ライフサイエンスコーパス: tumour

1 nd increased local invasion from the primary tumour.

2 dominant neoantigens in the subclones of the tumour.

3 ate PARP inhibitor treatment of HR-deficient tumours.

4 for immunotherapy in the treatment of solid tumours.

5 lf also a potential nutrient for tissues and tumours.

6 er immune-mediated regression of established tumours.

7 hanced TAM penetration throughout and within tumours.

8 chieving significant regression of the SW620 tumours.

9 nd cellular origins of lineage-specific lung tumours.

10 ion signature associated with BRCA1/2 mutant tumours.

11 expression and pimonidazole accumulation in tumours.

12 s, including survival prediction across many tumours.

13 ic and transcriptomic dimensions for complex tumours.

14 lower pH values in hypoxic regions of solid tumours.

15 s for schwannomas and other Merlin-deficient tumours.

16 on of the physical characteristics of rectum tumours.

17 on biological differences between or within tumours.

18 ally accumulate in or are designed to target tumours.

19 rences that exist between patients and their tumours.

20 esistance alleles across 1934 drug-resistant tumours.

21 very are based on orthotopic or subcutaneous tumours.

22 en de novo, low-frequency mutations in human tumours.

23 e in vivo models for future studies of these tumours.

24 tics with germline BRCA1 mutation-associated tumours.

25 omplex, is required for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequent dif

26 One such gene is Wilms' tumour 1 (WT1), which plays multiple roles in developmen

27 72-4.42]; p=0.0004), diameter of the largest tumour (1.07 per cm increase [1.04-1.11]; p<0.0001), log

28 -27.5]) and lowest in survivors of germ cell tumours (14.0 [11.5-16.6]).

29 s were administered to mice bearing the same tumours 20min prior to PDT treatment.

30 Here, we build a compendium of 2218 primary tumours across 12 human cancer types and systematically

31 ontaining geranylgeraniol can limit the anti-tumour activity of pitavastatin and diet should be contr

32 We assessed the safety and anti-tumour activity of standard-dose pembrolizumab in combin

33 vo studies are warranted to explore the anti-tumour activity of tivozanib in combinatorial approaches

34 re still being monitored for safety and anti-tumour activity.

35 prostate cancer, we identify alterations in tumours affecting the production of decarboxylated S-ade

36 ction in the characteristics associated with tumour aggressiveness, including invasion, migration, an

37 elial to amoeboid transition contributing to tumour aggressiveness.

38 d suppressor cells infiltrate in the primary tumour and distant organs with different time kinetics a

39 g platform towards early detection of cancer tumour and is anticipated to be exploited as a magnifice

40 noma cells, the most common Merlin-deficient tumour and the hallmark for NF2.

41 preferential accumulation of the complex in tumours and candidate biomarkers to analyse its effect o

42 of hypoxia (low oxygen) occur in most solid tumours and cells in these areas are the most aggressive

43 ients with bilateral multifocal (BMF) kidney tumours and clinical manifestations of Birt-Hogg-Dube (B

44 ave established mouse models for parathyroid tumours and uterine neoplasms that develop in the HPT-JT

45 ytic poxvirus would attract T cells into the tumour, and induce PD-L1 expression in cancer and immune

46 NA payload are transferred in the developing tumour, and provide functional evidence for an essential

47 e stratified by chemotherapy centre, site of tumour, and tumour stage.

48 estis, ovary, lymphoid cells, granulosa cell tumours, and a subset of malignant melanoma and thyroid

49 cant decrease in proliferation in 5/23 (22%) tumours, and that KRAS/BRAF mutant tumours were particul

50 edominantly in poor prognosis serous subtype tumours, and this genetic deletion is associated with po

51 vesicles (MVs), activates VEGF receptors and tumour angiogenesis through a unique 90 kDa form of VEGF

52 mic and proteomic strategy that interrogates tumour antigen peptides presented by major histocompatib

53 n of type III interferons and hence enhances tumour antigen presentation.

54 ction in vitro and in vivo; (c) labelling of tumour antigens in mouse models; and (d) use in affinity

55 Approximately 70% of these tumours are located in the gastrointestinal system (GI),

56 Hogg-Dube (BHD) syndrome, or with BMF kidney tumours as the only manifestation; however, their impact

57 d RGEPs, we can estimate the content of many tumours associated immune and stromal cell types, their

58 expression analyses identified a subgroup of tumours associated with hypoxia and HIF signalling.

59 Tumour-associated Th17-to-Treg cell conversion identifie

60 t with the high expression of Slco2a1 in the tumour-associated vascular endothelial cells.

61 s, suggesting the need of denser sampling of tumours at relapse.

62 omic and molecular alterations that fuel the tumour, average patient survival post-diagnosis remains

63 ng data bank, cancer registry and colorectal tumour bank we determine the prevalence of Lynch syndrom

64 Here we present a fitness model for tumours based on immune interactions of neoantigens that

65 converted from IL-17A(+)Foxp3(neg) cells in tumour-bearing mice.

66 The impact of SCNAs on tumour biology remains poorly understood.

67 ib, suggesting that acute treatment of small tumour biopsies is worthy of further exploration as a pr

68 cells determined in relation to pretreatment tumour burden correlated with clinical response.

69 imbalance between T-cell reinvigoration and tumour burden.

70 A histopathological examination of the CNS tumour can confirm a dedifferentiation of NEN in the dir

71 ent inhibited pERK1/2 phosphorylation in all tumours, caused a significant decrease in proliferation

72 erapies including chemotherapy aim to induce tumour cell death.

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

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

75 2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 host immune system to recognize and destroy tumour cells.

98 is affected by the similarity to endogenous tumour cells.

99 that targeted alterations are present in all tumour cells.

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

101 We consider methylation-based tumour classification highly relevant for the future dia

102 utilized to distinguish specific binding to tumour collagen from non-specific uptake.

103 ful therapeutic treatment for patients whose tumours contain a high fraction of replicating cells.

104 intra-tumoural balance in favour of enhanced tumour control.

105 isions are based on one or a few samples per tumour, creating uncertainty on whether alterations foun

106 trong therapeutic opportunities by targeting tumour dependencies on NMD-elicit mutations.

107 interaction of CRTH2 and NKp30 with elevated tumour-derived PGD2 and B7H6, respectively.

108 Using the tumour-derived RGEPs, we can estimate the content of man

109 erence gene expression profiles (RGEPs) from tumour-derived single-cell RNA sequencing data.

110 nvironment is very complex, and essential in tumour development and drug resistance.

111 ome rearrangements can initiate and maintain tumour development, and indicate a viable therapeutic wi

112 athway is a critical determinant not only in tumour development, but also in dictating the nature of

113 uccinylation, tumour cell proliferation, and tumour development.

114 of NFS1, whereas metastatic or primary lung tumours do not.

115 tal bifurcation (P), contiguous extrahepatic tumour (E), multifocal tumour (F), and spontaneous ruptu

116 h release half-lives did not achieve an anti-tumour effect.

117 ver, tivozanib synergistically enhanced anti-tumour effects of EGFR-directed therapies including erlo

118 pression and leukocyte adhesion in quiescent tumour endothelial cells with intact insulin receptors a

119 Tumour engraftment did not occur in one of the five immu

120 e shown to be safe and effective in reducing tumour expansion and lengthening the survival of intracr

121 Organotypic culture and human tumour explants were allowed to grow long-term (14-35 da

122 eceptor 1 [PD-1] antibody) in advanced solid tumours expressing programmed cell death ligand 1 (PD-L1

123 ntiguous extrahepatic tumour (E), multifocal tumour (F), and spontaneous rupture (R).

124 0-2, and did not have high-risk lesions for tumour flare (eg, >5 sites of visceral disease or bone l

125 for tumor formation.BRCA2 mutations promote tumour formation while also paradoxically causing cell l

126 ath to preserve barrier function and prevent tumour formation.

127 o derive the cellular composition of a solid tumour from bulk gene expression data by mathematical de

128 l prostate tissue and reduced in a subset of tumours from the Cancer Genome Atlas (TCGA).

129 Thus, small-cell lung cancer tumours generate their own microenvironment via activati

130 ) may be identified by sequencing metastatic tumour genomes to identify molecular markers at this let

131 nce of carcinoid syndrome (p<0.0001), as was tumour grade, stage, and primary tumour site (all p<0.00

132 Mammary or subcutaneous tumours grow despite suppression of NFS1, whereas metast

133 Patient-derived xenograft tumours growing in immunodeficient mice exhibited enhanc

134 te in tumours, resulting in greater rates of tumour growth and mortality.

135 e, NKG2D-sufficient mice display accelerated tumour growth associated with, an increased recruitment

136 ition of this axis results in suppression of tumour growth in a transgenic mouse model of breast canc

137 nd renal diseases, and in the progression of tumour growth in cancer, but current diagnosis and treat

138 vitro, leading to a significant reduction in tumour growth in mice.

139 TRPV4 activation also resulted in reduced tumour growth in vivo.

140 tment with AKT inhibitors causes synergistic tumour growth inhibition in vitro and in vivo.

141 lico model of dynamically coupled angiogenic tumour growth is specified to in-vivo and in-vitro data,

142 a reaction-diffusion equation based model of tumour growth to investigate how the invasion front is d

143 nic fibroblasts (MEFs) resulted in increased tumour growth, aberrant remodelling of the extracellular

144 tive Lgr5(+) cell ablation restricts primary tumour growth, but does not result in tumour regression.

145 er cells, whereas silencing in vivo inhibits tumour growth, increases cisplatin efficacy and OS.

146 ent cancer cells in vivo and interfered with tumour growth.

147 ort to trigger ferroptosis in vitro and slow tumour growth.

148 ) performance status of 0 or 1, MET-positive tumours (>/=25% of tumour cells with membrane staining o

149 antial change in trial methodology for solid tumours has taken place, in response to increased unders

150 e show that those devils that become host to tumours have otherwise greater fitness, with higher surv

151 ntext dependency, signalling plasticity, and tumour heterogeneity, and we offer a perspective on emer

152 three-dimensional TAM composition, tumour-to-tumour heterogeneity, response to colony-stimulating fac

153 Effective anti-tumour immunity in humans has been associated with the p

154 This lack of anti-tumour immunity is attributed to an absence of cell surf

155 s, thereby enhancing suppression of Th1 anti-tumour immunity.

156 ngs indicate that CDK4/6 inhibitors increase tumour immunogenicity and provide a rationale for new co

157 nitor therapy-induced genomic changes in the tumour in an inexpensive and minimally invasive manner.

158 ed enhanced hypoxia compared to the original tumours in immunocompetent humans, and hypoxia was reduc

159 Cs), as well as the suppression of germ cell tumours in mice.

160 within heterogeneous T cell populations from tumours in mice; these surface markers were also express

161 ls that TAM density was heterogeneous across tumours in the same animal, overall TAM density is diffe

162 lowed therapy of experimentally induced DFTD tumours in three Tasmanian devils.

163 h of cell line and patient-derived xenograft tumours in vivo.

164 Here we show that Th17 cells are a source of tumour-induced Foxp3(+) cells.

165 The results demonstrated that tumour-induced human monocyte-derived DCs exhibited syst

166 escence and SASP responses exhibit decreased tumour-inducing potential.

167 n breast cancer is associated with increased tumour infiltrating lymphocytes (TILs), however, MAPK ac

168 markers were also expressed on human PD1(hi) tumour-infiltrating CD8 T cells.

169 tumour-infiltrating immune cells vs >/=5% of tumour-infiltrating immune cells [IC2/3]), chemotherapy

170 xpression on <1% [IC0] or 1% to <5% [IC1] of tumour-infiltrating immune cells vs >/=5% of tumour-infi

171 therapy for melanoma, Runx3-deficient CD8(+) tumour-infiltrating lymphocytes failed to accumulate in

172 uman colorectal cancer stem cells (CSCs) are tumour initiating cells that can self-renew and are high

173 otein 3 (DLL3), a novel target identified in tumour-initiating cells and expressed in more than 80% o

174 orm 3D spheres (SPH), which retain stem-like tumour-initiating features.

175 understand how translational control affects tumour initiation and malignancy.

176 D631A) in mouse lung cells markedly enhances tumour initiation, a phenomenon mediated by Craf kinase

177 nitiating cell self-renewal, a surrogate for tumour initiation, and activated P-Stat3.

178 glycaemia and can be due either to beta-cell tumours (insulinomas) or beta-cell hyperplasia.

179 When the primary tumour is located in the pancreas, it is associated with

180 The hallmark of tumours is the ability of cancerous cells to promote vas

181 y and worse prognosis than 1p/19q co-deleted tumours, is unclear.

182 s that do not become infected, although high tumour loads lead to high mortality.

183 , how this altered metabolism contributes to tumour metastasis remains elusive.

184 C-produced CXCL12, an important chemokine in tumour metastasis, was markedly inhibited by TGFbeta.

185 were stratified by histology of the primary tumour, metastatic tumour size, and number of metastases

186 bitors prevent the release of NLGN3 into the tumour microenvironment and robustly block HGG xenograft

187 The tumour microenvironment is very complex, and essential i

188 t lack of sustained immune activation in the tumour microenvironment restricts antitumour immunity.

189 ies will need also to target elements of the tumour microenvironment that promote glioma progression.

190 target antigens, overcome immunosuppressive tumour microenvironments, reduce toxicities, and prevent

191 cy's law is applied to a 3-D realistic brain tumour model that is extracted from magnetic resonance (

192 y, with 100% survival over 60 days in a TC-1 tumour model.

193 ensity is different among separate pulmonary tumour models, nanotherapeutic drug delivery correlated

194 organoid cultures, FACS analysis and in vivo tumour models.

195 negative (A375Ppuro and PANC-1) subcutaneous tumour mouse models.

196 s exposure to anti-GD2 antibody therapy, and tumour MYCN amplification status.

197 changer NHE1 is an important modifier of the tumour nanoenvironment.

198 ad been previously treated with at least one tumour necrosis factor (TNF) antagonist (which had faile

199 , RIPK3, TRIF and ZBP1/DAI and inhibition of tumour necrosis factor (TNF), lipopolysaccharide or poly

200 ity-score matching tested the effect of anti-tumour necrosis factor alpha (TNFalpha) therapy exposure

201 Here we identify that tumour necrosis factor-alpha (TNFalpha) selectively redu

202 and leukocyte adhesion after treatment with tumour necrosis factor-alpha.

203 e 2016 revision of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues includes

204 vascular invasion (P < 0.001) and late stage tumours (P < 0.001) had AFP over 400 ng/ml.

205 Differences in the tumour pharmacokinetic profiles of EP-3533 and EP-3612 w

206 initiating cell and ultimately the resulting tumour phenotype.

207 reatment was associated with more unbalanced tumour phylogenetic trees, suggesting the need of denser

208 In silico benchmarking on simulated tumour phylogenies across a wide range of sample puritie

209 nt time kinetics and regulate spatiotemporal tumour plasticity.

210 kinase activity, and effectively accelerates tumour progression when activated in advanced lung adeno

211 nimal-morbidity chemotherapy (in the case of tumour progression)-for paediatric patients with desmoid

212 Although these processes alter tumour progression, their regulation is poorly understoo

213 ry factors are important factors that affect tumour progression.

214 and cell motility/contractility help mediate tumour progression.

215 we provide genetic evidence of an unexpected tumour-promoting effect of NKG2D in a model of inflammat

216 ant therapy, chemotherapy-free interval, and tumour PTEN status.

217 ific antigen levels as the representation of tumour quantity.

218 nd tumour reactivity assays, we predict that tumour reactive T cells are frequently present in NSCLC.

219 Using T-cell receptor-beta sequencing and tumour reactivity assays, we predict that tumour reactiv

220 accelerated epirubicin would improve time to tumour recurrence (TTR); and whether use of oral capecit

221 ffer new therapeutic approaches for limiting tumour recurrence.

222 y tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4 and CDK6.

223 rimary tumour growth, but does not result in tumour regression.

224 ming of CD8(+) T cells that mediate systemic tumour rejection (abscopal effect) in the context of imm

225 KRAS mutated tumours represent a large fraction of human cancers, but

226 Recent studies have shown that MSC tumour residence and their close interactions with infla

227 me, monitor minimal residual disease, assess tumour resistance to therapeutic agents, and potentially

228 itin, hepcidin and ferroportin expression in tumours respect to surrounding liver, whereas transferri

229 es and acute myeloid leukaemia, but complete tumour responses are infrequent and of short duration, p

230 therapy [BAT]) in this setting might induce tumour responses.

231 ltrating lymphocytes failed to accumulate in tumours, resulting in greater rates of tumour growth and

232 ssion network identified using TCGA prostate tumour RNA-sequencing identifies co-regulated cancer gen

233 their phylogenies from noisy and impure bulk tumour samples at unprecedented depth.

234 point mutation detection assays in preserved tumour samples can be imaged and analysed using mobile p

235 nd protein expression did not differ between tumour samples from variant and wild-type carriers.

236 quencing was successful for 97% (342/351) of tumour samples in the prospective cohort and showed 100%

237 rform an integrative analysis of human NSCLC tumour samples, patient-derived xenografts, murine model

238 chromosomal rearrangements in primary human tumour samples, with the potential to define chromosome

239 oach to target Hsp90 in cancer, that is, the tumour-secreted Hsp90alpha, instead of the intracellular

240 This novel tumour-selective pretargeting approach may be used to im

241 In human tumours separase is overexpressed, making it a potential

242 01), as was tumour grade, stage, and primary tumour site (all p<0.0001).

243 sy or surgery, and we classified patients by tumour site, clinical stage (TNM system), and post-surgi

244 lantation is indicated on the basis of large tumour size and anatomy that precludes the possibility o

245 e ductal adenocarcinoma of grade 1-3, with a tumour size of 3 cm or less (pT1-2), none to three posit

246 tory breast cancer to stage 3, regardless of tumour size or nodal spread.

247 histology of the primary tumour, metastatic tumour size, and number of metastases.

248 Modern cancer therapies aim at targeting tumour-specific alterations, such as mutations or neo-an

249 The focus of tumour-specific antigen analyses has been on single nucl

250 class of HLA-bound peptides that arise from tumour-specific mutations.

251 The tumour-specific origin of HBB is confirmed by sequence p

252 T-cell recognition of neoantigens, which are tumour-specific, mutated peptides presented on the surfa

253 es have revealed the molecular nature of the tumour specificity of CD40 signalling and explained the

254 is was based on histological analysis of the tumour specimen after biopsy or surgery, and we classifi

255 r of involved axillary lymph nodes, clinical tumour stage, oestrogen-receptor status, type and timing

256 by chemotherapy centre, site of tumour, and tumour stage.

257 hey underwent PET/CT imaging for the initial tumour staging and had no evidence of distant metastates

258 Intravital imaging enables to study dynamic tumour-stroma interactions within primary and metastatic

259 roportion of ctDNA originating from specific tumour subclones depend on multiple factors, making comp

260 CDK6 in human cancers might help to identify tumour subsets that undergo cell death and tumour regres

261 de signaling systems with both oncogenic and tumour-suppressing roles for cancer progression, such as

262 s, the FLCN H255Y mutant protein has lost it tumour suppressive function leading to the clinical mani

263 PML is a tumour suppressor and regulator of cell differentiation.

264 mRNA downregulation, suggesting an important tumour suppressor function.

265 noma (PDAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which i

266 Inactivation of the VHL (Von Hippel Lindau) tumour suppressor has long been recognised as necessary

267 gase MDM2, and leads to re-activation of the tumour suppressor p53 in various cancers.

268 The p53 tumour suppressor protein is a short-lived transcription

269 entify a novel Myst2-associated protein, the tumour suppressor protein Niam (Nuclear Interactor of AR

270 ers besides its well-established function as tumour suppressor.

271 ronic inflammation, through loss of the same tumour-suppressor pathways and eventual sporadic develop

272 export regulates the proteolysis of FOXO3A/4 tumour suppressors in the context of cancer and illustra

273 Association of undruggable tumour suppressors with drug targets informs therapeutic

274 slational mechanisms, blocks these important tumour suppressors.

275 omozygous deletions, aiming to identify rare tumour suppressors.

276 nt blockade (ICB) therapies can unleash anti-tumour T-cell responses.

277 with 309 samples of other extra-axial skull tumours that might histologically mimic meningioma varia

278 ations, which have been reported in atypical tumours that progressed from benign ones.

279 in-situ hybridisation of two cores of breast tumour tissue in a microarray, done in a central laborat

280 at HOXB13 expression does not differ between tumour tissue of G84E variant carriers and non-carriers.

281 nd acquired Thr790Met mutation detectable in tumour tissue or plasma.

282 PI3K status in tumour tissue was determined via central laboratory duri

283 o examine three-dimensional TAM composition, tumour-to-tumour heterogeneity, response to colony-stimu

284 ess of therapies that disrupt PD-L1-mediated tumour tolerance has highlighted the need to understand

285 will lead to a more refined therapy for this tumour type.

286 he Cancer Genome Atlas has sequenced primary tumour types obtained from surgical resections, much les

287 of lymphangiogenesis (in melanomas and other tumour types) is limited by the paucity of mouse models

288 events is highly variable within and across tumour types.

289 mutant that is frequently observed in other tumour types.

290 with the response to PD-1 blockade in other tumour types.

291 a with highest levels detected in metastatic tumours versus normal skin or benign skin lesions.

292 predictors of ctDNA release and analyse the tumour-volume detection limit.

293 To describe the evolution of a heterogeneous tumour, we evaluate its fitness as a weighted effect of

294 xcess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein MOrtality R

295 /23 (22%) tumours, and that KRAS/BRAF mutant tumours were particularly sensitive to the anti-prolifer

296 Adenosquamous lung tumours, which are extremely poor prognosis, may result

297 dc73(L/L)/PTH-Cre mice developed parathyroid tumours, which had nuclear pleomorphism, fibrous septati

298 All induced mice develop mammary tumours with 9qA1 (Yap1) and/or 6qA2 (Met) amplification

299 g genome-wide sequencing results from 28 366 tumours with complete manual curation of 23 489 individu

300 ng, and we observed mutual exclusivity among tumours with somatic NF-kappaB pathway aberrations and L