ライフサイエンスコーパス: solid tumour

1 t-effective manner with applicability to any solid tumour.

2 to 500 cell lines(1,2) spanning 21 types of solid tumour.

3 countered in the poorly angiogenic core of a solid tumour.

4 ng of the biology of this complex paediatric solid tumour.

5 luation of tisotumab vedotin is warranted in solid tumours.

6 zumab duocarmazine in patients with advanced solid tumours.

7 ntibody inhibitors in patients with advanced solid tumours.

8 argeting for the treatment of PDAC and other solid tumours.

9 usiasm for immunotherapy in the treatment of solid tumours.

10 ion at lower pH values in hypoxic regions of solid tumours.

11 or patient survival in the majority of human solid tumours.

12 erapeutic strategy to treat breast and other solid tumours.

13 hibitor currently in clinical development in solid tumours.

14 own salvage responses in multiple refractory solid tumours.

15 ited by extracellular acidity, a hallmark of solid tumours.

16 cer in the USA, and the most familial of all solid tumours.

17 e shown significant activity against several solid tumours.

18 ave been proposed to improve accumulation in solid tumours.

19 ealistically large and clinically detectable solid tumours.

20 y and rapidly profile structural variants in solid tumours.

21 l responses in some patients with metastatic solid tumours.

22 liative care services than are patients with solid tumours.

23 n patients with predefined types of advanced solid tumours.

24 ave not been considered for the treatment of solid tumours.

25 why overexpression of ORAOV1 is so common in solid tumours.

26 nge of cancers, including non-haematological solid tumours.

27 tions that are frequently encountered within solid tumours.

28 proliferative disease and contribute to some solid tumours.

29 nslocations underlie both haematopoietic and solid tumours.

30 d response rate in individuals with advanced solid tumours.

31 untreated brain metastases, and non-melanoma solid tumours.

32 s with melanoma, brain metastases, and other solid tumours.

33 sly treated recurrent or metastatic advanced solid tumours.

34 phenotypes including a reduced incidence of solid tumours.

35 pillary distances that are characteristic of solid tumours.

36 ours, have recently been described in common solid tumours.

37 and prognosis of various haematological and solid tumours.

38 somes and CIN, two common characteristics of solid tumours.

39 o with other haematological malignancies and solid tumours.

40 n patients with sarcoma and those with other solid tumours.

41 This concept is currently being tested in solid tumours.

42 moderately myelosuppressive chemotherapy for solid tumours.

43 ntered clinical studies for the treatment of solid tumours.

44 ) are effective adjuncts to the treatment of solid tumours.

45 tly being evaluated clinically in a range of solid tumours.

46 for the study of targeted therapies in other solid tumours.

47 well-tolerated approach for the treatment of solid tumours.

48 xplained why this might happen, at least for solid tumours.

49 ute leukaemia and high dose chemotherapy for solid tumours.

50 moderately myelosuppressive chemotherapy for solid tumours.

51 l', which overcomes these barriers unique to solid tumours.

52 use of valproate in human haematological and solid tumours.

53 synthesis in angiogenesis, such as found in solid tumours.

54 ng a place in the routine management of some solid tumours.

55 as in those with other cancers, particularly solid tumours.

56 , basket trial of durvalumab and olaparib in solid tumours.

57 mechanosensitive cation channel in multiple solid tumours.

58 receptor (CAR)-T cells for the treatment of solid tumours.

59 tologically confirmed advanced or metastatic solid tumours.

60 is the identification of immune cells within solid tumours.

61 ption for patients with NTRK fusion-positive solid tumours.

62 lable for patients with NTRK fusion-positive solid tumours.

63 with selected, previously treated, advanced solid tumours.

64 vering drugs to the edges and to the core of solid tumours.

65 ngle-agent activity in the common paediatric solid tumours.

66 ulation of patients with TRK fusion-positive solid tumours.

67 umab deruxtecan in HER2-expressing, advanced solid tumours.

68 atic BRAF(V600E) mutations and are typically solid tumours.

69 on and has single-agent activity in advanced solid tumours.

70 polymerase (PARP) inhibitors in a variety of solid tumours.

71 mour immunity and CAR T-cell therapy against solid tumours.

72 fety and tolerability in patients with mIDH1 solid tumours.

73 zumab deruxtecan in HER2-expressing advanced solid tumours.

74 tor-assessed Response Evaluation Criteria in Solid Tumours 1.1 progression-free survival and overall

75 l schedules (28-day cycles) in patients with solid tumours: (1) 4.0 mg or 3.2 mg CH5126766 three time

76 models that led to the eradication of small solid tumours (~100 mm(3)) and regression of large estab

77 CAR T cells have been less effective against solid tumours(3-5), in part because they enter a hypores

78 eal-world environments such as the gut(6,7), solid tumours(8,9), bioreactors(10) or soil(11).

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

80 d and glucose deprivation, stresses found in solid tumours, activated the upstream eukaryotic initiat

81 t delivery, where light is fed directly into solid tumours, allows PDT to be used for large, buried t

82 d 65 drugs: 47 (72%) drugs were approved for solid tumours and 18 (28%) were approved for haematologi

83 ntre phase 1 study in patients with advanced solid tumours and adequate organ function.

84 ty of crizotinib in children with refractory solid tumours and anaplastic large-cell lymphoma.

85 egions of hypoxia (low oxygen) occur in most solid tumours and cells in these areas are the most aggr

86 ciations between monthly treatment costs for solid tumours and clinical benefit in all assessed count

87 e the complexity and diversity of paediatric solid tumours and establish new models of recurrent dise

88 going clinical investigations for a range of solid tumours and haematological malignancies.

89 ry cancers encompass some of the most common solid tumours and have high rates of morbidity and morta

90 mental in clinical management of both common solid tumours and hematologic malignancies.

91 trospective review, patients with pancreatic solid tumours and history of previous extrapancreatic ca

92 CIN is observed in most solid tumours and is associated with both poor prognosis

93 moderately myelosuppressive chemotherapy for solid tumours and lymphomas during the first cycle of ch

94 charge is feasible in low-risk patients with solid tumours and lymphomas, at least in specialist cent

95 umour activity of this drug in patients with solid tumours and multiple myeloma harbouring RAS-RAF-ME

96 or standard care in ambulatory patients with solid tumours and no indication for anticoagulation publ

97 Of 136 patients with solid tumours and other lymphomas, eight had partial res

98 noclonal antibody, in patients with advanced solid tumours and to determine the optimum doses for fur

99 is currently being proposed to treat certain solid tumours and various other diseases.

100 .745-1.123) overall, 0.762 (0.609-1.766) for solid tumours, and 0.149 (0.090-0.247) for haematologica

101 tatic or locally advanced previously treated solid tumours, and adequate end-organ function.

102 ETATION: Dabrafenib is safe in patients with solid tumours, and an active inhibitor of Val600-mutant

103 macrophage infiltration into early avascular solid tumours, and extensions to study the interaction o

104 nts of type I collagen is a hallmark of many solid tumours, and fibrosis is a promising target in can

105 nd in sprouting endothelium during growth of solid tumours, and showed that the hepatitis C IRES is u

106 ponses in patients with NTRK fusion-positive solid tumours, and was well tolerated with a manageable

107 In 28 patients with BRAF-mutant non-melanoma solid tumours, apparent antitumour activity was noted in

108 Tumour-specific CD8 T cells in solid tumours are dysfunctional, allowing tumours to pro

109 Solid tumours are exposed to microenvironmental factors

110 Aggressive behaviours of solid tumours are highly influenced by the tumour microe

111 Solid tumours are infiltrated by effector T cells with t

112 A better mechanistic understanding of how solid tumours are rejected may aid the design of more ef

113 atients, the Response Evaluation Criteria in Solid Tumours are suboptimum to predict benefit.

114 ealth of transcriptomic and clinical data on solid tumours are under-utilized due to unharmonized dat

115 Paediatric solid tumours arise from endodermal, ectodermal, or meso

116 Neuroblastoma, the most common paediatric solid tumour, arises from defective neural crest cells.

117 es to prevent and treat bone metastases from solid tumours as well as myeloma bone disease.

118 ion study of ivosidenib monotherapy in mIDH1 solid tumours at 12 clinical sites in the USA and one in

119 on study, we enrolled patients with advanced solid tumours at one site in the UK and two sites in the

120 t patients with advanced TRK fusion-positive solid tumours based on a primary analysis set of 55 pati

121 ng ones--is a prerequisite for the growth of solid tumours beyond a diameter of approximately 2 mm.

122 vascularisation to permit the development of solid tumours beyond a threshold size, has focused atten

123 d 25 years and older with one of 12 types of solid tumours (bladder, breast, colon, endometrial, lary

124 dely used as coadjuvants in the treatment of solid tumours, but GC treatment may be associated with p

125 th placebo or standard care in patients with solid tumours, but it does not improve survival.

126 ectively eliminated CXCR4(+) cancer cells in solid tumours, but showed limited toxicity to normal CXC

127 R T-cell therapy responses, particularly for solid tumours, by combining CAR T-cell therapy with radi

128 practice for patients with diseases such as solid-tumour cancers, haematological malignancies, and c

129 generally considered to play a minor role in solid tumour carcinogenesis.

130 As in leukaemias, several childhood solid tumours carry balanced chromosomal translocations,

131 GRP78 has been reported to be secreted from solid tumour cells, participating in cell-cell communica

132 Further, like most solid tumours, colorectal cancer exhibits immune/inflamm

133 Solid tumours comprise mixtures of tumour cells (TCs) an

134 advanced or metastatic NTRK fusion-positive solid tumours comprising ten different tumour types and

135 The majority of solid tumours contain regions of hypoxia and it has rece

136 The therapeutic control of a solid tumour depends critically on the responses of the

137 nocarcinoma (PDAC) is one of the most lethal solid tumours despite the use of multi-agent conventiona

138 They explain why solid tumours develop resistance to targeted therapies i

139 t of several human leukaemias, their role in solid tumour development has been somewhat more controve

140 Solid tumours display varied oxygen levels and this char

141 dian era of radical surgical extirpation for solid tumours dominated the first half of the 20th centu

142 linical success has not yet been achieved in solid tumours due in part to the strong immunosuppressiv

143 ng to progress in the treatment of malignant solid tumours, earlier diagnosis by MRI and an ageing po

144 resectable or metastatic, or both) incurable solid tumour (eligible tumour types were anal, biliary,

145 e central nervous system are the most common solid tumour encountered.

146 ical behaviour and represent the most common solid tumour entity of childhood, accounting for approxi

147 nded phase 2 dose in patients with incurable solid tumours, especially those with melanoma and untrea

148 ic children, one consisting of children with solid tumours, excluding lymphomas (n = 409), the other

149 Solid tumours exhibit altered pH homeostasis with extrac

150 eath receptor 1 [PD-1] antibody) in advanced solid tumours expressing programmed cell death ligand 1

151 fine a unique molecular subgroup of advanced solid tumours for which larotrectinib is highly active.

152 facilitates anchorage-independent growth and solid tumour formation in vivo, whereas the activation o

153 imitations, anchorage-independent growth and solid tumour formation in vivo.

154 tional mutagen to identify genes involved in solid tumour formation.

155 how to derive the cellular composition of a solid tumour from bulk gene expression data by mathemati

156 12,294 patients with a variety of solid tumours from 17 randomised controlled trials were

157 diagnosis of advanced, malignant, incurable solid tumours from University of California at San Diego

158 n order to address this multiscale nature of solid tumour growth and its response to treatment, we pr

159 ll tumour cell burden by over 90% and reduce solid tumour growth in combination with the antioxidant

160 This paper reports a hybrid model of solid tumour growth in order to investigate the impact o

161 We propose a cellular automaton model of solid tumour growth, in which each cell is equipped with

162 of blood vessels, is a crucial component of solid tumour growth, linking the relatively harmless ava

163 ming metabolic stress is a critical step for solid tumour growth.

164 patients with metastatic or locally advanced solid tumours harbouring oncogenic NTRK1, NTRK2, and NTR

165 gical malignancies, its success in combating solid tumours has been limited.

166 usiasm, application of CAR T-cell therapy to solid tumours has had little success, although positive

167 The management of metastatic solid tumours has historically focused on systemic treat

168 Radical treatment of many solid tumours has moved from surgery to multimodal organ

169 substantial change in trial methodology for solid tumours has taken place, in response to increased

170 kpoint pathway, a frequent characteristic of solid tumours, has any effect on oncogene addiction.

171 f blood-borne cancers, but the advances with solid tumours have been modest.

172 Solid tumours have oxygen gradients and areas of near an

173 notherapeutic approaches, similarly to other solid tumours, have shown promising results so far.

174 ma has the highest case-fatality rate of any solid tumour, highlights the urgency for designing novel

175 has shown antitumour activity across various solid tumours; however, its initial development was limi

176 in a wide range of epithelial cells and some solid tumours; however, its role in breast cancer is onl

177 re remains a promising approach for treating solid tumours; however, the mechanisms of tumour neovasc

178 the most frequent, aggressive, extracranial solid tumour in childhood.

179 gical malignancies compared with people with solid tumours in a consecutive case series.

180 ble safety profile in patients with advanced solid tumours in a dose-escalation phase 1a trial.

181 tocol for monitoring the mutation profile of solid tumours in cancer patients.

182 Kidney tumours are among the most common solid tumours in children, comprising distinct subtypes

183 rapeutic and imaging molecules in metastatic solid tumours in humans.

184 The lower occurrence of solid tumours in individuals with DS supports the identi

185 work, thus blocking the angiogenic switch in solid tumours in mice.

186 as to whether there is a lower incidence of solid tumours in people with trisomy 21 (Down's syndrome

187 C oncogene is overexpressed in many types of solid tumours including the lethal castration-resistant

188 r activity against NTRK gene fusion-positive solid tumours, including CNS activity due to its ability

189 , has become the standard of care in several solid tumours, including colorectal cancer, renal-cell c

190 In multiple solid tumours, including gliomas, the mechanical propert

191 tumour-associated antigen expressed by many solid tumours, including non-small-cell lung cancer.

192 the overexpression of FRalpha in a range of solid tumours, including ovarian, lung and breast cancer

193 iew of the molecular landscape of paediatric solid tumours, including their underlying genomic altera

194 empt to stimulate an immune response against solid tumours, infiltration of effector cells into the t

195 tical model for the growth and invasion of a solid tumour into a domain of tissue (in this case breas

196 though the overall survival of children with solid tumours is 75%, that of children with recurrent di

197 nt of biological agents for the treatment of solid tumours is an area of considerable activity.

198 The progression of many solid tumours is driven by deregulation of multiple comm

199 variants acting as disease-drivers in common solid tumours is frequently small in size, but significa

200 As incidence of many solid tumours is much lower in DS, we speculated that di

201 P3, a purported tumour suppressor in various solid tumours, is expressed in erythroid cells.

202 tumour development in vivo, particularly in solid tumours, is not completely understood.

203 ith locally advanced or metastatic (or both) solid tumours known to express tissue factor.

204 ncer overexpressed) is overexpressed in many solid tumours, making a key contribution to the developm

205 In patients with solid tumour malignancies in the modified intention-to-t

206 The trial included adult patients with solid tumour malignancies receiving chemotherapy and tho

207 or herpes zoster prevention in patients with solid tumour malignancies receiving chemotherapy, but wa

208 was herpes zoster incidence in patients with solid tumour malignancies receiving chemotherapy, which

209 days after the fourth dose in patients with solid tumour malignancies receiving chemotherapy.

210 icacy against herpes zoster in patients with solid tumour malignancies was 63.6% (97.5% CI 36.4 to 79

211 In patients with solid tumour malignancies, serious adverse events were s

212 ntial agents for the treatment of a range of solid tumour malignancies.

213 on, from 2.6 (95%CI 2.6-2.7) in those with a solid tumour malignancy to 12.3 (95%CI 11.3-13.2) in tho

214 ng the specific immune cell composition of a solid tumour may be essential to predict a patient's res

215 The delivery of therapeutic drugs to solid tumours may be impaired by structural and function

216 s guideline describes a standard approach to solid tumour measurements and definitions for objective

217 The solid tumour microenvironment includes nerve fibres that

218 adjuvant therapy when surgical resection of solid tumours might leave behind residual microscopic di

219 Compared with patients with solid tumours (n=4414), there were no significant differ

220 for DPB1*0201 as compared with children with solid tumours [odds ratio (OR), 95% confidence interval

221 Osteosarcoma is the most common solid tumour of childhood.

222 encing of 500 adult patients with metastatic solid tumours of diverse lineage and biopsy site.

223 Lymphomas are solid tumours of the immune system.

224 tients with stable or progressing metastatic solid tumours, on single-agent chemotherapy or hormonal

225 or herpes zoster prevention in patients with solid tumour or haematological malignancies.

226 rmed, PD-L1-positive, relapsed or refractory solid tumour or lymphoma, and a Lansky Play/Karnofsky Pe

227 wing cellular populations, such as biofilms, solid tumours or developing embryos, is thought to be do

228 adults with recurrent or refractory non-CNS solid tumours or lymphoma.

229 1-2 trial of patients (aged <30 years) with solid tumours or lymphomas recruited from 28 hospitals i

230 eligible patients had advanced or metastatic solid tumours or multiple myeloma harbouring RAS-RAF-MEK

231 dose-escalation cohort and 29 patients with solid tumours or multiple myeloma were included in the b

232 significantly more children than those with solid tumours or normal infants typed for DPB1 alleles c

233 rts of patients with different INI1-negative solid tumours or synovial sarcoma.

234 cal assessment of alisertib in patients with solid tumours, particularly those with breast cancer and

235 der acidic conditions such as those found in solid tumours (pH approximately 6), and effectively inhi

236 two single-stage expansion cohorts within a solid-tumour phase 1 trial.

237 The majority of assays used for solid tumour profiling use DNA sequencing to interrogate

238 of modified Response Evaluation Criteria in Solid Tumours (RECIST version 1.1) in cancer immunothera

239 ers based on Response Evaluation Criteria In Solid Tumours (RECIST) criteria.

240 according to Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1, including two comple

241 response by Response Evaluation Criteria in Solid Tumours [RECIST]) in evaluable patients who receiv

242 r cytologically confirmed advanced malignant solid tumours refractory to previous therapies, and an E

243 st 20 years of age in Japan and had advanced solid tumours (regardless of HER2 expression in dose esc

244 least 20 years old in Japan and had advanced solid tumours (regardless of HER2 expression in dose esc

245 Regulatory enhancer elements in solid tumours remain poorly characterized.

246 enetically distinct clones within developing solid tumours remain poorly understood.

247 Drug penetration into solid tumours remains a major challenge in the effective

248 All solid tumours require a vascular supply in order to prog

249 The growth of solid tumours requires a blood supply provided by re-mod

250 in vivo targets for antibodies in lungs and solid tumours, respectively.

251 Abnormal vascularization of solid tumours results in the development of microenviron

252 kidney injury [NSCLC], hypoglycaemia [other solid tumours], retinopathy [urothelial carcinoma], and

253 From 1 January 2013 to 31 December 2013, solid tumour samples (including non-small-cell lung carc

254 Three haematological and five solid tumour second primary malignancies in the placebo

255 with three (1%) haematological and nine (4%) solid tumour second primary malignancies in the placebo

256 18 (8%) haematological and 14 (6%) solid tumour second primary malignancies were diagnosed

257 The binding to tumours, solid tumour slices and tumour cells correlated well wit

258 alysed whole-exome sequencing data from 5777 solid tumours, spanning 19 cancer types from The Cancer

259 scovery of tumour initiating cells (TICs) in solid tumours, studies focussing on their role in cancer

260 al decline at the end of life to people with solid tumours, suggesting similar care needs.

261 responses, and it is overexpressed in human solid tumours, suggesting that it has an important funct

262 d clinical benefit in patients with advanced solid tumours supporting further investigation of the co

263 o potential beneficial effects in some other solid tumours, the choice of anaesthetic method had no i

264 tion of treatment responses in patients with solid tumours, therefore, often fail to detect successfu

265 Unlike most solid tumours, thickness rather than cytological markers

266 for epigenetic differentiation therapy of a solid tumour through EZH2 inhibition.

267 d permeability and retention (EPR) effect in solid tumours to increase accumulation at the target sit

268 e mouse models of breast carcinoma and other solid tumours to show that selective CDK4/6 inhibitors n

269 ogation in vitro of heterogeneous cells from solid tumours together with their native microenvironmen

270 cytomas and paragangliomas (PCC/PGL) are the solid tumour type most commonly associated with an inher

271 e factor, which is expressed across multiple solid tumour types and is associated with poor clinical

272 ficacy has been demonstrated across multiple solid tumour types within clinical trials.

273 ied a frequent 5p13 amplification in several solid tumour types, including lung (56%), ovarian (38%),

274 ell tumours are superior to those with other solid tumour types, there are still many areas that requ

275 on-small-cell lung cancer (NSCLC), and other solid tumour types.

276 xia is also problematic for the treatment of solid tumours using these techniques.

277 For cancers, such as common solid tumours, variants in the genome give a selective g

278 rding to the Response Evaluation Criteria in Solid Tumours version 1.1 or the International Neuroblas

279 onse) as per Response Evaluation Criteria in Solid Tumours (version 1.1) by independent central revie

280 evaluated by Response Evaluation Criteria in Solid Tumours, version 1.1) were observed in patients wi

281 reted in the tumour microenvironment of many solid tumours, was assessed.

282 For drugs indicated for solid tumours, we assessed clinical benefit using ASCO-V

283 models as surrogates for three common human solid tumours, we describe a standardised workflow for s

284 o investigate the function of CAR T cells in solid tumours, we transferred hCD19-reactive CAR T cells

285 were enrolled to the study: 29 patients with solid tumours were included in the dose-escalation cohor

286 criptions of the altered metabolic nature of solid tumours were reported by Otto Warburg almost a cen

287 Eligible patients had incurable solid tumours, were 18 years or older, and had adequate

288 d a total of 4599 patients with RCC or other solid tumours, were selected from 223 articles screened

289 for oncolytic adenoviruses in patients with solid tumours when administered intratumorally, resultin

290 een shown to preferentially replicate within solid tumours when injected from a distal site, and all

291 harmacokinetics of avelumab in patients with solid tumours while assessing biological correlatives fo

292 ients naive to chemotherapy with a malignant solid tumour who were scheduled to receive cisplatin-bas

293 uited adults (aged >=18 years) with advanced solid tumours who had received one or more previous line

294 tic or locally advanced NTRK fusion-positive solid tumours who received entrectinib orally at a dose

295 tion (ie, patients with NTRK fusion-positive solid tumours who were TRK inhibitor-naive and had recei

296 astatic non-CNS primary, TRK fusion-positive solid tumour, who had received standard therapy previous

297 hase) of the study were aged 1-18 years with solid tumours with measurable or evaluable disease (by R

298 d the UK with locally advanced or metastatic solid tumours with variable HER2 status who were refract

299 and young adults with refractory or relapsed solid tumours, with known or expected PD-L1 expression.

300 ome evidence of clinical activity in various solid tumours, with partial confirmed or unconfirmed res