mice formed with shorter lat

181 Tumors induced in St6gal1-null animals were more differe

182 s, Treg cell reprogramming was suppressed by tumor-induced indoleamine 2,3-dioxygenase (IDO) and vacc

183 Anti-Fn14 antibodies prevented tumor-induced inflammation and loss of fat and muscle ma

184 sis that fatigue results from propagation of tumor-induced inflammation to the brain and activation o

185 models and human cancer patients showed that tumor-induced inflammatory mediators induce MDSC differe

186 ent is created by the tumor and dominated by tumor-induced interactions.

187 Tumor-induced liver NKT cells, especially type I NKT cel

188 of either RelB or NIK completely blocked the tumor-induced loss of trabecular bone.

189 These characteristics of tumor-induced lymph drainage could be useful for diagnos

190 , the Vegfr3-reporter allowed us to tracking tumor-induced lymphangiogenesis at the tumor periphery a

191 ere, we show that SOX18 is also critical for tumor-induced lymphangiogenesis, and we show that suppre

192 alpha4beta1 then promotes growth factor and tumor-induced lymphangiogenesis, as genetic loss of inte

193 Y991A knock-in mice blocks growth factor and tumor-induced lymphangiogenesis, as well as tumor metast

194 studies have revealed that monocyte-derived tumor-induced macrophages represent a major tumor-associ

195 ve T cells: 1) naive T cells cocultured with tumor-induced MDSC have reduced L-selectin; 2) T cells i

196 underlying iNOS expression and regulation in tumor-induced MDSCs are unknown.

197 Here, we demonstrated that tumor-induced MDSCs exhibit significantly decreased spon

198 Furthermore, tumor-induced MDSCs exhibited diminished STAT1 and NF-ka

199 and standardization of criteria classifying tumor-induced MDSCs have led to unified descriptions and

200 that the Tnf promoter was hypermethylated in tumor-induced MDSCs in vivo.

201 Instead, tumor-induced MDSCs showed increased SETD1B expression a

202 ted myeloid populations highly homologous to tumor-induced MDSCs with respect to phenotype, function,

203 SETD1B, was enriched at the nos2 promoter in tumor-induced MDSCs, and inhibition or silencing of SETD

204 vo Strikingly, although IRF8 was silenced in tumor-induced MDSCs, iNOS expression was significantly e

205 NOS expression was significantly elevated in tumor-induced MDSCs, suggesting that the expression of i

206 face Fas receptor decreased significantly in tumor-induced MDSCs.

207 whereas expression of Bcl-xL is increased in tumor-induced MDSCs.

208 cing of SETD1B diminished iNOS expression in tumor-induced MDSCs.

209 ions of immunotherapy for melanoma stem from tumor-induced mechanisms of immune evasion that render t

210 Genetic ablation of Id2 delayed tumor-induced mortality, and pharmacologic inhibition of

211 Hsp70/90 expression in tumor cells abrogates tumor-induced muscle catabolism and wasting in cultured

212 rase activity in mouse muscle attenuated LLC tumor-induced muscle catabolism.

213 ignaling pathway responsible for the bulk of tumor-induced muscle proteolysis.

214 a suggest that p300 is a key mediator of LLC tumor-induced muscle wasting whose acetyltransferase act

215 specific p300 knockout were resistant to LLC tumor-induced muscle wasting.

216 ressing EVs are necessary and sufficient for tumor-induced muscle wasting.

217 Tumor-induced myeloid-derived suppressor cells (MDSC) co

218 hat phenotypically and functionally resemble tumor-induced myeloid-derived suppressor cells (MDSCs),

219 afts showed that SOX18 is reexpressed during tumor-induced neolymphangiogenesis.

220 Cav-2 promotes subcutaneous tumor growth and tumor-induced neovascularization using two independent s

221 ressor cells and contribute significantly to tumor-induced neovascularization.

222 ain-derived endothelial cells, as a model of tumor-induced neovasculation.

223 cal or systemic blockade of VEGFR1 prevented tumor-induced nerve remodeling and attenuated cancer pai

224 ping effective targets for the inhibition of tumor-induced neurogenesis and tumor progression.

225 to which mammary tumor resection attenuates tumor-induced neuroinflammation and sickness behavior fo

226 onstrate that chronic acidic stress in solid tumors induced OCT-4 expression in fibroblasts and other

227 he conjugative opines produced by crown gall tumors induced on plants by the bacteria.

228 Using a fly model of tumor-induced organ wasting, we observed aberrant MEK ac

229 ate cancer metastasis include targeting both tumor-induced osteoblastic lesions and underlying osteoc

230 on tumor cells by RNA interference abrogates tumor-induced osteoclast formation.

231 ng that MCP-1, in addition to IL-8, mediates tumor-induced osteoclastogenesis and bone resorption.

232 ate drug zoledronic acid (ZOL) would inhibit tumor-induced osteolysis and reduce tumor growth and inv

233 interface plays an important role in mammary tumor-induced osteolysis and suggest that cathepsin G is

234 of MMP13 at the TB interface is important in tumor-induced osteolysis and suggest that MMP13 is a pot

235 r, AZD4547 suppressed osteoclastogenesis and tumor-induced osteolysis in an orthotopic breast cancer

236 We then examined tumor-induced osteolysis in both RelB-/- and NIK-/- mice

237 Perpetuation of tumor-induced osteolysis requires a continuous supply of

238 ZOL-mediated inhibition of tumor-induced osteolysis was characterized by reduced nu

239 Furthermore, tumor-induced osteolysis was significantly reduced in mi

240 ignificantly contributes to tumor growth and tumor-induced osteolysis whereas osteoclast-derived MMP-

241 To determine the functional role of MMP13 in tumor-induced osteolysis, mice with Cl66 mammary tumors

242 -20 may be a novel target in treating breast tumor-induced osteolysis.

243 chanism through which MMP-7 mediates mammary tumor-induced osteolysis.

244 vo inhibition of cathepsin G reduces mammary tumor-induced osteolysis.

245 The pathogenesis of tumor-induced osteomalacia involves tumor expression of

246 Tumor-induced osteomalacia is a rare acquired metabolic

247 Data suggest that tumor-induced oxidative stress may promote both VEGFR1 u

248 Tumor-induced perturbations in the endocrine, immune and

249 as well as their potential association with tumor-induced polarization states and immunosuppressive

250 on of PR as a single genetic change in these tumors induced progesterone resistance indicating that p

251 ot affect subcutaneous primary tumor growth, tumor-induced recruitment of inflammatory cells or T cel

252 ainst DYRK1A in mice bearing HNSCC xenograft tumors induced regression of tumor growth.

253 Tumor-induced remodeling of the microenvironment relies

254 + BMCs that were recruited to the responding tumors induced resident tissue fibroblasts to express ge

255 Tumor-induced senescence of T cells is induced by solubl

256 Moreover, overexpression of Adm in tumors induced sentinel lymph node lymphangiogenesis and

257 pression to tumor promotion is mediated by a tumor-induced shift in the local immune state, and despi

258 systemic effects, including reversal of the tumor-induced shrinkage of sinusoidal vessels and altere

259 , colony formation, migration, invasion, and tumor-induced skeletal lesions in femoral bone.

260 e, Gata2 deletion in established Kras mutant tumors induced striking regression.

261 c model Ags, we demonstrate that alleviating tumor-induced suppression along with vaccination against

262 apy in MM may function in part by subverting tumor-induced suppression of canonical Wnt signaling in

263 To identify tumor-induced suppressor cells, we transferred spleen ce

264 ors and host tissues play essential roles in tumor-induced systemic wasting and cancer cachexia, incl

265 ppaB activity and prevent the development of tumor-induced systolic dysfunction and atrophy.

266 The contribution of GM2 gangliosides to tumor-induced T cell death was supported by the finding

267 austion during chronic infections; and (iii) tumor-induced T cell dysfunction.

268 o dissect the molecular pathways involved in tumor-induced T cell dysfunction.

269 e for using anti-PD-1 blocking Ab to reverse tumor-induced T cell exhaustion in NSCLC patients.

270 together with PD-1-PD-L1 blockade to reverse tumor-induced T cell exhaustion/dysfunction in patients

271 CD11c(+) cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacki

272 Using a tumor-induced T cell tolerance model, we find that expan

273 n of tumor Ags, which results in reversal of tumor-induced T cell tolerance.

274 These investigations identified tumor-induced T-cell hyporesponsiveness as a form of clo

275 Tumor-induced T-cell tolerance is a major mechanism that

276 Consequently, anti-Jagged therapy overcame tumor-induced T-cell tolerance, increased the infiltrati

277 and displayed a superior capacity to reverse tumor-induced T-cell tolerance.

278 Using a tumor-induced temperature sensitivity model, we showed t

279 a suppressive oligodeoxynucleotide, blocked tumor-induced temperature sensitivity.

280 These findings suggest that IgG4 promoted by tumor-induced Th2-biased inflammation may restrict effec

281 Metastatic mammary tumors induced the accumulation of distinct populations

282 ancer could provide a strategy to counteract tumor-induced thrombosis and organ failure as well as to

283 ements for costimulatory signals to overcome tumor-induced tolerance and have significant implication

284 ancer, outlining interventions that mitigate tumor-induced tolerance and highlighting several combina

285 These findings suggest the role of Chop in tumor-induced tolerance and the therapeutic potential of

286 sildenafil abrogates Treg proliferation and tumor-induced tolerance in antigen-specific T cells.

287 one molecular mechanism that contributes to tumor-induced tolerance.

288 s produced by them play an essential role in tumor-induced Treg expansion.

289 aling molecules and studied their effects on tumor-induced Treg expansion.

290 ws that an IL-12-IFN-gamma axis can suppress tumor-induced Treg proliferation.

291 and stimulated interferon-beta secretion in tumors, induced tumor regression with durable antitumor

292 This study demonstrates that tumor-induced up-regulation of S100A9 protein is critica

293 nscriptome analysis revealed CB1R-dependent, tumor-induced up-regulation of the hepatic expression of

294 UR) effectively suppressed the growth of HCC tumors induced using the hydrodynamic tail vein injectio

295 attern, geographic necrosis and infiltrating tumor-induced vascular proliferation closely resembling

296 cular endothelial growth factor (VEGF-A) and tumor-induced VEC-Y658 phosphorylation in vivo.

297 e genetic evidence that FAK is a mediator of tumor-induced VP in the brain.

298 n additional role of astrocytes in mediating tumor-induced VP.

299 dramatically extended lifespan by inhibiting tumor-induced weight loss although having only moderate

300 reporter system that is capable of tracking tumor-induced weight loss, an early marker of cachexia.