ライフサイエンスコーパス: solid tumour

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

2 ng in defective peptide transport in a human solid tumour.

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

4 usiasm for immunotherapy in the treatment of solid tumours.

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

6 phenotypes including a reduced incidence of solid tumours.

7 pillary distances that are characteristic of solid tumours.

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

9 and prognosis of various haematological and solid tumours.

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

11 o with other haematological malignancies and solid tumours.

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

13 This concept is currently being tested in solid tumours.

14 moderately myelosuppressive chemotherapy for solid tumours.

15 ntered clinical studies for the treatment of solid tumours.

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

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

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

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

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

21 ute leukaemia and high dose chemotherapy for solid tumours.

22 moderately myelosuppressive chemotherapy for solid tumours.

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

24 use of valproate in human haematological and solid tumours.

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

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

27 Regions of hypoxia are a common feature of solid tumours.

28 rtant in both the genesis and maintenance of solid tumours.

29 an be used to deliver enzyme to a variety of solid tumours.

30 a notion is clearly lacking, particularly in solid tumours.

31 ignancy, but also in translocations found in solid tumours.

32 hypoxia) and necrosis are common features of solid tumours.

33 lay a role in the development of many common solid tumours.

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

35 erapeutic strategy to treat breast and other solid tumours.

36 hibitor currently in clinical development in solid tumours.

37 own salvage responses in multiple refractory solid tumours.

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

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

40 e shown significant activity against several solid tumours.

41 ave been proposed to improve accumulation in solid tumours.

42 ealistically large and clinically detectable solid tumours.

43 y and rapidly profile structural variants in solid tumours.

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

45 l responses in some patients with metastatic solid tumours.

46 liative care services than are patients with solid tumours.

47 n patients with predefined types of advanced solid tumours.

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

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

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

51 tions that are frequently encountered within solid tumours.

52 proliferative disease and contribute to some solid tumours.

53 nslocations underlie both haematopoietic and solid tumours.

54 d response rate in individuals with advanced solid tumours.

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

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

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

58 The results have generally been negative in solid tumours, although some have been more promising in

59 er who are undergoing active treatment for a solid tumour and 70-90% among those with advanced diseas

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

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

62 In this study, we evaluated 79 human solid tumours and cell lines for genetic abnormalities i

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

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

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

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

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

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

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

70 lity of antibodies or antibody conjugates to solid tumours and the difficulty in obtaining tumour-spe

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

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

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

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

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

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

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

78 ormal tissue which implies that cells within solid tumours are capable of maintaining their level of

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

80 Solid tumours are exposed to microenvironmental factors

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Solid tumours display varied oxygen levels and this char

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

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

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

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

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

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

105 Solid tumours exhibit altered pH homeostasis with extrac

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

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

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

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

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

111 12,294 patients with a variety of solid tumours from 17 randomised controlled trials were

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

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

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

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

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

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

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

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

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

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

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

123 Solid tumours have oxygen gradients and areas of near an

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

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

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

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

128 ne are common in cancer, occurring in 30% of solid tumours in adults.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 Osteosarcoma is the most common solid tumour of childhood.

151 Wilms' tumour (WT) is one of the most common solid tumours of childhood, occurring in 1 in 10,000 chi

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

153 Lymphomas are solid tumours of the immune system.

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

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

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

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

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

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

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

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

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

163 Regulatory enhancer elements in solid tumours remain poorly characterized.

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

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

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

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

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

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

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

171 18 (8%) haematological and 14 (6%) solid tumour second primary malignancies were diagnosed

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

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

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

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

176 Unlike most solid tumours, thickness rather than cytological markers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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