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 hagocytic marker phosphatidylserine on dying tumour cells.

3 metastatic niches and settlement of residual tumour cells.

4 have been compared to aerobic glycolysis in tumour cells.

5 r immunity in vitro and in mice bearing MC38 tumour cells.

6 i-tumour immunity and induced ferroptosis in tumour cells.

7 metabolic adaptation capacity of RAS-mutant tumour cells.

8 es suppresses Wnt/beta-catenin signalling in tumour cells.

9 e granule proteins that can potentially kill tumour cells.

10 restores TGF-beta responses in ALK-positive tumour cells.

11 d by inactivation of antigen presentation by tumour cells.

12 inhibits the growth of APC mutant colorectal tumour cells.

13 cell cycle arrest and cellular senescence in tumour cells.

14 dominant expression in clustered circulating tumour cells.

15 ally to nfP2X(7) expressed on the surface of tumour cells.

16 of interest, such as those from pathogens or tumour cells.

17 antitumour cytokines and effectively killing tumour cells.

18 clear if they had an impact on the growth of tumour cells.

19 host immune system to recognize and destroy tumour cells.

20 is affected by the similarity to endogenous tumour cells.

21 that targeted alterations are present in all tumour cells.

22 o disease stage and baseline PD-L1 status of tumour cells.

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

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

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

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

27 ce metastatic growth of already disseminated tumour cells.

28 gents by increasing their bioavailability in tumour cells.

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

30 es, including those derived from circulating tumour cells.

31 ctive oxygen species and causes apoptosis of tumour cells.

32 apeutic target to overcome immune evasion by tumour cells.

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

34 acrophages engulf and destroy haematopoietic tumour cells.

35 normal tissues and to TAA expression loss in tumour cells.

36 M1c(-)HLA-A2(+) leukaemia cells or HLA-A2(-) tumour cells.

37 between mobile leucocytes and proliferating tumour cells.

38 the effectiveness of the immune response to tumour cells.

39 s of the major histocompatibility complex on tumour cells.

40 Oncogenic KRAS alters the metabolism of tumour cells(3) in several ways, including increased glu

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

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

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

44 Tumour cells adapt to nutrient deprivation in vivo, yet

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

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

47 However, tumour cells also upregulated the expression of PD-L1, w

48 tumours: 1) loss of antigen presentation on tumour cells and 2) upregulation of TGFbeta and activate

49 cells, thereby decreasing target density on tumour cells and abating T cell activity by promoting fr

50 ade present distinct metabolic challenges to tumour cells and an altered tumour metabolism associated

51 te antitumour responses by direct killing of tumour cells and by participating in cellular networks t

52 of tumour components (including circulating tumour cells and circulating tumour DNA) in bodily fluid

53 ed invasiveness of tumour-microtube-positive tumour cells and glioma growth.

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

55 ics used during cancer surgery may influence tumour cells and immunological response.

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

57 0%) had increased percentages of Galectin-9+ tumour cells and of Foxp3+ lymphocytes, respectively.

58 bitor-mediated elimination of EGFR-amplified tumour cells and propagation of EGFR non-amplified cell

59 unnatural sugars for metabolic labelling of tumour cells and subsequent development of tumour-target

60 isruption of positive-feedback loops between tumour cells and the bone microenvironment.

61 the aberrant glycosylation patterns found in tumour cells and the constituent cell types of the tumou

62 es a complex and dynamic interaction between tumour cells and the immune system.

63 tage process involves contribution from both tumour cells and the tumour stroma to release metastatic

64 data indicate that the interactions between tumour cells and their environment shape the evolutionar

65 operties in the tumour and can regulate both tumour cells and their microenvironment to promote gliom

66 erogeneity, the complex interactions between tumour cells and their microenvironment, and the details

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

68 , its progression, and the interplay between tumour cells and their surrounding microenvironment have

69 em x(c)(-), impairs the uptake of cystine by tumour cells, and as a consequence, promotes tumour cell

70 support tumour growth, increase migration of tumour cells, and remodel the ECM in distant organs to a

71 e ferroptosis-specific lipid peroxidation in tumour cells, and that increased ferroptosis contributes

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

73 lipogenesis-related genes, proliferation of tumour cells, and tumorigenesis in mice.

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

75 However, metastatic tumour cells are exposed to highly perfused and immunoac

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

77 identified double-stranded RNA derived from tumour cells as an upstream signal that induces expressi

78 Within the bone, these disseminated tumour cells, as well as those arising in the context of

79 ed brain metastasis, disrupting invasion and tumour cell association with the brain vasculature, phen

80 Finally, we highlight how tumour cell-autonomous mechanisms might be exploited by

81 ew developments illustrating the key role of tumour cell-autonomous signalling after radiotherapy.

82 that the therapeutic mechanisms operate via tumour-cell-autonomous effects on flux through one-carbo

83 Mechanistically, tumour cells avidly consumed methionine and outcompeted

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

85 (CTCs) and bone marrow-derived disseminated tumour cells (BM-DTCs) can offer clinically relevant bio

86 Furthermore, tumour cell-bound CD47 is implicated in this process.

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

88 SDME expression enhances the phagocytosis of tumour cells by tumour-associated macrophages, as well a

89 Tumour cells can escape from the primary tumour site and

90 orm because they preferentially replicate in tumour cells, can be engineered to express transgenes th

91 c therapies, which are directly cytotoxic to tumour cells, cancer immunotherapy relies on the host's

92 ing culture medium, and their consumption by tumour cells, causes proliferation to be localised at th

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

94 Identification of the lethal tumour cell clones is required to improve survival of pa

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

96 Recombinant TGF-beta1 or tumour cell conditioned medium (TCM) elevated alpha-SMA,

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

98 Our results indicate that the glycocalyx of tumour cells controls the binding and biological activit

99 Tumour cell conversion into a different histological sub

100 binding to tumours, solid tumour slices and tumour cells correlated well with the Y(1)R affinities.

101 from baseline, or conversion of circulating tumour cell count (from >=5 cells per 7.5 mL blood at ba

102 ation method, with balancing for circulating tumour cell count at screening, to receive 400 mg or 300

103 13 (30.2%; 17.2-46.1) of 43; and circulating tumour cell count conversion was achieved in 15 (53.6%;

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

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

106 ncreasing evidence suggests that circulating tumour cells (CTCs) and bone marrow-derived disseminated

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

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

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

110 Circulating tumour cells (CTCs) survive circulatory cytotoxicity, ex

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

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

113 While tumour cell death can result in response to therapy, the

114 the MCL1 inhibitor AZD5991, driving profound tumour cell death that requires BAK/BAX, BIM and BMF, an

115 erapies including chemotherapy aim to induce tumour cell death.

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

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

118 n to generate a pharmacologically actionable tumour cell dependence for survival.

119 Triggered by tumour cell-derived factors like transforming growth fac

120 f alphaKG in p53-deficient tumours can drive tumour-cell differentiation and antagonize malignant pro

121 ycle-specifically results in increased 5hmC, tumour-cell differentiation and decreased tumour-cell fi

122 5-hydroxymethylcytosine (5hmC) accompany the tumour-cell differentiation that is triggered by p53, wh

123 This has to be considered for the design of tumour cell directed nanocarriers to improve the deliver

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

125 Here we show that tumour cells disrupt methionine metabolism in CD8(+) T c

126 y implicated, in providing an exit route for tumour cell dissemination and metastases.

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

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

129 Plasticity in tumour cells drives their transformation towards a pheno

130 The presence of disseminated tumour cells (DTCs) in bone marrow is predictive of poor

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

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

133 How disseminated tumour cells engage specific stromal components in dista

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

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

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

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

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

139 y revealed diffusely and deeply infiltrating tumour cells extending through the dermis, subcutis, orb

140 matically investigate the role of fusions in tumour cell fitness, we utilized RNA-sequencing data fro

141 of metabolic dependencies that contribute to tumour cell fitness.

142 C, tumour-cell differentiation and decreased tumour-cell fitness.

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

144 Tumour cells frequently utilize glutamine to meet bioene

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

146 e binding may also be useful to discriminate tumour cells from healthy cells.

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

148 tion and death generates an cellular flow of tumour cells from the spheroid rim towards its core.

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

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

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

152 ential for tumour initiation and maintaining tumour cell growth in cell culture and xenografts(2,3).

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

154 free amino acids that can be used to support tumour cell growth under nutrient-limiting conditions(2)

155 ainst lipid peroxidation, NO production, and tumour cells growth.

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

157 However, Hsp90alpha-knockout tumour cells have not only lost their own constitutive m

158 AKR1B10(High) tumour cells have reduced glycolytic capacity and depend

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

160 in which defects in DNA repair pathways make tumour cells highly sensitive to the inhibition of PARP

161 PDL1 can be expressed on the surface of tumour cells, immune cells and other cells in the tumour

162 CEMIP depletion in tumour cells impaired brain metastasis, disrupting invas

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

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

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

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

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

168 f mTOR inhibition, rather than the intrinsic tumour cells in GBM.

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

170 ight into the metabolism of normal cells and tumour cells in vivo.

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

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

173 teractions between microglia and AKT1+ brain tumour cells in zebrafish (Chia et al., 2018).

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

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

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

177 and the reducing intracellular conditions of tumour cells induced systemic cytotoxic T-cell responses

178 thought to occur via seeding of circulating tumour cells into the brain microvasculature; within thi

179 ncer subgroups through their effects on both tumour cell-intrinsic and non-cell-autonomous cancer hal

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

181 THBS1 silencing inhibits tumour cell invasion and growth, alone and in combinatio

182 and cancer stem cell traits in disseminated tumour cells is provided by bone vascular niche E-select

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

184 ssion of MHC class II-restricted antigens by tumour cells is required at the site of successful rejec

185 roximity between cytotoxic T lymphocytes and tumour cells is required for effective immunotherapy.

186 Lactate, which is converted from pyruvate in tumour cells, is widely known as an energy source and me

187 lt of the dysregulated metabolic activity of tumour cells, leading to impaired antitumour immune resp

188 1) are also critical for survival of certain tumour cell lines during replication stress, making it a

189 er, HIV-1 restriction by human TRIM5alpha in tumour cell lines is minimal(21) and inhibition of such

190 against Caco-2 and MCF-7 cancer cell lines (tumour cell lines of intestinal and mammary origin, resp

191 d composition and parameters associated with tumour cell lines such as their sensitivity to hypoxia o

192 lation events in two triple- negative breast tumour cell lines, MFM223 and SUM52, that exhibit amplif

193 s assessed by antiproliferation assay on two tumour cell lines, whereas for investigation of type of

194 been identified as dysfunctional in numerous tumour cell lines.

195 In the present study, tumour cell lines: A549 (lung), HCT116 (colon) and MCF-7

196 tumour cells, and as a consequence, promotes tumour cell lipid peroxidation and ferroptosis.

197 flect the mechanical trapping of circulating tumour cells, liver metastasis is also dependent, at lea

198 While tumour cells may be an important source of TAAs for T ce

199 uential paracrine-signalling events, such as tumour-cell-mediated differentiation of macrophages and

200 his establishes a link between nutrition and tumour cell metabolism that may allow for tumour-specifi

201 dietary manipulation can specifically affect tumour-cell metabolism to mediate broad aspects of cance

202 We found that SOX11+DCIS tumour cells metastasize to brain and bone at greater fr

203 Radiotherapy-induced tumour cell micronuclei activate cytosolic nucleic acid

204 eration of the sEV-mediated communication of tumour cells might be a therapy-induced host response, w

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

206 1 from disparate cellular sources, including tumour cells, myeloid or other immune cells can similarl

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

208 cell proliferation and survival, circulating tumour cell number, seeding of cancer cells in distant o

209 er relies in large part upon identifying the tumour cell of origin.

210 In melanoma, tumour cells often experience low glutamine levels, whic

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

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

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

214 gression either directly by interacting with tumour cells or indirectly by shaping the tumour microen

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

216 ble and lead to cell death in nearby exposed tumour cells, osteoblasts and osteoclasts.

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

218 That work includes evaluation of tumour cell PD-L1 expression, gene expression signatures

219 Tumour cell phagocytosis by antigen presenting cells (AP

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

221 Increased tumour cell phagocytosis subsequently enhances antigen c

222 cess driven by the feedback between evolving tumour cell phenotypes and microenvironmentally driven s

223 Further deciphering the molecular basis of tumour cell plasticity has the potential to contribute t

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

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

226 cally have been stymied by drug toxicity and tumour cell plasticity.

227 a particular case owing to the vast size of tumour cell populations, chromosomal instability and its

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

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

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

231 function of the RNA-editing enzyme ADAR1 in tumour cells profoundly sensitizes tumours to immunother

232 Because tumour cells proliferate in suboptimal environments, and

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

234 The pressure created by the localisation of tumour cell proliferation and death generates an cellula

235 ling-related signalling pathways to modulate tumour cell proliferation and the tumour microenvironmen

236 45Ala), reduces gene expression and inhibits tumour cell proliferation and tumour growth.

237 cles produced under these conditions promote tumour cell proliferation and turnover and modulate bloo

238 of chick embryos, we observed a reduction of tumour cell proliferation as well as a reduction in hypo

239 ntributed to control protein acetylation and tumour cell proliferation by inhibiting calcineurin and

240 If and how mechanical cues regulate tumour cell proliferation is currently not fully studied

241 ion in these parameters, such as the rate of tumour cell proliferation or sensitivity to hypoxia, can

242 2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development.

243 dipokine regulation, linked to a decrease of tumour-cell proliferation.

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

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

246 tance to palbociclib occurred as a result of tumour cell re-wiring leading to increased expression of

247 Our work supports the notion that some tumour cells reactivate a developmental metabolic progra

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

249 Lysis of tumour cells releases tumour-specific antigens that trig

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

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

252 in vivo, highly proliferative stem cells and tumour cells require OxPhos for efficient growth and gen

253 MErT is not a simple mirror image of EMT as tumour cells retain a transcriptional "memory" following

254 ecifically due to the lack of eHsp90alpha on tumour cell-secreted exosomes.

255 ered the lung environment more vulnerable to tumour cell seeding and growth.

256 ng excess stress and inflammatory responses, tumour-cell shedding and pro-angiogenic and/or growth fa

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

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

259 lity protein class I (MHC I) proteins on the tumour cell surface, promoting robust intratumoral infil

260 sion and also that nfP2X(7) is essential for tumour cell survival.

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

262 Solid tumours comprise mixtures of tumour cells (TCs) and tumour-adjacent cells (TACs), and

263 f mitochondrial function selectively targets tumour cells that are dependent on oxidative phosphoryla

264 lass of extracellular vesicles released from tumour cells that are now understood to facilitate commu

265 Most disseminated tumour cells that arrive in distant tissues, surrounded

266 A network of communicating tumour cells that is connected by tumour microtubes medi

267 distinct and profound selective pressure on tumour cells that, in turn, shapes the metastatic proces

268 unequal segregation of ecDNA from a parental tumour cell to offspring cells rapidly increases tumour

269 Immunohistochemical staining revealed the tumour cells to be AE1/AE3, CK7, GCDFP-15, E-cadherin, a

270 r show that pericyte derived Cyr61 instructs tumour cells to elevate expression of the proangiogenic/

271 ronment, which is required for disseminating tumour cells to engraft distant sites(4-6).

272 toylation that decreases PD-L1 expression in tumour cells to enhance T-cell immunity against the tumo

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

274 mune checkpoints that are often exploited by tumour cells to evade immunosurveillance have emerging r

275 by MHC class I molecules and the ability of tumour cells to impair antigen presentation as they evol

276 ticles, and silencing of ITCH sensitizes the tumour cells to irradiation treatment.

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

278 Dissemination of tumour cells to the bone marrow is an early event in bre

279 etastatic' niche that supports the spread of tumour cells to the liver(2,3).

280 tic target to enhance the sensitivity of the tumour cells to the treatment.

281 initiation of biological processes to revert tumour cells to undifferentiated aggressive states via p

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

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

284 Only two trials of an autologous renal tumour cell vaccine and of the vascular endothelial grow

285 Gemogenovatucel-T is an autologous tumour cell vaccine manufactured from harvested tumour t

286 astoma tumours consisting of patient-derived tumour cells, vascular endothelial cells and decellulari

287 umorigenesis when it arises within incipient tumour cells versus stromal cells, and how these roles c

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

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

290 ells and the number of circulating 4T1 mouse tumour cells were measured.

291 cularis muscle bundles and nerve fibers; the tumour cells were noted to have a monotonous histiocytoi

292 atumoral compartment-or knockdown of C3aR in tumour cells-were both protective against tumour growth.

293 tions are responsible for drug-resistance of tumour cells which impacts on the efficacy of treatment.

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

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

296 gher levels of glycolytic enzymes in primary tumour cells, which we corroborated by flow cytometric a

297 We first evaluate means of labelling tumour cells with CpG adjuvant, we then go on to demonst

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

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

300 Interactions of tumour cells with the surrounding microenvironment play