ライフサイエンスコーパス: tumor-associated

1 s generally assumed that CD8(+) TILs will be tumor-associated Ag (TAA) specific, it is unknown whethe

2 etting, they imply that the range of CTL and tumor-associated Ag combinations that may be effectively

3 ective against lymphoma, and lowly expressed tumor-associated Ag should be considered as potential ta

4 ies a polyclonal population of high-affinity tumor-associated Ag-specific CD8(+) T cells, which produ

5 g the frequency of cytotoxic, high-affinity, tumor-associated Ag-specific cells.

6 cer immunotherapy are often directed against tumor-associated Ags also expressed in normal tissues.

7 Cancer cells harbor high-affinity tumor-associated Ags capable of eliciting potent antitum

8 ving field that exploits T cell responses to tumor-associated Ags to induce tumor rejection.

9 s melanoma are used to extract a snapshot of tumor-associated alteration in the serum.

10 and -deficient tumor tissues and (b) sorted tumor-associated and -resident colonic macrophage subpop

11 helial markers, we performed a microarray on tumor-associated and nonmalignant endothelium collected

12 hat inhibit oncogenic signaling pathways and tumor-associated angiogenesis, as well as by the recent

13 tric solid tumor with high expression of the tumor associated antigen disialoganglioside GD2.

14 Survivin is a tumor-associated antigen (TAA) that inhibits apoptosis a

15 ession of PD-1, TIM3, and LAG3 was higher on tumor-associated antigen (TAA)-specific CD8(+) TIL, comp

16 ETAA1 (Ewing tumor-associated antigen 1), also known as ETAA16, was i

17 esis and progression, MUCL1 is an attractive tumor-associated antigen and a potential therapeutic tar

18 thelial cell adhesion molecule (HEPCAM) is a tumor-associated antigen frequently expressed in carcino

19 eptor (CAR)-engineered T cells targeting the tumor-associated antigen interleukin-13 receptor alpha 2

20 e normal tissues by specifically targeting a tumor-associated antigen that is also expressed on those

21 ognizing a naturally processed and presented tumor-associated antigen with a chimeric PD-1:28 recepto

22 inhibitor, that can, without using exogenous tumor-associated antigen(s), eliminate various large tum

23 expressed Y-encoded minor H antigen or to a tumor-associated antigen, although poorly effective if i

24 on and function of CD8 T cells recognizing a tumor-associated antigen.

25 ) and chimeric antigen receptors recognizing tumor-associated antigens (TAAs) can now be engineered t

26 apeutic monoclonal antibodies (mAbs) against tumor-associated antigens (TAAs) is that their mechanism

27 Donor-derived immunity against tumor-associated antigens (TAAs) may exert selective ant

28 se expression of tumor-specific antigens and tumor-associated antigens (TAAs) that can activate antit

29 show that CD8 T-cell responses to viral and tumor-associated antigens are greatly underestimated in

30 of HSV can be retargeted to cells expressing tumor-associated antigens by single-chain antibodies fus

31 TEX carrying tumor-associated antigens can interfere with antitumor i

32 onstraints have led to a relative paucity of tumor-associated antigens for antibody targeting in onco

33 for spontaneous CD8+ T cell priming against tumor-associated antigens has generated renewed interest

34 Autoantibodies raised against tumor-associated antigens have shown high promise as cli

35 sfer of T-cell receptors (TCRs) specific for tumor-associated antigens is a promising approach for ca

36 t secondary CD8 T-cell response specific for tumor-associated antigens other than WT1.

37 Many tumors overexpress tumor-associated antigens relative to normal tissue, suc

38 ting either MHC class I or II neoantigens or tumor-associated antigens rendered up to 60% of the tota

39 tic cells and enhanced cross-presentation of tumor-associated antigens to CD8 T cells.

40 les of neutrophils and B cells in presenting tumor-associated antigens to T cells in this combination

41 Small organic ligands, selective for tumor-associated antigens, are increasingly being consid

42 tumor microenvironment, primed to recognize tumor-associated antigens, can occur in response to immu

43 proliferation of CD8(+) T cells specific to tumor-associated antigens, resulting in cancer-specific

44 nses to cancer by stimulating the release of tumor-associated antigens.

45 sing patient T cells redirected to recognize tumor-associated antigens.

46 rgeted therapies, such as mAbs, that bind to tumor-associated antigens.

47 eta secretion by activation of c-Met induced tumor-associated astrocytes to secrete the c-Met ligand

48 anism of acquired therapy resistance through tumor-associated B cells with important clinical implica

49 nism of acquired drug resistance mediated by tumor-associated B cells-derived IGF-1.

50 ipt levels in tumors and IGF-1 expression in tumor-associated B cells.

51 microenvironment, which is mediated by human tumor-associated B cells.

52 is sensitive to wild-type BAF180, but not a tumor-associated BAF180 mutant.

53 ivo, Ang-4 stimulated a 4.5-fold increase in tumor-associated blood vessel permeability compared with

54 TORC1 versus mTORC2 in cancer, their role in tumor-associated blood vessels and tumor immunity, and p

55 d in ex vivo T-ALL cells, and coculture with tumor-associated, but not normal thymic DCs, sustained I

56 The tumor-associated calcium signal transducer 2 (TACSTD2/Tr

57 ession modulated drug vector distribution in tumor-associated capillaries.

58 ivery and vector distribution differences in tumor-associated capillary bed at different stages of di

59 Sialyl Thomsen-nouveau (STn) is a tumor-associated carbohydrate antigen (TACA) that is ove

60 pentasaccharide fragments of the Le(a)Le(x) tumor-associated carbohydrate antigen alpha-L-Fuc-(1-->4

61 fficient synthesis of three analogues of the tumor-associated carbohydrate antigen Le(a)Le(x).

62 with other interesting biomolecules, such as tumor-associated carbohydrate antigens (TACAs).

63 inhibitory activity/selectivity against the tumor associated carbonic anhydrase (CA, EC 4.2.1.1) iso

64 escribe targeting of aberrantly glycosylated tumor-associated cell membrane mucin MUC1 using chimeric

65 Molecular profiles of tumors and tumor-associated cells hold great promise as biomarkers

66 ppaB RelA interaction as a target to enhance tumor-associated DC function to support or enhance antit

67 signals driving T-ALL growth, and implicate tumor-associated DCs and their mitogenic signals as ausp

68 It is established that tumor-associated DCs are defective in their ability to c

69 As a result, tumor-associated DCs are no longer able to stimulate ade

70 s provide the first evidence that endogenous tumor-associated DCs supply signals driving T-ALL growth

71 or targets) for reducing TIM-3 expression on tumor-associated DCs, we explored the molecular mechanis

72 h concomitant expression of their ligands by tumor-associated DCs.

73 of c-Src in mice reduced TIM-3 expression on tumor-associated DCs.

74 eraction between FOXO3 and NF-kappaB RelA in tumor-associated DCs.

75 of T cell Ig and mucin protein-3 (TIM-3) on tumor-associated dendritic cells (DCs) attenuates antitu

76 signaling are believed to be responsible for tumor-associated ECM remodeling.

77 Treatments of brain tumor associated edema with systemically delivered dexam

78 Tumor-associated edema and necrosis were lessened, resul

79 Tumor-associated endothelial cells (TECs) regulate tumor

80 tal Cell, Lin et al. (2017) demonstrate that tumor-associated endothelial cells can give rise to oste

81 t the tumor-induced bone derives partly from tumor-associated endothelial cells that have undergone e

82 node endothelial cells and highly induced on tumor-associated endothelium.

83 isoforms) and hCA IX and XII (transmembrane, tumor-associated enzymes).

84 abrogated tumor cell apoptosis and depleted tumor-associated eosinophils, accompanied by a decrease

85 The anti-apoptotic function and tumor-associated expression of heat-shock protein 70 (HS

86 e hepatocytes influences the network for the tumor-associated fibroblast environment.

87 umbers of SMC and non-SMC, which were mostly tumor-associated fibroblasts (TAF).

88 Moreover, tumor-associated fibroblasts from mouse PDA were also re

89 Traction force microscopy revealed that tumor-associated fibroblasts generate larger forces on s

90 on from Th2 to Th1 type while remodeling the tumor-associated fibroblasts, collagen, and blood vessel

91 that cells of mesenchymal origin, including tumor-associated fibroblasts, degrade substantial amount

92 xenograft tumors, suggesting the presence of tumor-associated fibroblasts.

93 lating mesenchymal precursors as a source of tumor-associated fibroblasts.

94 against tumor development via inhibition of tumor-associated fibrosis, stromal TGFbeta1 production,

95 s synaptic transmission, as well as critical tumor-associated functions.

96 During the productive infection of tumor-associated gammaherpesviruses, both virions and VL

97 gene expression profiling and designated 50 tumor-associated genes as the NFE2L2-associated molecula

98 of BRD4 binding was increased expression of tumor-associated genes such as NOTCH1 and RBPJ, as well

99 osylation state of live zebrafish and detect tumor-associated glycans in mice, the ability to image g

100 Fusion proteins targeting CD20 or tumor-associated glycoprotein 72 (TAG-72) mediated the s

101 astic progression, and unique alterations in tumor-associated glycosylation may also serve as a disti

102 l ones hCA VA and VB, and the transmembrane, tumor associated hCA IX and XII.

103 ion.IMPORTANCE Cells lytically infected with tumor-associated herpesviruses produce a high proportion

104 scaffold to obtain potent inhibitors of the tumor-associated human carbonic anhydrases (hCAs) IX and

105 For instance, we show that the tumor-associated human repeat human satellite repeat II

106 he expression of PD-L1, PD-1, and subsets of tumor associated immune cells.

107 engineering cell-based therapies to overcome tumor associated immune dysfunction and thereby identifi

108 of tumor immune crosstalk and the resulting tumor-associated immune cell activity.

109 Membranous PD-L1 expression in tumor and tumor-associated immune cells was assessed by a clinical

110 e effects of GBM standard on care therapy on tumor-associated immune cells, and review several approa

111 valuable for the study of subtle changes in tumor-associated immune cells.

112 e chemotaxis, resulting in repression of the tumor-associated immune system.

113 Tumor-associated immunosuppression aids cancer cells to

114 rticle we demonstrate that reovirus augments tumor-associated immunosuppression immediately following

115 rapy in PDAC tumors include a high number of tumor-associated immunosuppressive cells and a uniquely

116 d CTLA4(+)/CD86(+) complexes indicative of a tumor-associated immunosuppressive phenotype.

117 This work suggests that the establishment of tumor-associated inflammation and immunity critically de

118 effector molecule GADD45beta that restricts tumor-associated inflammation and T-cell trafficking int

119 The mechanisms regulating tumor-associated inflammation are incompletely understoo

120 r types, our findings suggest that targeting tumor-associated inflammation via anti-ERK5 therapy may

121 sion correlated with reduced accumulation of tumor-associated inflammatory cells, likely caused by di

122 For gliomas, the tumor-associated inflammatory response is pivotal to sup

123 er gemcitabine to malignant cells expressing tumor-associated integrins.

124 erivatives acted as potent inhibitors of the tumor-associated isoform hCA XII.

125 inhibition while poorly inhibiting the other tumor-associated isoform hCA XII.

126 anhydrase ligand with high affinity for the tumor-associated isoform IX (CAIX), which can transport

127 ype agents: small molecule inhibitors of the tumor-associated kinases MEK and PI3K or the pro-inflamm

128 enotype characterized by low infiltration of tumor-associated leukocytes, particularly macrophages an

129 ding KLRB1 (encoding CD161), largely reflect tumor-associated leukocytes.

130 These cells play a major role in rebuilding tumor-associated lymphatic and blood vessels, thereby pr

131 t and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived su

132 restingly, HOXB7 overexpression also induced tumor-associated macrophage (TAM) recruitment and acquis

133 Tumor-associated macrophage (TAM) significantly contribu

134 prised of discrete MHC-II(hi) and MHC-II(lo) tumor-associated macrophage (TAM) subpopulations that or

135 er, MUC1-ST induced macrophages to display a tumor-associated macrophage (TAM)-like phenotype, with i

136 -infiltrating CD8(+) and CD4(+) T cells, and tumor-associated macrophage activation.

137 Here, we report that caspase-1 promotes tumor-associated macrophage differentiation by cleaving

138 endogenous regulatory mechanisms underlying tumor-associated macrophage differentiation remain large

139 accumulation of lipid droplets and promoting tumor-associated macrophage differentiation.

140 xpression by T cells is necessary for proper tumor-associated macrophage expression of IFNgamma-induc

141 Nuclear density, tumor-associated macrophage infiltration, and nuclear mo

142 mune checkpoints other than PD-1; modulating tumor-associated macrophage phenotype from tumor-promoti

143 3.5 million measured cells, we identified 17 tumor-associated macrophage phenotypes, 22 T cell phenot

144 tumor-induced macrophages represent a major tumor-associated macrophage population, which can furthe

145 peutic approach to prevent tumor progression.Tumor associated macrophages (TAMs) promote cancer progr

146 s to IH accelerated tumor progression with a tumor associated macrophages (TAMs) shift towards a pro-

147 Armored CAR T cells mediated depletion of tumor associated macrophages and resisted endogenous PD-

148 cells restored activation of proinflammatory tumor-associated macrophages (TAM) and intratumoral immu

149 Tumor-associated macrophages (TAM) and myofibroblasts ar

150 Tumor-associated macrophages (TAM) are important compone

151 Tumor-associated macrophages (TAM) are known to limit th

152 Tumor-associated macrophages (TAM) contribute to all asp

153 Accumulation of tumor-associated macrophages (TAM) correlates with malig

154 among them being of monocytic origin such as tumor-associated macrophages (TAM) or myeloid-derived su

155 In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to one h

156 with tumor-associated neutrophils (TAN) and tumor-associated macrophages (TAM) versus females, and t

157 nt creates an immunosuppressive signature on tumor-associated macrophages (TAM), which favors express

158 d markedly in primary melanomas and CD163(+) tumor-associated macrophages (TAM).

159 ber and metastatic potential of infiltrating tumor-associated macrophages (TAM).

160 nd constitutive TTP expression in late-stage tumor-associated macrophages (TAM).

161 h contributes to differentiation of MDSCs to tumor-associated macrophages (TAMs) and DCs.

162 Tumor-associated macrophages (TAMs) are abundant in glio

163 Tumor-associated macrophages (TAMs) are essential compon

164 nant disease progression, both apoptosis and tumor-associated macrophages (TAMs) are often associated

165 In cancer, tumor-associated macrophages (TAMs) are recruited to the

166 pressor cells (MDSCs) and differentiation of tumor-associated macrophages (TAMs) are the major factor

167 Accumulation of tumor-associated macrophages (TAMs) associates with mali

168 Tumor-associated macrophages (TAMs) can influence ovaria

169 Tumor-associated macrophages (TAMs) expressing the multi

170 The role of tumor-associated macrophages (TAMs) in cancer is often c

171 ensive reports have defined the dual role of tumor-associated macrophages (TAMs) in tumor development

172 myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) into tumor microenvi

173 Tumor-associated macrophages (TAMs) play an essential ro

174 In particular, tumor-associated macrophages (TAMs) produce many cytokin

175 Tumor-associated macrophages (TAMs) promote tumor develo

176 In this context, tumor-associated macrophages (TAMs) represent key regula

177 Among tumor-infiltrating immune cells, tumor-associated macrophages (TAMs) take a center stage

178 of cancers is known to favor polarization of tumor-associated macrophages (TAMs) to alternatively act

179 ted within the tumor microenvironment induce tumor-associated macrophages (TAMs) to differentiate int

180 PD-L1 is also expressed by nonmalignant tumor-associated macrophages (TAMs), but the relationshi

181 The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs), either of periphera

182 , we analyzed its expression and function in tumor-associated macrophages (TAMs).

183 Dual therapy also led to changes in tumor-associated macrophages (TAMs).

184 t M1-type macrophages, and the occurrence of tumor-associated macrophages (TAMs).

185 undly influence or depend on the function of tumor-associated macrophages (TAMs).

186 ionable, given the well-known limitations of tumor-associated macrophages (TAMs).

187 ), resident natural killer cells (NKRs), and tumor-associated macrophages (TAMs).

188 ocytes that appear in the circulation and as tumor-associated macrophages (TAMs).

189 Our data demonstrates that tumor-associated macrophages also form them.

190 umor-bearing mice also exerted morphology of tumor-associated macrophages and expressed high levels o

191 eveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute

192 s and a correlation between B7-H4-expressing tumor-associated macrophages and FoxP3(+) regulatory T c

193 s, subsequently affecting the recruitment of tumor-associated macrophages and IL17A synthesis.

194 Recruitment of tumor-associated macrophages and neutrophils (TAM and TA

195 ctivity suppresses alternative activation of tumor-associated macrophages and the growth of colon can

196 rowth, but instead increased the presence of tumor-associated macrophages and the metastatic spread o

197 cal for cytokine and chemokine production in tumor-associated macrophages and was necessary for the g

198 Tumor-associated macrophages are increasingly viewed as

199 Other immune cells such as tumor-associated macrophages can have other pro-tumorige

200 Tumor-associated macrophages constitute a major componen

201 -derived xenograft resulted in a shift among tumor-associated macrophages from the immunosuppressive

202 e of Immunity, Zhu et al. (2017) report that tumor-associated macrophages in a mouse model of pancrea

203 cretion of proinflammatory cytokine IL6 from tumor-associated macrophages in a TLR7/8-dependent manne

204 We confirmed increased tumor-associated macrophages in bevacizumab-resistant gl

205 large-scale single-cell RNA-seq analysis of tumor-associated macrophages in gliomas has unveiled a n

206 (FLIM) as a means to non-invasively identify tumor-associated macrophages in the intact mammary tumor

207 Since B7-H4 is expressed on tumor cells and tumor-associated macrophages in various cancer types, th

208 In contrast, there was a paucity of NLRC4+ tumor-associated macrophages observed in human metastati

209 Furthermore, tumor-associated macrophages of the corresponding tumors

210 Interactions between tumor cells and tumor-associated macrophages play critical roles in the

211 d use of these inhibitors as tools to ablate tumor-associated macrophages that enable malignant progr

212 We also defined a population of tumor-associated macrophages that increase dramatically

213 immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one, w

214 cinoma cells secrete VEGFA, which stimulates tumor-associated macrophages to produce CXCL1 in the pri

215 ary malignant cell-secreted VEGFA stimulates tumor-associated macrophages to produce CXCL1, which rec

216 of cancer immunotherapies aiming to polarize tumor-associated macrophages toward an antitumor phenoty

217 PD-L1 is expressed on tumor cells, tumor-associated macrophages, and other cells in the tum

218 ied CtsZ, which is predominantly supplied by tumor-associated macrophages, as the compensatory protea

219 induces not only an expected deprivation of tumor-associated macrophages, but also an accumulation o

220 expression in epithelial cells is induced by tumor-associated macrophages, contributing to the recipr

221 In contrast to tumor-associated macrophages, myeloid-derived suppressor

222 sized that a tumor-extrinsic factor, notably tumor-associated macrophages, promotes and contributes t

223 Compared to tissue-resident tumor-associated macrophages, these newly differentiated

224 osis in tumor cells, as well as depletion of tumor-associated macrophages, vascular ectasia, and hemo

225 ted on the surface of macrophages, including tumor-associated macrophages.

226 but not primary tumor growth, which involves tumor-associated macrophages.

227 as revealed the extensive presence of NLRC4+ tumor-associated macrophages.

228 by driving the recruitment of MMP9-positive tumor-associated macrophages.

229 nd their presence correlated with that of M2 tumor-associated macrophages.

230 target genes in CD163(+) tissue-resident and tumor-associated macrophages.

231 NF1 deficiency resulted in increased tumor-associated macrophages/microglia infiltration.

232 The identified tumor-associated metabolic changes support theories of d

233 s a result of impaired stratification of the tumor-associated microbiota and toll-like receptor signa

234 gical roles of endothelial cells, microglia, tumor-associated microglia/macrophage, neurons, astrocyt

235 nal dysfunction by operating at the level of tumor-associated microglial activation.

236 Identifying the tumor associated molecules that regulate neutrophil infi

237 A third population, which resembles tumor-associated monocytes, expresses a large number of

238 This study investigated the role of tumor-associated MPhi in lung cancer.

239 ed LLC1 tumor growth and metastasis, shifted tumor-associated MPhi toward M1 polarization, suppressed

240 Expression of tumor-associated MUC1 (tMUC1) positively correlated with

241 d characterized 13 IgGs specific for several tumor-associated MUC1 epitopes with a wide range of bind

242 We also characterize NOTCH3 tumor-associated mutations that result in activation of

243 Here, we demonstrate that tumor-associated mutp53 promotes cancer cell survival up

244 mounting evidence has demonstrated that many tumor-associated mutp53 proteins not only lose the tumor

245 modulation of KDR/ID2 signaling may restrict tumor-associated myeloid cells and could potentially be

246 Its importance, however, in tumor-associated myeloid cells is unknown.

247 Tumor-associated myeloid cells, including dendritic cell

248 he estimation of recruitment and activity of tumor-associated myeloid immune cells.

249 However, an outlier subset of tumor-associated ncRNAs, typically of recent evolutionar

250 tes (CTLs) directly recognize and respond to tumor-associated neoantigens (TANs) in much the same way

251 to alphaVbeta3 integrins present in both the tumor-associated neovasculature and on the surface of ov

252 RT-recruited tumor-associated neutrophils (RT-Ns) exhibited an increa

253 se tumors were more heavily infiltrated with tumor-associated neutrophils (TAN) and tumor-associated

254 ted data about the phenotype and function of tumor-associated neutrophils (TANs) in humans.

255 uced pulmonary neutrophilic inflammation and tumor-associated neutrophils were reduced in Tlr2/4(-/-)

256 epitopes is a hallmark of many cancers, and tumor-associated oligosaccharides are actively investiga

257 The tumor-associated osteoblasts in PCa bone metastasis spec

258 for protecting tumor-infiltrating cells from tumor-associated oxidative stress-mediated repression.

259 t a potent CD8(+) T cell responses employing tumor-associated peptide antigens, are typically ineffec

260 anistic insight on proteasomal regulation of tumor-associated peptide/HLA antigen complexes, and yiel

261 These findings provide insight into tumor-associated PMNs and reveal a context-specific capa

262 captures TNBC heterogeneity and informs how tumor-associated properties interact to affect prognosis

263 Furthermore, matriptase is unique among tumor-associated proteases in that epithelial stem cell

264 This hypothesis was supported using the tumor-associated protein He4, which, when endocytosed by

265 ly reported as an interferon (IFN)-inducible tumor-associated protein, harbors nucleic acid-binding d

266 found that the VJ-independent components of tumor-associated repertoires diverge more from their cor

267 This not only expands the range of tumor-associated self-antigens that are amenable for T-c

268 Therapeutic strategies that target tumor-associated sialosides may therefore potentiate ant

269 Here, we investigate the roles of tumor-associated signals in regulating endothelial cell

270 tumorigenic capacity of BMCs in response to tumor-associated signals.

271 Cancer cells exert mastery over the local tumor-associated stroma (TAS) to configure protective im

272 Furthermore, ormeloxifene depleted tumor-associated stroma in xenograft tumor tissues by in

273 llenge, we investigated the transcriptome of tumor-associated stroma isolated from TNBC (n = 57).

274 Tumor tissue and tumor-associated stroma showed evident changes in their

275 ells (MSCs) that are actively recruited into tumor-associated stroma, we assessed the impact of MSCs

276 tic evaluation of the functional capacity of tumor-associated stromal cells revealed that myeloid cel

277 romal cells, induce partial reprogramming of tumor-associated stromal cells, and respond to therapy.

278 ingly proceeds indirectly through ERalpha in tumor-associated stromal fibroblasts.

279 as potent anticancer properties and depletes tumor-associated stromal tissue by inhibiting the SHH si

280 We considered that tumor-associated T cells might promote malignancy via di

281 tion regulates the activity and expansion of tumor-associated T cells.

282 ical response resulting in the production of tumor-associated (TA) autoantibodies.

283 o demonstrated more substantial expansion of tumor-associated TCR clones in the peripheral blood 3 we

284 reg cells suppressed anti-tumor responses in tumor-associated tertiary lymphoid structures (TA-TLSs).

285 zed that VWF fibers in tumor vessels promote tumor-associated thromboembolism and metastasis.

286 Tumor-associated variants of VHL differentiate between t

287 neal ovarian cancer allowed visualization of tumor-associated vasculature and its contrast against no

288 The structure and molecular signature of tumor-associated vasculature are distinct from those of

289 ously unappreciated role in the formation of tumor-associated vasculature which could possibly offer

290 ment model under the influence of functional tumor-associated vasculature.

291 mechanism with high selectivity for CRC and tumor-associated vasculature.

292 impairs virus function, and we suggest that tumor-associated viruses may be more likely to contain D

293 red GUCY2C signaling, eliminating intestinal tumors associated with a high calorie diet.

294 r cells and its expression in primary breast tumors associated with a higher likelihood of metastatic

295 mutations in the catalytic subunit of PKA in tumors associated with Cushing's syndrome, a kidney diso

296 that MUC1, TAK1 and TRAF6 are upregulated in tumors associated with decreased survival and that MUC1-

297 he treatment of ovarian and other epithelial tumors associated with elevated levels of EGFR and espec

298 o excessive cortisol production, and also in tumors associated with fibrolamellar hepatocellular carc

299 established to accelerate new treatments for tumors associated with neurofibromatosis type 1 (NF1).

300 xpression defines basal-like and HER2 breast tumors associated with poor clinical outcome.