ライフサイエンスコーパス: tumour cell

1 LL3 expression (expression in 50% or more of tumour cells).

2 that targeted alterations are present in all tumour cells.

3 acrophages engulf and destroy haematopoietic tumour cells.

4 ivity-dependent increase in EGFR activity in tumour cells.

5 ead to apoptosis, necrosis, and autophagy of tumour cells.

6 n by reducing the proliferative potential of tumour cells.

7 strategy to decrease metastatic capacity of tumour cells.

8 bute to the evolution of treatment-resistant tumour cells.

9 ment of successful metastases from surviving tumour cells.

10 wide analyses and their ability to eliminate tumour cells.

11 lular contact nor factors released by BCR(+) tumour cells.

12 host immune system to recognize and destroy tumour cells.

13 surveys or somatic mutation catalogues from tumour cells.

14 t promotes proliferation in advanced primary tumour cells.

15 novel synthetic lethal approach to targeting tumour cells.

16 nts with PD-L1 expression on at least 50% of tumour cells.

17 in those samples are actually present in all tumour cells.

18 els redirected the metastasis of bone-tropic tumour cells.

19 t payload gradually releases to neighbouring tumour cells.

20 suppressor, inducing G1 cell cycle arrest in tumour cells.

21 ce metastatic growth of already disseminated tumour cells.

22 gents by increasing their bioavailability in tumour cells.

23 rom combinations with drugs targeting BCR(-) tumour cells.

24 es, including those derived from circulating tumour cells.

25 ctive oxygen species and causes apoptosis of tumour cells.

26 apeutic target to overcome immune evasion by tumour cells.

27 is affected by the similarity to endogenous tumour cells.

28 ht correlate with PD-L1 expression levels in tumour cells.

29 ized growth of transplanted MMTV-PyMT breast tumours cells.

30 ISPR/Case9 knocking out Hsp90alpha nullifies tumour cells' ability to migrate, invade and metastasize

31 ontrolled proliferation, a subset of primary tumour cells acquires additional traits/mutations to tri

32 ed form of RXRalpha (tRXRalpha), produced in tumour cells, activates phosphoinositide 3-kinase (PI3K)

33 Understanding how tumour cells adapt themselves to survive hypoxia may hel

34 Thus, Amigo2 regulated tumour cell adhesion to liver endothelial cells and form

35 allows the characterization of heterogeneous tumour cells along with neighbouring stromal and immune

36 ate; it involves contributions from both the tumour cell and tumour microenvironment ('host', which i

37 taneously into mice to localize transplanted tumour cells and deliver immunomodulatory factors in a c

38 w targeting of multiple surface receptors on tumour cells and endothelial or immune cells in the tumo

39 umoral heterogeneity, which is shaped by the tumour cells and immune cells in the surrounding microen

40 by modifying the populations of circulating tumour cells and it could be extended to other cancer me

41 nt correlation between high EGFR activity in tumour cells and macrophage-tumour cell proximity was fo

42 inistration, triggers photodynamic damage of tumour cells and microvessels, and simultaneously initia

43 g a mutually beneficial relationship between tumour cells and neurons.

44 0%) had increased percentages of Galectin-9+ tumour cells and of Foxp3+ lymphocytes, respectively.

45 ly, the effects of CDK4/6 inhibitors both on tumour cells and on regulatory T cells are associated wi

46 oxaliplatin and pyrolipid-induced PDT kills tumour cells and provokes an immune response, resulting

47 s inhibitors that selectively kill aneuploid tumour cells and repress translation of specific messeng

48 Functional interplay between tumour cells and their neoplastic extracellular matrix p

49 SCLC, analysed by PD-L1 expression levels on tumour cells and tumour-infiltrating immune cells and in

50 ith PD-L1 immunohistochemistry expression on tumour cells and tumour-infiltrating immune cells, sugge

51 s negatively with phagocytic potency against tumour cells, and blockade of PD-1-PD-L1 in vivo increas

52 ctivation of Notch signalling in a subset of tumour cells, and the presence of these cells may serve

53 erates cell:cell repulsion events that drive tumour cells apart.

54 forces to increase immune cytokine-mediated tumour cell apoptosis.

55 s interactions between the immune system and tumour cells are governed by a complex network of cell-c

56 HER2(-) subpopulations: HER2(+) circulating tumour cells are more proliferative but not addicted to

57 cell hypothesis, that a small population of tumour cells are responsible for tumorigenesis and cance

58 s known about the immediate fate of incoming tumour cells as they colonize this tissue, and even less

59 ort the clinical use of miRNA or circulating tumour cells as useful prognostic markers for this disea

60 ession was scored by immunohistochemistry in tumour cells (as percentage of PD-L1-expressing tumour c

61 In tissues and tumours, cell behaviours are regulated by multiple time-

62 d Tim-3 in lymphocytes, and of Galectin-9 in tumour cells between paired primary and recurrent NPC fr

63 irculating tumour cells in blood and overall tumour cell burden by over 90% and reduce solid tumour g

64 y was defined as expression in 1% or more of tumour cells by immunohistochemistry.

65 press fatty acid synthesis and elongation in tumour cells by targeting ATP citrate lyase and fatty ac

66 Tumour cells can use strategies that make them resistant

67 d form of mitochondrial energy metabolism in tumour cells, causing changes in mitochondrial enzyme ac

68 ous ferumoxytol treatment before intravenous tumour cell challenge prevented development of liver met

69 known about the mechanisms through which the tumour cell co-opts a normal fibroblast.

70 efficient at phagocytosis of haematopoietic tumour cells, compared with non-haematopoietic tumour ce

71 nduction in macrophages that are cultured in tumour cell-conditioned media as well as an iNOS activit

72 ytansinoids, indiscriminately radiosensitize tumour cells, conjugating these potent anti-tubulins to

73 nd provide trophic support to neuroendocrine tumour cells, consistent with a pro-tumorigenic role.

74 henotypes within patient-derived circulating tumour cells, contributing to progression of breast canc

75 n to selectively bind to a model circulating tumour cell (CTC) line, MCF-7, a metastatic breast cance

76 wth in a highly aggressive NSCLC circulating tumour cell (CTC) patient derived explant (CDX) mouse mo

77 Circulating tumour cells (CTCs) are rare tumour cells found in the c

78 Metastasis-competent circulating tumour cells (CTCs) experience oxidative stress in the b

79 The role of circulating tumour cells (CTCs) in advanced oesophageal cancer (EC)

80 Primary tumours liberate circulating tumour cells (CTCs) into the blood and we have developed

81 erial effects on the analyses of circulating tumour cells (CTCs) selected from the peripheral blood o

82 C) is characterized by prevalent circulating tumour cells (CTCs), early metastasis and poor prognosis

83 FBXL4 deletion is detectable in circulating tumour cells (CTCs), making it a potential prognostic bi

84 selective CDK4/6 inhibitors not only induce tumour cell cycle arrest, but also promote anti-tumour i

85 These compounds induce tumour cell death and enhance cytotoxicity with chemothe

86 that this inflammatory milieu may potentiate tumour cell death by supporting immune activation and in

87 a with monoclonal antibody, 1G6-D7, enhanced tumour cell death under hypoxia.

88 tibody decreased proliferation and increased tumour cell death, but did not affect survival when comb

89 Knocking out Hsp90beta leads to tumour cell death.

90 mour-associated endothelial cells to enhance tumour cell death.

91 erapies including chemotherapy aim to induce tumour cell death.

92 athway redundancy in GBM and, hence, promote tumour cell death.

93 potential quantitative imaging biomarker for tumour cell density and is widely used to detect early t

94 s regulated by increased HER2 expression and tumour-cell density involving microRNA-mediated progeste

95 ial super-enhancer-associated genes on which tumour cells depend.

96 ellular immunity against viral infection and tumour cells depends on antigen presentation by major hi

97 n of tumorigenesis in orthotopic circulating tumour cell-derived tumour models.

98 Mechanistically, host hepatocyte, but not tumour cell-derived vascular endothelial growth factor (

99 Rather than targeting tumour cells directly, elements of the tumour microenvir

100 e responses are known to select (immunoedit) tumour cells displaying immunoevasive properties.

101 cancer progression, although the pathways of tumour cell dissemination are unclear.

102 ce that tumour-infiltrated mMDSCs facilitate tumour cell dissemination from the primary site by induc

103 ing the effects of SNS signalling to prevent tumour cell dissemination through lymphatic routes may p

104 s indicate that loss of VHL could be driving tumour cell dissemination through stabilization of HIF-1

105 mour lymphatic architecture and lymphogenous tumour cell dissemination.

106 K2 phosphorylation/activation to enhance the tumour cell DNA damage response.

107 Unlike in tumour cells, DNA mutations are rare in CAFs, raising th

108 termined that phagocytosis of haematopoietic tumour cells during SIRPalpha-CD47 blockade was strictly

109 and CD47 expressed on tumour cells, improves tumour cell elimination in vitro and in vivo, suggesting

110 Cancer stem cells (CSC) are a subset of tumour cells endowed with stem-like properties, which pl

111 n and around tumours to provide pathways for tumour cell escape.

112 ell interactions and the mechanisms by which tumour cells evade antitumour immunity, the field of can

113 tion, highlighting the complexities by which tumour cells evade chemotherapeutic interventions and ac

114 substantial destruction of patients' kidney tumour cells ex vivo.

115 We find that bulk AML tumour cells exhibit distinct open chromatin loci that r

116 addition to being highly heterogeneous, GBM tumour cells exhibit high adaptive capacity to targeted

117 Patient-derived acute myeloid leukaemia tumour cells exhibit high sensitivity to CC-885, indicat

118 BCR(-) tumour cells exhibit increased GSK3beta activity and are

119 reliance on aerobic glycolysis, in promoting tumour cell exosome release.

120 Here we show that tumour cell exosomes secretion is controlled by pyruvate

121 operate as a paracrine signal that sustains tumour cell expansion and progression, suggesting that a

122 umours, 84% of whom had acquired circulating tumour cells expressing HER2.

123 Among patients with at least 50% of tumour cells expressing PD-L1, overall survival was sign

124 First, CDK4/6 inhibitors activate tumour cell expression of endogenous retroviral elements

125 vasculogenic mimicry (VM), a process whereby tumour cells form 'endothelial-like' vessels.

126 Circulating tumour cells (CTCs) are rare tumour cells found in the circulatory system of certain

127 Tumour cells frequently overexpress the ligand for PD-1,

128 Here we analyse circulating tumour cells from 19 women with ER(+)/HER2(-) primary tu

129 Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zon

130 lls by almost two-fold in primary culture of tumour cells from Apc(Min/+) mice.

131 These pathways protect tumour cells from DNA damage and replication stress and

132 RC1 metabolic checkpoint, thereby protecting tumour cells from MYC-driven cell death, and indeed, MYC

133 Tumour cells fulfil the bioenergetic and biosynthetic ne

134 The non-coding regions of tumour cell genomes harbour a considerable fraction of t

135 Among the 102 tumour cell genomes we analyse, small insertions are fre

136 ession of CSC markers in CCA-SPH compared to tumour cells growing as monolayers.

137 y proliferates by fermentation, analogous to tumour cells growing by aerobic glycolysis, whereas on n

138 so costimulate T-cell activation and promote tumour cell growth and metastasis.

139 they have been implicated in suppression of tumour cell growth by inhibition of canonical Wnt signal

140 ated KRAS at the plasma membrane and induced tumour cell growth in vitro and in vivo.

141 ed in decreased GRP78 secretion and impaired tumour cell growth in vitro.

142 ed that extracellular lumican decreases PDAC tumour cell growth in xenograft and syngeneic orthotopic

143 ability to cause a significant reduction in tumour cell growth, irrespective of TP53 status, using a

144 caused a profound cell growth inhibition in tumour cells harbouring KRAS mutations.

145 genomic analysis across large populations of tumour cells has provided key insights into cancer biolo

146 Although HER2(+) and HER2(-) circulating tumour cells have comparable tumour initiating potential

147 Yet, imaging of tumour cell heterogeneity and the hallmarks of cancer ha

148 Elevated tumour cell heterogeneity is linked with progression, th

149 r matrix represents a nutrient reservoir for tumour cells highlighting the metabolic flexibility of t

150 on originating from stromal cells and affect tumour cells, highlighting the potent inhibitory effect

151 guide RNAs, and profiled genes whose loss in tumour cells impaired the effector function of CD8(+) T

152 to make a distinction between LS174T and U87 tumour cells implanted in the mouse brain.

153 rophages, or of its ligand CD47 expressed on tumour cells, improves tumour cell elimination in vitro

154 non-neuroendocrine fate switch in 10-50% of tumour cells in a mouse model of small-cell lung cancer

155 sed metastasis of weakly metastatic, non-EMT tumour cells in a paracrine manner, in part by non-cell

156 ccine (Candid#1) preferentially replicate in tumour cells in a variety of murine and human cancer mod

157 tment of immune cytokine, reduce circulating tumour cells in blood and overall tumour cell burden by

158 sites, bacteria, blood cells and circulating tumour cells in blood.

159 or ganglioneuroblastoma at diagnosis or have tumour cells in bone marrow with increased urinary catec

160 ve focused on the identification of residual tumour cells in the bone marrow using flow cytometry or

161 although insulin is mitogenic for intestinal tumour cells in vitro, impaired insulin action in the tu

162 at targeted polymeric particles delivered to tumour cells in vivo amplify the apoptotic effect of a s

163 heterogeneity of EGFR signalling activity in tumour cells in vivo.

164 delays the growth of primary and metastatic tumour cells in vivo.

165 Circulating tumour cells in women with advanced oestrogen-receptor (

166 mour cells, compared with non-haematopoietic tumour cells, in response to SIRPalpha-CD47 blockade.

167 oss of alpha3(V) chains normally produced by tumour cells, in which they affect growth by enhancing t

168 of the protein tyrosine phosphatase PTPN2 in tumour cells increased the efficacy of immunotherapy by

169 In ARID1A mutant tumour cells, inhibition of ATR triggers premature mitot

170 HER2(+) and HER2(-) circulating tumour cells interconvert spontaneously, with cells of o

171 sed highly leaky hepatic vasculatures permit tumour cell intravasation and extravasation.

172 rates a microenvironment that contributes to tumour cell invasion and angiogenesis.

173 lling to create a permissive environment for tumour cell invasion and promotion of distant metastasis

174 may contribute to genome instability and to tumour cell invasion.

175 ated melanoma patients, MHC-II positivity on tumour cells is associated with therapeutic response, pr

176 ce of TGFbeta, this CXCL12 effect of MSCs on tumour cells is relieved.

177 We show that VEGFC derived from tumour cells is required for stress to induce lymphatic

178 The PTEN level in PTEN-loss brain metastatic tumour cells is restored after leaving the brain microen

179 This allows for potent tumour cell killing, and an overall decreased metastatic

180 Here we show that, in tumour cells lacking LKB1, NUAK1 activity is maintained

181 this adaptive PTEN loss in brain metastatic tumour cells leads to an increased secretion of the chem

182 epithelial cell line MCF10A and the uMUC1(-) tumour cell line U87.

183 A subset of tumour cell lines exhibit dependence on MCL1 expression

184 ollection of 533 genetically annotated human tumour cell lines.

185 Cultured circulating tumour cells maintain discrete HER2(+) and HER2(-) subpo

186 s establishes miR-22 as a novel regulator of tumour cell metabolism, a function that could contribute

187 rogression and acts as critical regulator of tumour cell metabolism.

188 reveals a potential mechanism that promotes tumour cell migration and infers a strategy to decrease

189 e secretion or biogenesis leads to defective tumour cell migration associated with increased formatio

190 estabilization, suppressed EMT and decreased tumour cell migration, invasion, and metastasis.

191 Glutamine starvation rendered tumour cells more resistant to Chk1 inhibitor-induced DN

192 cells undergoing active replication rendered tumour cells more resistant to Chk1 inhibitor-induced DN

193 e therapies for cancer resulting in enhanced tumour cell motility.

194 To colonize distant organs, circulating tumour cells must overcome many obstacles through mechan

195 1 from disparate cellular sources, including tumour cells, myeloid or other immune cells can similarl

196 Tumour cells not only are activated by genetic and epige

197 -expressed in CSCs when compared to non-stem-tumour-cells (nsTCs).

198 Methods to reliably define tumour cell of origin from primary, bulk tumour cell sam

199 Moreover, we show that the tumour cell of origin influences the frequency of malign

200 tially minimises the radiation damage to non-tumour cells of healthy tissues.

201 en receptors (CARs), so that they can combat tumour cells once they are reinfused.

202 rporate immune-based therapies into existing tumour cell or endothelial-derived therapies-eg, with ki

203 at least 1% PD-L1 expression detected on the tumour cells or in tumour stroma, as determined by immun

204 ion of DCs loaded with allogeneic-IgG-coated tumour cells or intratumoral injection of allogeneic IgG

205 evel of PD-L1 expression (ie, at least 1% of tumour cells or stroma that were PD-L1-positive by immun

206 opulation TC1/2/3 or IC1/2/3 (>/=1% PD-L1 on tumour cells or tumour-infiltrating immune cells).

207 Many types of human tumour cells overexpress the dual-specificity phosphatas

208 nt increase in the expression of Galectin-9+ tumour cells (p < 0.001) and Foxp3+ lymphocytes (p < 0.0

209 has been reported to be secreted from solid tumour cells, participating in cell-cell communication i

210 The greatest focus has been on tumour-cell PD-L1 expression.

211 e pro-phagocytic receptor(s) responsible for tumour cell phagocytosis is(are) largely unknown.

212 e switching and provide proof that targeting tumour cell plasticity is a viable therapeutic opportuni

213 widely accepted that dynamic and reversible tumour cell plasticity is required for metastasis, howev

214 with poor outcomes because of heterogeneous tumour cell population including mature non-stem-like ce

215 arising from either intra or extraprostatic tumour cell populations, at early and late stages in the

216 amically maintained within a wide variety of tumour cell populations.

217 mour cells rather than less advanced central tumour cell populations.

218 ital to support both mature and immature GBM tumour cell populations.

219 ty also generated protective effects against tumour-cell populations that lacked the HER2 receptor.

220 ng data but heterogeneity in the fraction of tumour cells present across samples hampered accurate qu

221 Because tumour cells proliferate in suboptimal environments, and

222 jC histone demethylases (KDMs) are linked to tumour cell proliferation and are current cancer targets

223 characterize the effects of dexamethasone on tumour cell proliferation and death, and to identify gen

224 sunitinib or axitinib resulted in decreased tumour cell proliferation and enhanced cell death, where

225 45Ala), reduces gene expression and inhibits tumour cell proliferation and tumour growth.

226 ing antioxidant, anti-inflammatory and human tumour cell proliferation inhibitory assays.

227 g mice, dexamethasone pretreatment decreased tumour cell proliferation without affecting tumour cell

228 2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development.

229 -driven increase in Akt activation, and thus tumour cell proliferation, as a potential mechanism of d

230 by reverting EMT/CSC phenotype and promoting tumour cell proliferation.

231 EGFR activity in tumour cells and macrophage-tumour cell proximity was found to in part account for t

232 ffect lymphoma growth, BCR-negative (BCR(-)) tumour cells rapidly disappear in the presence of their

233 te from evolutionary advanced extraprostatic tumour cells rather than less advanced central tumour ce

234 Inhibition of cyclin D3-CDK6 in tumour cells reduces flow through the PPP and serine pat

235 rine, which are often rapidly metabolised by tumour cells, regulate rapamycin-resistant mTORC1 in a P

236 function of PKM2, an enzyme associated with tumour cell reliance on aerobic glycolysis, in promoting

237 Tumour cells rely on specific tropomyosin-containing act

238 nancy, yet the intrinsic effects of force on tumour cells remain poorly understood.

239 erscores a potential mechanism through which tumour cells retaining elevated levels of plasticity acq

240 ine tumour cell of origin from primary, bulk tumour cell samples has been a challenge.

241 ng each cell of origin tested, from bulk AML tumour cell sampling.

242 Tumour cells secrete exosomes that are involved in the r

243 ple signalling pathways; HER2(-) circulating tumour cells show activation of Notch and DNA damage pat

244 m, LUV-TRAIL being more efficient in killing tumour cells, showing no effect on the integrity of endo

245 s antigen melanoma antigen-A4 (MAGE-A4) as a tumour cell-specific RAD18-binding partner and an activa

246 al role for NUAK1 in supporting viability of tumour cells specifically when MYC is overexpressed.

247 mune memory and decreased activities against tumour-cell subpopulations with low targeting receptor l

248 gradable polymeric particles tethered to the tumour cell surface via polyethylene glycol linkers, inc

249 They use antibodies that are specific to tumour cell-surface proteins and, thus, have tumour spec

250 growth but lead to paradoxical promotion of tumour cell survival upon treatment with mTOR inhibitors

251 the view that BCR signalling is required for tumour cell survival.

252 r suppressor and other proteins critical for tumour cell survival.

253 C, CS1, CD319), expressed on macrophages and tumour cell targets.

254 our cells (as percentage of PD-L1-expressing tumour cells TC3>/=50%, TC2>/=5% and <50%, TC1>/=1% and

255 R-mediated crosstalk between vasculature and tumour cells that can be exploited to improve the effica

256 plication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutatio

257 cision medicines exert selective pressure on tumour cells that leads to the preferential growth of re

258 y, lung metastases mainly consist of non-EMT tumour cells that maintain their epithelial phenotype.

259 umour cells to survive likely comes from the tumour cells themselves or its associated stromal cells.

260 microenvironment that can shelter incipient tumour cells, thus allowing them to proliferate and prog

261 increased the sensitivity of A2058 and U2OS tumour cells to Chk1 inhibition.

262 amine starvation restored the sensitivity of tumour cells to Chk1 inhibitor-induced DNA damage.

263 demonstrate that defects in ARID1A sensitize tumour cells to clinical inhibitors of the DNA damage ch

264 -deficient HCT116 cells, and also sensitizes tumour cells to doxorubicin and 5-Fluorouracil.

265 en disrupted in mouse, modify the ability of tumour cells to establish metastatic foci, with 19 of th

266 This multi-stage process requires tumour cells to survive in the circulation, extravasate

267 Altered metabolism is needed for tumour cells to survive in this environment, but the met

268 g tumour, whatever factor(s) that allows the tumour cells to survive likely comes from the tumour cel

269 es ovarian tumour progression and sensitizes tumour cells to the treatment of PI3K/AKT inhibitor.

270 SCLC, especially cancers expressing PD-L1 on tumour cells, tumour-infiltrating immune cells, or both.

271 he apoptotic effect of an immune cytokine on tumour cells under fluid shear exposure by as much as 50

272 Pleural disseminated, mutant KRAS bearing tumour cells upregulate and systemically release chemoki

273 ransfected this biosensor into EGFR-positive tumour cells using targeted lipopolyplexes bearing EGFR-

274 pression patterns in colon cancer versus non tumour cells using the previously selected suitable norm

275 ly enhance the outgrowth of brain metastatic tumour cells via enhanced proliferation and reduced apop

276 novel strategy for the genetic profiling of tumour cells via integrated "amplification-to-detection"

277 3 provides a strategic survival advantage to tumour cells via its effects on mTOR.

278 nt to a novel role for calcium in supporting tumour cell viability and clarify the synthetic lethal i

279 ant inhibition of tumour growth, circulating tumour cell viability and decreased metastasis.

280 tumour cell proliferation without affecting tumour cell viability, but reduced survival when combine

281 In presence of CXCL12, CXCR7 expression on tumour cells was decreased.

282 (31)P-NMR-detecatable metabolite content of tumour cells was examined.

283 Depletion of Hsp90alpha secretion from the tumour cells was permissive to cytotoxicity by hypoxia,

284 ncer with PD-L1 expression on at least 1% of tumour cells were randomly assigned (1:1:1) in blocks of

285 -like signalling from metabolically stressed tumour cells, whereas tumour growth depends on active am

286 or secreted exclusively by aggressive breast tumour cells, which induces CAF conversion.

287 omote cytotoxic T-cell-mediated clearance of tumour cells, which is further enhanced by the addition

288 ations may propagate immunoglobulin-crippled tumour cells, which usually represent a minority of the

289 high-burden tissues were similar to primary tumour cells, which were more heterogeneous and expresse

290 er of PTEN-targeting microRNAs to metastatic tumour cells, while astrocyte-specific depletion of PTEN

291 port to implicate mitophagy in regulation of tumour cells with high CD44 expression, representing a p

292 tment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug,

293 ls, a non-degradable IP3R3 mutant sensitizes tumour cells with low or no PTEN expression to photodyna

294 s of 0 or 1, MET-positive tumours (>/=25% of tumour cells with membrane staining of >/=1+ staining in

295 Here we show that both human and mouse tumour cells with normal expression of PTEN, an importan

296 ereas supplementation of Hsp90alpha-knockout tumour cells with recombinant Hsp90alpha, but not Hsp90b

297 monoclonal antibodies to specifically target tumour cells with the highly potent killing activity of

298 pothesize that metastases are seeded by rare tumour cells with unique properties, which may function

299 ortantly, in clinical breast cancer cohorts, tumour cell Wnt7a expression correlates with a desmoplas

300 This approach is effective in cultured human tumour cells, xenografts and mouse models of colorectal