ライフサイエンスコーパス: primary tumour

1 multiple competing subclones within a single primary tumour.

2 fter apparently curative surgery removed the primary tumour.

3 ay arise from a minority of cells within the primary tumour.

4 metastasis and a xenograft derived from the primary tumour.

5 because cells have already escaped from the primary tumour.

6 eminated cells after surgical removal of the primary tumour.

7 , depending upon the ER concentration in the primary tumour.

8 stinct characteristics and genetics from the primary tumour.

9 ter the apparently successful treatment of a primary tumour.

10 tics of metastases than is available for the primary tumour.

11 markedly different biology from that of the primary tumour.

12 (ECM) and increased local invasion from the primary tumour.

13 ded from different clones present within the primary tumour.

14 the adjuvant setting after resection of the primary tumour.

15 ours and metastases, as well as the injected primary tumours.

16 rcinoma (HCC) following surgical ablation of primary tumours.

17 nome-wide DNA copy number alterations in 701 primary tumours.

18 tions of histopathologically well-classified primary tumours.

19 pattern reminiscent of that reported in some primary tumours.

20 with colorectal cancer had surgery to remove primary tumours.

21 7%) neuroblastoma cell lines and 10/50 (20%) primary tumours.

22 majority of events were classified as second primary tumours.

23 ng late ipsilateral and contralateral second primary tumours.

24 which very rarely has p53 gene mutations in primary tumours.

25 sent in five lines and at least three of ten primary tumours.

26 tastases in 55% of the animals that produced primary tumours.

27 romatin accessibility in lung adenocarcinoma primary tumours.

28 ic large cell lymphoma (ALCL) cell lines and primary tumours.

29 deficient wtGIST and 3/6 cases had multiple primary tumours.

30 tastatic microenvironment after resection of primary tumours.

31 Moreover, among metastases from the same primary tumour, 100% of the driver mutations in 17 patie

32 36%] of 9169 patients; p=0.0003), have colon primary tumours (1116 [84%] of 1334 patients vs 5603 [66

33 indeterminate uptake across all IC (mean PPV primary tumour 36%, nodes 48%).

34 d despite surgical or radiation treatment of primary tumours, ~50% of patients progress to metastatic

35 umour cells from 19 women with ER(+)/HER2(-) primary tumours, 84% of whom had acquired circulating tu

36 Of these six mutations, two were in primary tumours (a colorectal cancer and a breast cancer

37 al-like breast cancer: peripheral blood, the primary tumour, a brain metastasis and a xenograft deriv

38 show that within a predominantly epithelial primary tumour, a small proportion of tumour cells under

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

40 illed and conservative surgery to remove the primary tumour; adjuvant therapies are also given before

41 Gliomas are the most common primary tumours affecting the adult central nervous syst

42 egulated in approximately 90% and 86% of all primary tumours analysed, respectively.

43 d in men, with higher SUV(max) values of the primary tumour and a more advanced CT-based stage of the

44 es dissemination of cancer cells away from a primary tumour and colonization at distal sites.

45 Identification of the primary tumour and development of a tailored site-specif

46 d-derived suppressor cells infiltrate in the primary tumour and distant organs with different time ki

47 hat after metastatic cancer cells escape the primary tumour and enter the circulation, their interact

48 ong time intervals between cells leaving the primary tumour and growth of overt metastases(2,3).

49 They also carry information about the primary tumour and have the potential to be valuable bio

50 ons, providing growth advantages both in the primary tumour and in the lung microenvironment.

51 lysis of 100 single cells from a monogenomic primary tumour and its liver metastasis indicated that a

52 aimed to evaluate initial PET/CT features of primary tumour and locoregional metastatic lymph nodes (

53 ed disease stage, and SUV(max) values of the primary tumour and lymph nodes.

54 resolved transcriptomics from 55 samples of primary tumour and metastases (liver, lung and peritoneu

55 ry to determine the PD-L1 status in both the primary tumour and metastatic lymph nodes.

56 reduced neutrophil infiltration to both the primary tumour and metastatic sites.

57 These cells detach from the primary tumour and move from the bloodstream to a new si

58 were 91, 25, 20, 13 and 55, 70, 18 and 3 for primary tumour and nodes respectively.

59 Patients aged 18 or older with a controlled primary tumour and one to five metastatic lesions, Easte

60 uality of life in patients with a controlled primary tumour and one to five oligometastatic lesions.

61 ed to identify transcriptomic differences in primary tumour and peritumoral adipose tissue between ob

62 Radiotherapy directly interferes with the primary tumour and possibly reverses some immunosuppress

63 um associated with relapse, we sequenced the primary tumour and relapse genomes from eight AML patien

64 ed that a single clonal expansion formed the primary tumour and seeded the metastasis.

65 At 20 mg/kg growth of both the primary tumour and the number of metastatic deposits in

66 orrelations between PET/CT parameters of the primary tumour and those of metastatic axillary LNs.

67 SF1A methylation status in a large series of primary tumour and tumour lines; (b) chromosome 3p allel

68 o delineate the immune crosstalk between the primary tumour and tumour-draining lymph nodes and how t

69 e is mounting evidence that resection of the primary tumour and/or localised radiotherapy (locoregion

70 We studied primary tumours and 156 lymph nodes from 32 patients wit

71 Notably, PARP14 is highly expressed in HCC primary tumours and associated with poor patient prognos

72 myc-induced apoptosis by Cbfa1 as explanted primary tumours and cell lines from CD2-Cbfa1-G1/CD2-myc

73 that are unique to breast cancer cell lines, primary tumours and colon cancer cells.

74 and assessed transcriptional profiles in 43 primary tumours and copy number profiles in 38 primary t

75 r sub-clonal expression of a PA signature in primary tumours and for dominant expression in clustered

76 nts with LN metastases had relatively larger primary tumours and higher SUVmax values.

77 All primary tumours and histologically involved lymph nodes

78 Loss of FBXL4 was also detected in primary tumours and it was highly associated with progno

79 collected at autopsy together with available primary tumours and longitudinal metastatic biopsies tak

80 rspective, I examine how genetic analyses of primary tumours and matched metastases can distinguish b

81 Comparison of primary tumours and matched relapse samples showed a str

82 ductal carcinomas and express E-cadherin in primary tumours and metastases(4).

83 tant p53 resulted in the rapid appearance of primary tumours and metastases.

84 ctively suppressed the growth of MLL3-mutant primary tumours and metastases.

85 We find that both primary tumours and micrometastases display transcriptio

86 mediates regression of both light-irradiated primary tumours and non-irradiated distant tumours by in

87 nd SNAIL in the metastases compared with the primary tumours and renal vein tumour thrombi.

88 ous degrees of genetic heterogeneity between primary tumours and their distant metastases.

89 ter region CpG island was hypermethylated in primary tumours and tumour cell lines.

90 d expression of the human CAVEOLIN-1 gene in primary tumours and tumour-derived cell lines.

91 ases, N2 disease, or poor differentiation of primary tumour), and previous adjuvant treatment with ox

92 d early, before the last clonal sweep in the primary tumour, and early divergence was enriched for pa

93 to AJCC staging criteria, ulceration of the primary tumour, and patient sex.

94 ions and a large deletion not present in the primary tumour, and was significantly enriched for 20 sh

95 agnosis of lung cancer and no other previous primary tumour, and who were mentally fit with sufficien

96 LMO1 expression (P = 0.028) in neuroblastoma primary tumours, and ablates GATA3 binding (P < 0.0001).

97 hway was significantly higher in BMs than in primary tumours, and SERPINI1 was the most frequently mu

98 e driver mutations beyond those required for primary tumours, and that phylogenetic trees across meta

99 The primary tumours arising from the S100A4-expressing cells

100 ironment-ideally, recovering the role of the primary tumour as an immunogenic hub.

101 oma cells thus reducing tumour growth in the primary tumour as well as at metastatic sites.

102 methylation occurs frequently (> or =20% of primary tumours) at CASP8, SLIT2 and RASSF1A in Wilms' t

103 in size who had a complete resection of the primary tumour between Jan 1, 2000, and Dec 31, 2010.

104 cimens from patients and of 28 corresponding primary tumour biopsies confirmed the score's effectiven

105 ell RNA-seq of CD45(+) cell populations from primary tumours, blood and lungs demonstrated that IL11

106 ivity, and that fusion-positive ES cells and primary tumours both express low or undetectable levels

107 er seems to arise from a single clone in the primary tumour but can exhibit subclonal heterogeneity a

108 Disseminated cancer cells from primary tumours can seed in distal tissues, but may take

109 the increasing use of primary cell cultures, primary tumour cell explants, early passage cell lines,

110 wing uncontrolled proliferation, a subset of primary tumour cells acquires additional traits/mutation

111 Cancer metastasis requires that primary tumour cells evolve the capacity to intravasate

112 Strong nuclear expression of maspin within primary tumour cells is correlated with increased surviv

113 st to higher levels of glycolytic enzymes in primary tumour cells, which we corroborated by flow cyto

114 lls from high-burden tissues were similar to primary tumour cells, which were more heterogeneous and

115 tion, but promotes proliferation in advanced primary tumour cells.

116 -) mice that phenotypically resemble nascent primary tumour cells.

117 In a melanoma mouse model, primary tumour clearance depends on the STING signalling

118 d-stage blood, we detect both metastatic and primary tumour clones, even years after removal of the p

119 ial epigenetic re-programming of early-stage primary tumours compared with late-stage metastases.

120 1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role

121 specialization, for example, dominating the primary tumour, contributing to metastatic populations,

122 e in-frame deletion of 30 base pairs) in six primary tumours, corresponding to an overall mutation fr

123 lysis of human disseminated cancer cells and primary tumours corroborated the relevance of these find

124 ication (a biomarker for bone metastasis) in primary tumours could predict the treatment outcomes of

125 Similarly, 10/15 primary tumour cultures (including three matched to norm

126 ressed induction of GADD45alpha was found in primary tumour cultures compared and to matched peripher

127 s), an algorithm that mines pan-cancer human primary tumour data to identify mutation-specific SL par

128 and growth rate in mice implanted with both primary tumour-derived GBMNS and GBMDC.

129 henotypically distinct clones derived from a primary tumour-derived human prostate cancer cell line (

130 was largely abandoned when no differences in primary tumour development were found between athymic nu

131 that protects immunocompetent hosts against primary tumour development, but this idea was largely ab

132 Symptoms, time frame between primary tumour diagnosis and the finding of metastases,

133 ly consistent with a subsequent or suspected primary tumour diagnosis, when available (23/26 patients

134 colorectal cancer who had surgery to remove primary tumours done by colorectal surgeons or non-color

135 cidental detection of one or more additional primary tumours during computed tomography (CT) staging

136 by ongoing copy number evolution during the primary tumour expansion.

137 ognosis, we examined seven cell lines and 87 primary tumours for co-amplification of candidate genes

138 somatic, and those evaluated occurred in the primary tumour from which the cell line was derived.

139 Care (TCC) protocol, we calculated GARD for primary tumours from 20 disease sites treated using stan

140 lassify lung cancer histologies, distinguish primary tumours from metastases to the lung from other s

141 Studies on GTICs have focused on primary tumours from which GTICs could be isolated and t

142 lastic stroma, ultimately recapitulating the primary tumours from which they arose.

143 g AML relapse: (1) the founding clone in the primary tumour gained mutations and evolved into the rel

144 e investigated the role of DDR1b and DDR2 on primary tumour growth and experimental lung metastases.

145 ings identified divergent effects of DDRs on primary tumour growth and experimental lung metastasis i

146 suggesting a differential role for DDR1b in primary tumour growth and lung colonization.

147 models of vascular permeability, emphysema, primary tumour growth and metastasis.

148 of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression.

149 ) phenotype has been implicated in promoting primary tumour growth and progression to metastatic dise

150 enhanced tumorigenicity in murine models of primary tumour growth and pulmonary metastases.

151 lation of haematopoietic FAK does not affect primary tumour growth but enhances the incidence of meta

152 vealed that these cells do not contribute to primary tumour growth but, instead, constitute a pool of

153 spatial memory impairment without affecting primary tumour growth or causing sickness behaviour.

154 etastasis enhancer that has little impact on primary tumour growth or dissemination but promotes effe

155 at selective Lgr5(+) cell ablation restricts primary tumour growth, but does not result in tumour reg

156 CTC-derived cultures has minimal effects on primary tumour growth, but it greatly increases apoptosi

157 mination and metastasis, but dispensable for primary tumour growth.

158 Caspase-8 status was not a predictor of primary tumour growth; rather, caspase-8 selectively pot

159 Many primary tumours have low levels of molecular oxygen (hyp

160 MR deficiencies, respectively, regardless of primary tumour histology.

161 With a single biopsy of a primary tumour in 14 patients, the likelihood of missing

162 motherapy, and is helpful in identifying the primary tumour in patients who present with axillary ade

163 risk of developing local recurrence or a new primary tumour in previously irradiated areas.

164 Ts were classified as a possible or probable primary tumour in two (1%) of 278 patients with distant

165 dh(low) cancer cells, and silencing Phgdh in primary tumours increases metastasis formation.

166 n metastasis and xenograft compared with the primary tumour indicate that secondary tumours may arise

167 Cancer cells that transit from primary tumours into the circulatory system are known as

168 When the primary tumour is located in the pancreas, it is associa

169 reful monitoring for development of a second primary tumour is necessary, with further investigation

170 In young male patients, the primary tumour is usually in the testis, in other patien

171 d metastases, and HOTAIR expression level in primary tumours is a powerful predictor of eventual meta

172 n of vascular endothelial growth factor C in primary tumours is associated with increased disseminati

173 Eliciting immune responses against primary tumours is hampered by their immunosuppressive m

174 ajor clinical problem as serial re-biopsy of primary tumours is often not a clinical option.

175 1269a expression in their surgically removed primary tumours is strongly associated with risk of CRC

176 ic colorectal cancer, we show that, although primary tumours largely adopt LGR5(+) intestinal stem-li

177 Primary tumours liberate circulating tumour cells (CTCs)

178 es differentiates metastatic cell lines from primary tumour lines.

179 denocarcinoma may not be associated with the primary tumour localisation.

180 ive Oncology Group (ECOG) performance score, primary tumour location [colon vs rectum], previous trea

181 active web response system and stratified by primary tumour location, to either tucatinib plus trastu

182 Of the primary tumours, malignant lesions are more frequent tha

183 arly lesions in mice and before any apparent primary tumour masses are detected, there is a sub-popul

184 establishing transcription-factor mapping in primary tumour material, we show that there is plasticit

185 demonstrate that, even after removal of the primary tumour, MDSCs contribute to the development of p

186 All IC were accurate for prediction of primary tumour (mean NPV 85.0% (84.6-85.3), PPV 85.0% (8

187 Patients were stratified by histology of the primary tumour, metastatic tumour size, and number of me

188 In common with the primary tumours, methylation-associated gene silencing o

189 The xenograft retained all primary tumour mutations and displayed a mutation enrich

190 The comparison of relapse-specific versus primary tumour mutations in all eight cases revealed an

191 elevant doses (5 x 2 Gy) to newly-presenting primary tumours (n = 12); the addition of concurrent cis

192 n was stratified by Breslow thickness of the primary tumour, N stage according to AJCC staging criter

193 were stratified according to the site of the primary tumour, nodal status (N0 or N1 vs N2 or N3), and

194 ree independent observers, who segmented the primary tumour of 20 NSCLC patients twice, to manual sli

195 ized fibrous tumour of the pleura) is a rare primary tumour of the pleura of mesenchymal origin.

196 validated transcriptomic differences in the primary tumours of obese patients compared with those of

197 Primary tumours of the bony spine and adjacent soft tiss

198 Gliomas are the most common primary tumours of the central nervous system, with near

199 ci arise independently and directly from the primary tumour or give rise to each other, i.e. metastas

200 CpG island, this is not methylated in either primary tumours or in tumour-derived cell lines in which

201 Intestinal melanomas can be primary tumours or metastases of cutaneous, ocular, or a

202 sis contain fewer genetic abnormalities than primary tumours or than DCCs from patients with metastas

203 t an early stage of tumour evolution (in the primary tumour) or at a later evolutionary stage (where

204 vival (time to relapse, secondary colorectal primary tumour, or death due to all causes), and overall

205 ancer-related mortality, irrespective of the primary tumour origin.

206 ding a unique cohort of 5 'trios' of matched primary tumour, PDX, and PDO.

207 Detachment of cells from the primary tumour precedes metastatic progression by facili

208 NQO1 expression in the primary tumour predicts response to neoadjuvant chemothe

209 mutations and increased proliferation within primary tumour regions.

210 Primary tumours release extracellular vesicles (EVs), in

211 differential protein expression between the primary tumours, renal vein tumour thrombi and metastase

212 and clinical strategies that do not rely on primary tumour responses.

213 iated with poor clinical outcome observed in primary tumours reveal gene signatures that predict clin

214 hism in colon and lung cancer cell lines and primary tumours revealed a small number of mutations, su

215 cer cells acquiring neuronal mitochondria in primary tumours revealed their selective enrichment at m

216 In cancer, the primary tumour's organ of origin and histopathology are

217 comprehensive genomic characterization of 22 primary tumours sampled before and after 4 months of neo

218 cs, and RNA-seq data from cancer cell lines, primary tumour samples and healthy tissue samples.

219 is of enhancer elements in a large series of primary tumour samples reveals insights into cis-regulat

220 for such heterogeneity and often investigate primary tumour samples that might not be representative

221 Additionally, primary tumour samples were enriched for FBW7 inactivati

222 whole-genome CNVseq was applied to 300 FFPE primary tumour samples, obtained from a large-scale epid

223 1739 AZURE patients contributed primary tumour samples, of whom 865 (50%) had two assess

224 cancer and who gave consent for use of their primary tumour samples.

225 We developed an automated system for scoring primary tumour sections of 91 late-stage ovarian cancer

226 Our meta-analysis shows that LRT of the primary tumour seems to improve overall survival in de n

227 ls that receive mitochondria from neurons in primary tumours, shedding new light on how the nervous s

228 sis of IMP3 status (positive vs negative) in primary tumours showed hazard ratios of 5.84 (95% CI 3.6

229 te genes between BBM tumours and originating primary tumours shows dysregulation of DNA methylation o

230 therapy drug, cisplatin, enables significant primary tumour shrinkage and metastasis prevention.

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

232 caused by cancer cells that migrate from the primary tumour site (the mammary duct) through the blood

233 rows, it induces systemic effects beyond the primary tumour site and affects the macroenvironment, fo

234 radiotherapy to 70 Gy in 33 fractions to the primary tumour site and cervical lymphadenopathy.

235 Tumour cells can escape from the primary tumour site and colonize the bone microenvironme

236 eceived subsequent local radiotherapy to the primary tumour site followed by maintenance therapy.

237 ustained expression of CXCL12 by MSCs in the primary tumour site inhibits metastasis through reductio

238 be a useful approach to unmask the original primary tumour site of cancer of unknown primary cases a

239 consolidation, and radiation therapy to the primary tumour site plus meta-iodobenzylguanidine avid m

240 invade and, hence, guide cells away from the primary tumour site to an extracortical location.

241 tly associated with tumour grade, stage, and primary tumour site, and leads to shorter survival compa

242 l only every 2 weeks, and were stratified by primary tumour site, previous surgery with curative inte

243 treated with these agents regardless of the primary tumour site.

244 eristics of brain metastases relative to the primary tumour so that they can inform targeted therapy

245 equencing of matching peripheral and central primary tumour specimens reveals various region-specific

246 least four positive axillary lymph nodes or primary tumour stage T3-4 disease were eligible to parti

247 metastases arise from a random selection of primary tumour subclones or whether they are enriched fo

248 imary outcome of the study was the effect of primary tumour subtype, age, and sex and on severe acute

249 and kidney cancer cell lines and in several primary tumours such as endometrial carcinomas, malignan

250 duced mouse models of cancer have shown that primary tumour susceptibility is thereby enhanced in imm

251 ilateral axillary LNs (SUVmax-LN), SUVmax of primary tumour (SUVmax-T) and NT ratios (SUVmax-LN/SUVma

252 One patient had three primary tumours synchronously.

253 eomic analysis to identify biomarkers in the primary tumour that predict response to neoadjuvant chem

254 analyses indicate that the cells within the primary tumours that gave rise to metastases are genetic

255 n metastatic tumours but also in a subset of primary tumours that were likely to subsequently develop

256 In the human cases, compared with primary tumours, the metastatic deposits had a significa

257 less responsive to first-line therapies than primary tumours, they acquire resistance to successive t

258 n the area of breast immediately next to the primary tumour; this is despite the finding that two-thi

259 The NPM-ALK kinase is active in primary tumour tissue and forms a multimeric complex wit

260 ) to predict the pathological node status in primary tumour tissue from three independent cohorts of

261 om brain metastases compared to same-patient primary tumour tissue.

262 unogenic, non-canonical peptide sequences in primary tumour tissue.

263 possibility in some cases of downstaging the primary tumour to avoid mastectomy, and to allow breast-

264 ltaneously satisfying a critical need of the primary tumour to be fed by the vasculature.

265 notypic changes enabling cancer cells from a primary tumour to disseminate and colonize at distant or

266 umour immunity by exploiting the capacity of primary tumours to act as antigen depots.

267 imary tumours and copy number profiles in 38 primary tumours to discover molecular subgroups of atypi

268 etastasis is the spread of cancer cells from primary tumours to distant organs and is the cause of 90

269 and did immunohistochemical analyses on 125 primary tumours to evaluate clinicopathological signific

270 the progression of a significant fraction of primary tumours to the metastatic stage.

271 n technique, stratified by hospital, site of primary tumour, tumour size, planned radiotherapy, and i

272 in at least a 4:1 ratio on the basis of sex, primary tumour type, age at diagnosis, smoking status, c

273 reflect differences in the behaviour of the primary tumour types from which the cell lines were deri

274 though The Cancer Genome Atlas has sequenced primary tumour types obtained from surgical resections,

275 hereas NMDAR activation is autocrine in some primary tumour types, human and mouse B2BM cells express

276 differential diagnosis for the origin of the primary tumour using routinely acquired histology slides

277 In responders, surgical excision of the primary tumour was attempted, followed by myeloablation

278 The primary tumour was semi-automatically delineated in the

279 Primary tumour was semi-automatically or manually segmen

280 In both primary tumours, we also identified an unexpectedly abun

281 f translocation in 21 myeloma cell lines and primary tumours, we show that the novel, karyotypically

282 n two others PIK3CA mutations present in the primary tumour were no longer detected at the time of pr

283 ding to the oestrogen-receptor status of the primary tumour were not statistically significant (pinte

284 In a subgroup of 41 subjects whose primary tumours were allelotyped, the fractional allelic

285 371 patients with localised primary tumours were further investigated by use of surv

286 Twenty-five primary tumours were judged to carry only wild type p53

287 ith a second tumour, the most frequent first primary tumours were melanoma (eight patients, 17.8%), l

288 l driver-gene mutations detected in these 14 primary tumours were present among all their metastases.

289 Curative therapy depends on control of the primary tumour, which can arise at many distinct anatomi

290 mic profiles, suggesting all are independent primary tumours, which are consistent with comprehensive

291 20%, minimisation by hospital site, site of primary tumour, WHO performance status, 16-week CT scan

292 r (CRC) undergoing curative resection of the primary tumour will develop metastases in the subsequent

293 Primary tumours will give us the statistical power to dr

294 Local treatment of the primary tumour with the established modalities of radiot

295 Two lines and one primary tumour with this translocation selectively expre

296 Primary tumours with aberrant TSC1 pre-mRNA splicing wer

297 cell lines correlate with distinct groups of primary tumours with different outcomes.

298 in addition colorectal tumour cell lines and primary tumours with low RASSF2 levels show decreased MS

299 In primary tumours with multiple samples, 97% of driver-gen

300 pathway analysis has been from study of the primary tumour, with little attention to the metastatic