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 In the colon and liver, the tumors induced active stromal reaction, whereas in the s

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

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

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

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

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

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

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

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

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

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

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

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

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

18 helial cell proliferation in vitro and block tumor-induced angiogenesis in vivo.

19 Understanding tumor-induced angiogenesis is a challenging problem with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 ted at blocking human cancer progression and tumor-induced angiogenesis.

41 g and reduce breast cancer cell invasion and tumor-induced angiogenesis.

42 e progression of solid tumors via abrogating tumor-induced angiogenesis.

43 portance of early inflammatory leukocytes in tumor-induced angiogenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 nly for tumor growth within the bone but for tumor-induced bone gain, a response resembling bone lesi

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

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

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

63 mportant resistance mechanism initiated from tumor-induced bone.

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

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

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

67 s a critical role in the induction of breast tumors induced by 4T1 cells by enhancing the expression

68 Moreover, mouse mammary tumors induced by 7,12-dimethylbenz(a)anthracene treatme

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

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

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

72 Low-grade superficial papillary tumors induced by activated H-ras had no detectable Rb f

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

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

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

76 Of the urogenital tumors induced by arsenic plus diethylstilbestrol, 80% w

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

78 the expression of SK1 and COX-2 in rat colon tumors induced by azoxymethane (AOM) and the relationshi

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

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

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

82 Prevention of tumors induced by environmental carcinogens has not been

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 tedly, with a phenotype identical to that of tumors induced by the JSRV Env, indicating that factors

99 2 expression levels were elevated in mammary tumors induced by the Neu (ErbB-2) oncogene, homozygous

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

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

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

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

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

105 ung cancers (NSCLC) as well as in mouse lung tumors induced by urethane.

106 a feature not previously described in other tumors induced by Wnt in mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 ge therapeutic vaccination is invalid due to tumor-induced dysfunction of CD8+ T cells.

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

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

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

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

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

136 Ephrin-A1 knockdown reduced tumor-induced endothelial cell migration in vitro and mi

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

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

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

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

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

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

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

144 ut the role and the regulation of SK1 during tumor-induced hypoxia or about SK1 regulation and HIFs.

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

146 Tumor-induced immune defects can weaken host immune resp

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

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

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

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

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

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

153 Tumor-induced immune suppression can permit tumor cells

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

155 Tumor-induced immune suppression involves the accumulati

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

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

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

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

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

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

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

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

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

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

166 ion in the face of a multitude of normal and tumor-induced immunoregulatory mechanisms.

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

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

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

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

171 Tumor-induced immunosuppression plays a key role in tumo

172 Tumor-induced immunosuppression remains one of the major

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

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

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

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

177 relevant immunotherapies requires reversing tumor-induced immunosuppression.

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

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

180 mouse tumor models, PDE5 inhibition reverses tumor-induced immunosuppressive mechanisms and enables a

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

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

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

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

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

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

187 Tumors induced in St6gal1-null animals were more differe

188 ata support a novel mechanism explaining how tumor-induced inactivation of proximal TCR signaling reg

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

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

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

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

193 ytes (TIL) are defective in cytolysis due to tumor-induced inhibition of proximal TCR-mediated signal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 terestingly, depletion of STAT5 in this same tumor induced more pronounced cell death compared with S

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

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

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

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

221 and lymphocytes combined with a reduction in tumor-induced myeloid suppressor cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 eptide (PTHrP) is a major factor involved in tumor-induced osteolysis caused by breast cancers that h

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

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

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

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

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

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

244 -20 may be a novel target in treating breast tumor-induced osteolysis.

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

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

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

248 Tumor-induced osteomalacia is a rare acquired metabolic

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

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

251 actor requirements by a process that we term tumor-induced progression of the microenvironment.

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

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

254 Such tumor-induced regulatory T cells (TMTregs) arose both fr

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

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

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

258 metastasizing, VEGF-A-overexpressing primary tumors induced sentinel lymph node lymphangiogenesis.

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

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

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

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

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

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

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

268 austion during chronic infections; and (iii) 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 The injection of AdSDF-1alpha into tumors induced the inflammatory enlargement and the accu

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

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

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

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

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

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

289 sitions that were morphologically similar to tumor-induced transitions.

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

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

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

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

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

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.