ライフサイエンスコーパス: tumour

1 is the most common and most aggressive brain tumour.

2 c characteristics of an individual and their tumour.

3 res resembling those observed in human Wilms tumour.

4 highly aggressive, difficult to treat brain tumour.

5 gene have been found in 5% of biliary tract tumours.

6 oving to effectively deliver therapeutics to tumours.

7 from 22 right-sided and 64 left-sided colon tumours.

8 ndocrine transformation in lung and prostate tumours.

9 d ideally be used in the management of these tumours.

10 ally silenced in both human and murine liver tumours.

11 erapy used for malignant thyroid mesenchymal tumours.

12 microenvironment after resection of primary tumours.

13 key role in the establishment of metastatic tumours.

14 tant role in immune responses to viruses and tumours.

15 mmunity and CAR T-cell therapy against solid tumours.

16 s with unresectable gastrointestinal stromal tumours.

17 and proteomic data to classify breast cancer tumours.

18 need to be explored to treat p53- deficient tumours.

19 y lymphoid structures in these CD8(+)CD20(+) tumours.

20 e surgical or radiation treatment of primary tumours, ~50% of patients progress to metastatic disease

21 rld environments such as the gut(6,7), solid tumours(8,9), bioreactors(10) or soil(11).

22 Here, we show that, for a range of solid tumours, a cyclic octapeptide labelled with a near-infra

23 sive nature of malignant thyroid mesenchymal tumours, a multidisciplinary team-based approach should

24 mal properties and can therefore be used for tumour ablation in mice, and that they have high optical

25 egration of the imaging signals triggered by tumour acidosis.

26 is of whole genomes, comprising thousands of tumours across populations worldwide, with the aim of id

27 B, and C, which has been shown to have anti-tumour activity against NTRK gene fusion-positive solid

28 human and mouse tumours and limits the anti-tumour activity of IL-18 in mice.

29 munity that suppressed the growth of distant tumours after rechallenge.

30 The inflammatory environment within tumours also influences responses to many therapies, inc

31 d in KIRC from an array dataset including 26 tumour and 26 adjacent normal tissue samples.

32 entify transcriptomic differences in primary tumour and peritumoral adipose tissue between obese pati

33 complex interplay between the clear cell RCC tumour and peritumoral adipose tissue microenvironment m

34 , parasympathetic and sensory) interact with tumour and stromal cells to promote the initiation and p

35 e-cell analysis identified the phenotypes of tumour and stromal single cells, their organization and

36 py based on the genetics and biology of each tumour and the clinical characteristics of each patient.

37 e between fresh biopsied samples of the oral tumour and the surgical resection margin with more than

38 cally the best method to detect a pancreatic tumour and to determine surgical resectability.

39 th ligand 1 or IFNGR1 elicited a robust anti-tumour and/or anti-metastatic effect.

40 nting evidence that resection of the primary tumour and/or localised radiotherapy (locoregional thera

41 Applied to data from 2658 tumours and 38 cancer types, TrackSig permits pan-cancer

42 Nonetheless, eosinophils infiltrate multiple tumours and are equipped to regulate tumour progression

43 xpression analysis of matched primary breast tumours and bone metastasis-derived patient-derived xeno

44 ns between monthly treatment costs for solid tumours and clinical benefit in all assessed countries,

45 increases the concentration of glutamine in tumours and its downstream metabolite, alphaKG, without

46 ently upregulated in diverse human and mouse tumours and limits the anti-tumour activity of IL-18 in

47 nce of the probes in mouse models of mammary tumours and of metastatic lung cancer, as well as during

48 mechanisms underlying TGFbeta signalling in tumours and their microenvironment and discuss approache

49 horts included only patients with resectable tumours, and a formalin-fixed, paraffin-embedded tumour

50 y modality for the treatment of intracranial tumours, and its use has been expanded for the treatment

51 lung cancer, mesothelioma, thymic epithelial tumours, and other pulmonary neuroendocrine neoplasms) a

52 CD68+ macrophages within human head and neck tumours, and show that images grouped semi-quantitativel

53 Tumour-associated antigens (TAAs) comprise a large set o

54 ould include bone-targeted agents to inhibit tumour-associated osteolysis and prevent skeletal morbid

55 ing of the treatment barriers imposed by the tumour-associated stroma, and from the development of no

56 the presence of 10% or less residual viable tumour at the time of surgery.

57 sation (WHO) classification categorises bone tumours based on their similarity to normal adult tissue

58 predict will alter extensile tensions on the tumour basement membrane.

59 e via nanoparticles improves the survival of tumour-bearing mice after irradiation.

60 ed to receive no tumour bed boost (n=605) or tumour bed boost (n=603).

61 enrolled and randomly assigned to receive no tumour bed boost (n=605) or tumour bed boost (n=603).

62 gned, by use of a minimisation algorithm, to tumour bed boost or no tumour bed boost, following conve

63 isation algorithm, to tumour bed boost or no tumour bed boost, following conventional whole breast ra

64 g pursued for predicting clinically relevant tumour behaviours, such as treatment response and emerge

65 ty and evolving mutations as a surrogate for tumour biopsy.

66 amples, E-cadherin-expressing and -deficient tumours both invade collectively and metastasize equally

67 remodelling of the basement membrane promote tumour budding, while stiffening of the basement membran

68 to arise from a single clone in the primary tumour but can exhibit subclonal heterogeneity at the ge

69 effect on the growth of primary subcutaneous tumours, but resulted in depletion of circulating melano

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

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

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

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

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

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

76 Mechanistically, tumour cells avidly consumed methionine and outcompeted

77 Tumour cells frequently utilize glutamine to meet bioene

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

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

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

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

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

83 have been compared to aerobic glycolysis in tumour cells.

84 e granule proteins that can potentially kill tumour cells.

85 metastatic niches and settlement of residual tumour cells.

86 hagocytic marker phosphatidylserine on dying tumour cells.

87 nd transcriptome analysis on a large ovarian tumour cohort and develop a machine learning approach to

88 t following fractionated radiation in murine tumours consistent with clinical reports.

89 ose of Western cohorts: specifically, 41% of tumours contained mutations in FOXA1 and 18% each had de

90 e length of the mouse small intestine and in tumours contrast with previous reports of discrete conce

91 Local tumour control and tumour regression were extracted as t

92 40 Gy in 15 fractions over 3 weeks for local tumour control, and is as safe in terms of normal tissue

93 er expression of AGXT, PTGER3 and SLC12A3 in tumours correlates with worse prognosis in KIRC patients

94 Albumin accumulation in tumours could reflect a role of albumin in transport of

95 dly, early priming of CD4(+) T cells against tumour-derived antigens also required cDC1, and this was

96 Thus, in the setting of tumour-derived antigens, cDC1 function as an autonomous

97 s such, early studies focused on the role of tumour-derived cohesin mutations in the fidelity of chro

98 a checkpoint that can limit immune-mediated tumour destruction.

99 enhanced cross-sectional images in terms of tumour detection.

100 its silencing in vivo drastically decreased tumour development and progression, likely through a mol

101 late phases are better for visualisation of tumour enhancement.

102 ecology, supporting the concept that purely tumour epithelium-centric metrics of aggressiveness may

103 es of 23,427 tumours, identifying aspects of tumour evolution including probable orders in which CAAs

104 Thus, CAAs predict cancer prognosis, shape tumour evolution, metastasis and drug response, and may

105 nts that often occur in parallel, throughout tumour evolution.

106 Analyses of tumour extracts revealed specific alterations in Hippo p

107 Studies reporting treatment of benign tumours, extraocular tumours, or other forms of stereota

108 with compensatory effects leading to robust tumour fitness maintained throughout the tumour progress

109 topographically and morphologically distinct tumour foci.

110 n about how aneuploidy itself contributes to tumour formation and progression.

111 Strikingly, we could block tumour formation completely by re-expressing Asense (hom

112 The few mutations in tumour genes that can be evaluated (eg, ATM and DAXX) ar

113 ions between the tumour microenvironment and tumour genotype are highlighted, providing important clu

114 Upfront tumour genotyping is now considered an essential step in

115 mine the relationship between PET-CT derived tumour glucose uptake as measured by maximum standard gl

116 wild-type growth factors, as well as reduced tumour growth (associated with PDGF-BB delivery) and vas

117 also resulted, in vivo, in a suppression of tumour growth and a decrease in the number of mouse circ

118 ntified divergent effects of DDRs on primary tumour growth and experimental lung metastasis in the HT

119 econstitution suppressed cell proliferation, tumour growth and invasion, both in vitro and in vivo.

120 ection of surgical site infection as well as tumour growth and other systemic inflammatory responses

121 ntial dietary intervention to block melanoma tumour growth and sensitize tumours to targeted therapy

122 praphysiological levels of D-mannose inhibit tumour growth and stimulate regulatory T cell differenti

123 Neither DDR1b nor DDR2 expression altered tumour growth at the primary site.

124 on, that were associated with stimulation of tumour growth by DDRs and collagen I.

125 nergize with anti-PD1 therapy in suppressing tumour growth in mouse models of cancer.

126 uting to tumour immune evasion and promoting tumour growth in mouse models.

127 ontaneous autoimmunity but protected against tumour growth in multiple cancer models.

128 In vivo, tumour growth of implanted human TNBC cells and the numb

129 ncer, and loss of carboxypeptidase D reduced tumour growth.

130 for quantitative longitudinal monitoring of tumour growth.

131 metabolism and HSC senescence that promotes tumour growth.

132 Patients with PD-L1 positive tumours (>=1%) had significantly shorter OS than patient

133 situ (with or without a high-grade Ta or T1 tumour) had a complete response within 3 months of the f

134 approval for the treatment of patients with tumours harbouring NTRK fusions and MMR deficiencies, re

135 ts with metastatic or locally advanced solid tumours harbouring oncogenic NTRK1, NTRK2, and NTRK3 gen

136 uently over-expressed in cancer and promotes tumour heterogeneity and therapy resistance.

137 urothelial carcinoma are extreme examples of tumour heterogeneity.

138 iencies, respectively, regardless of primary tumour histology.

139 erent data sets, including genomic profiles, tumour histopathology, radiological images, proteomic an

140 o the detection and characterisation of bone tumours; however, magnetic resonance imaging (MRI) is th

141 Here, we analyse CAA profiles of 23,427 tumours, identifying aspects of tumour evolution includi

142 d immune reactivity, thereby contributing to tumour immune evasion and promoting tumour growth in mou

143 We also assessed the tumour immune microenvironment in a prospective cohort o

144 ation, do not typically generate robust anti-tumour immune responses.

145 strategy for the generation of adaptive anti-tumour immune responses.

146 ach to molecularly classify and characterize tumour-immune phenotypes.

147 a target for bolstering T-cell-mediated anti-tumour immunity and CAR T-cell therapy against solid tum

148 erstanding the origin and fate of T cells in tumour immunity is the lack of quantitative information

149 P signalling during viral infection and anti-tumour immunity(1-5).

150 isit classical concepts concerning viral and tumour immunity, which will be critical to fully underst

151 cross-talk that is required for optimal anti-tumour immunity.

152 esting that IL-18 therapy could enhance anti-tumour immunity.

153 olecules and provide anti-microbial and anti-tumour immunity.

154 melanoma (UM) is the most common intraocular tumour in adults and despite surgical or radiation treat

155 ment of xenograft pancreatic cancer (BxPC-3) tumours in a murine model.

156 The lower occurrence of solid tumours in individuals with DS supports the identificati

157 Immune surveillance against pathogens and tumours in the central nervous system is thought to be l

158 ritumoural tissue, and 20.7% (17.4-31.7%) in tumours in vivo.

159 vity against NTRK gene fusion-positive solid tumours, including CNS activity due to its ability to pe

160 rest), nodal status (N0 vs rest), number of tumour-infiltrating lymphocytes (continuous variable), s

161 leukin-18 (IL-18) pathway are upregulated on tumour-infiltrating lymphocytes, suggesting that IL-18 t

162 Extensive tumour inflammation, which is reflected by high levels o

163 n II activity, high levels of ki-67 and high tumour-initiating abilities are characteristic of invasi

164 ensive metabolic reprogramming occurs during tumour initiation and progression in renal cell carcinom

165 nges in H3K27 trimethylation but its role in tumour initiation remains obscure.

166 verse molecular mechanisms presumed to drive tumour initiation, maintenance and recurrence across ind

167 nto the biological behaviour of various bone tumours is highlighted.

168 blood-brain barrier, namely malignant brain tumours, ischaemic stroke and haemorrhagic traumatic con

169 select appropriate adjuvant therapy based on tumour Ki67.

170 ing lactate being a more prominent source of tumour lactate in efficient metastasizers.

171 ow-grade epilepsy associated neuroepithelial tumour (LEAT), vascular malformation, and hippocampal sc

172 Tumours leverage ECM remodelling to create a microenviro

173 istopathological reports depicting cystic or tumour-like lesions were included in the study.

174 n (FLCN) and is characterized by benign skin tumours, lung and kidney cysts and renal cell carcinoma(

175 orrelated with patient survival and relevant tumour markers, and its silencing in vivo drastically de

176 rate that, even after removal of the primary tumour, MDSCs contribute to the development of premetast

177 in patients with PD-L1 immune cell-positive tumours, median overall survival was 25.0 months (95% CI

178 Now, the study of tumour metabolism is being redefined by the development

179 In this context, tumour metabolism itself is a checkpoint that can limit

180 ne cells, constituting a complex and dynamic tumour micro-environment (TME).

181 have fuelled ongoing efforts to exploit the tumour microenvironment (TME) for therapy, but strategie

182 th tumour cells or indirectly by shaping the tumour microenvironment (TME).

183 mical and biophysical characteristics of the tumour microenvironment and aim to enable studies of can

184 te many of the physiological features of the tumour microenvironment and have been shown to be far su

185 s with myeloid and fibroblastic cells in the tumour microenvironment and ongoing immune surveillance(

186 that shed light on interactions between the tumour microenvironment and tumour genotype are highligh

187 FGF2 is induced in the tumour microenvironment following fractionated radiation

188 releasing tumour-specific antigens into the tumour microenvironment highlights the potential for mCD

189 pment of novel approaches to re-engineer the tumour microenvironment in favour of effective anticance

190 d a chemokine cascade, which will favour the tumour microenvironment in terms of distant metastasis.

191 ts are focusing on modulating the pancreatic tumour microenvironment to enhance the efficacy of the i

192 The profound impact of the tumour microenvironment, reflected in the efficacy of im

193 germinal centre B cells and ASCs within the tumour microenvironment.

194 d is a critical regulator of immunity in the tumour microenvironment.

195 y underlie the dual potential of TANs in the tumour microenvironment.

196 d by the development of new molecular tools, tumour modelling systems and precise instrumentation tog

197 he method on two case studies with syngeneic tumour models which are challenging due to high variabil

198 A high tumour mutational burden (hypermutation) is observed in

199 tive value, although blood-based measures of tumour mutational burden did not have predictive value i

200 Patients with tumour mutational burden in the lower two terciles seem

201 Tumour mutational burden might have some predictive valu

202 However, patients with high tumour mutational burden seem to have a less pronounced

203 es, including biologics (in particular, anti-tumour necrosis factor (TNF) agents).

204 Since the early 2000s, anti-tumour necrosis factor (TNF) treatment has significantly

205 roles for pro-inflammatory cytokines such as tumour necrosis factor, IL-1beta and IL-17.

206 ctivity of the Rab3 and Rab27 small GTPases, tumour necrosis factor-alpha (TNF-alpha)-induced signall

207 iagnosis, including leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft-tissue sarcom

208 Traditional staging of HNSCC using the tumour-node-metastasis system has been supplemented by t

209 of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Canc

210 ed transcriptomic differences in the primary tumours of obese patients compared with those of a norma

211 that B cell signatures were enriched in the tumours of patients who respond to treatment versus non-

212 In 21 cases of borderline ovarian tumours, of which 11 were regarded as malignant and 10 w

213 Tumours often contain B cells and plasma cells but the a

214 ing treatment of benign tumours, extraocular tumours, or other forms of stereotactic radiosurgery wer

215 a clinically viable therapeutic strategy for tumours overexpressing the epidermal growth factor recep

216 rtance of functionally interrogating diverse tumour phenotypes driven by individual, yet related, var

217 a proof-of-concept method to infer the total tumour pressure, that is the sum of the fluid and solid

218 ratified by platinum-free interval, residual tumour, previous antiangiogenic therapy, and study group

219 ultiple tumours and are equipped to regulate tumour progression either directly by interacting with t

220 osphorylation and fuel lipogenesis, enabling tumour progression through metabolic reprogramming.

221 pts liver metabolic homeostasis and promotes tumour progression.

222 ust tumour fitness maintained throughout the tumour progression.

223 TANs can be part of tumour-promoting inflammation by driving angiogenesis, e

224 ograft mouse resection model with no sign of tumour recurrence.

225 possible means supporting early detection of tumour recurrence.

226 programmed cell death 1 (PD1) can result in tumour regression in preclinical models and can improve

227 Local tumour control and tumour regression were extracted as the primary outcomes

228 in vivo or in the setting of help-dependent tumour rejection.

229 Nano-formulations that are responsive to tumour-related and externally-applied stimuli can offer

230 d, as the mechanisms that underlie how these tumours remodel the neuronal milieu towards increased ac

231 IQR 21.4-28.1) and 35 of 41 patients who had tumour resection were progression free.

232 While hypoxia renders tumours resistant to many conventional therapies, little

233 ison with published data from 2,554 prostate tumours revealed that the genomic alteration signatures

234 st defences, suggesting that their effect on tumour risk may in part be accounted for by their influe

235 f C57BL/6J wild-type mice, and in normal and tumour samples from Apc(Min/+) mice.

236 assessed in formalin-fixed paraffin-embedded tumour samples using the FoundationOne CDx assay (Founda

237 phosphate (CA4P) is a microtubule-disrupting tumour-selective vascular disrupting agent (VDA).

238 ER, data from 435 (35%) of 1254 patients for tumour size (T1 vs rest), nodal status (N0 vs rest), num

239 Clinically, tumour SLC43A2 correlated negatively with T cell histone

240 lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft-tissue sarcomas, and bone cancer) by compar

241 xpressing carcinomas, subsequently releasing tumour-specific antigens into the tumour microenvironmen

242 int inhibitors demonstrates the potential of tumour-specific CD8(+) T cells to prevent and treat canc

243 can be circumvented by CAR-T cells targeting tumour-specific driver gene mutations, such as the four-

244 the processing of two substrates by multiple tumour-specific enzymes produce a fluorescent signal wit

245 Tumour-specific suprabasal stiffness gradients are gener

246 oid growth is parameterised by multicellular tumour spheroid (MCTS) data.

247 The mathematical model for tumour spheroid growth is parameterised by multicellular

248 tinuum models of microbead infiltration into tumour spheroids as they rely on resolving the trajector

249 Here, the response of tumour spheroids formed from two established human cance

250 to correlate the efficacy of some drugs with tumour stage.

251 centre B-cell or non-germinal centre B-cell tumour subtype and double or triple expressor status wer

252 tcome of the study was the effect of primary tumour subtype, age, and sex and on severe acute respira

253 ients with cancer, considering age, sex, and tumour subtype.

254 Diverse applications-particularly in tumour subtyping-have demonstrated the importance of int

255 at has been widely applied in the context of tumour subtyping.

256 DNA repair, replication fork maintenance and tumour suppression, and its therapeutic relevance.

257 Mechanistically, the tumour-suppressive effects of mutant p53 were driven by

258 We also establish H1 as a bona fide tumour suppressor and show that mutations in H1 drive ma

259 prostate cancer, SPOP seems to function as a tumour suppressor by targeting several proteins, includi

260 drocarbon receptor (AHR) pathway as a potent tumour suppressor in a SHH medulloblastoma mouse model.

261 ide genetic evidence for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critic

262 Alternative tumour suppressor pathways need to be explored to treat

263 Both human TSC1 and TSC2 are important tumour suppressors, and mutations in them underlie the d

264 clude that MEGF11 plays an important role in tumour survival and that overexpression of MEGF11 induce

265 PTEN hamartoma tumour syndrome (PHTS) is an umbrella term encompassing

266 to advances in therapeutic organ repair and tumour targeting.

267 Similarly to soft tissue tumours, the World Health Organisation (WHO) classificat

268 The hypermutator-phenotype of dMMR tumours theoretically enables high evolvability but thei

269 ollagen and DDRs in supporting the growth of tumours thriving within a collagen-rich stroma.

270 urs, and a formalin-fixed, paraffin-embedded tumour tissue block available for analysis.

271 me and DNA methylation data for 208 pairs of tumour tissue samples and matched healthy control tissue

272 two breast cancer cell-lines and two patient tumour tissue samples through a qPCR instrument and fina

273 ntly improved specificity and sensitivity to tumour tissue.

274 Variant histologies in tumour tissues that have developed distinct morphologica

275 ctivation as well as the oxidative status in tumours to clarify the mechanisms involved in a multiple

276 ne lipid diversity, which further sensitizes tumours to metabolic stress.

277 o block melanoma tumour growth and sensitize tumours to targeted therapy via epigenetic reprogramming

278 The high tumour-to-normal tissue ratio offered by TMRET in combin

279 erations to date, obtained by characterizing tumour transcriptomes from 1,188 donors of the Pan-Cance

280 IHC outperformed MSI for tumour triage and reliably identified both germline and

281 objective response to pembrolizumab for each tumour type according to the Response Evaluation Criteri

282 tuned to improve the representation of these tumour types.

283 tation signatures associated with particular tumour types.

284 selectively imaging and delivering drugs to tumours typically leverage differentially upregulated su

285 imating the probability of complication-free tumour under different treatment protocols.

286 specificity; 64% MSI-H and 73% MMR deficient tumours unexplained by LS or MLH1-hypermethylation had s

287 tem are occluded for the first and the whole tumour vasculature is destroyed for the latter.

288 to the Response Evaluation Criteria in Solid Tumours version 1.1 or the International Neuroblastoma R

289 a substantial and immediate occlusion of the tumour vessels followed by haemorrhage within the tissue

290 for the amplification of imaging contrast in tumours via the temporal integration of the imaging sign

291 This substantial and sustained decrease in tumour volume suggests that the proposed drug delivery a

292 For drugs indicated for solid tumours, we assessed clinical benefit using ASCO-VF and

293 In Kaplan-Meier analysis, patients whose tumours were CCS Low had a longer Progression Free Inter

294 internal compositions (the proportion of the tumour which is proliferating, hypoxic/quiescent and nec

295 itional knockout mice also generates similar tumours, which are rescued by deletion of YAP1 and its p

296 Glioblastoma (GBM) is a brain tumour with high invasiveness and poor prognosis.

297 Tumours with an immunosuppressive microenvironment respo

298 of the study were aged 1-18 years with solid tumours with measurable or evaluable disease (by Respons

299 hteen pipelines for the reconstruction of 10 tumours with multi-region sampling.

300 ight be a potential therapeutic strategy for tumours with RNF43 mutations.

301 usion MRI signal permits monitoring of brain tumours without invasive intervention.