ライフサイエンスコーパス: brain tumour

1 cers, P=0.006 for breast cancers, P=0.05 for brain tumours).

2 transport of paclitaxel and methotrexate in brain tumour.

3 ears) had a confirmed diagnosis of cancer or brain tumour.

4 the most common and most aggressive primary brain tumour.

5 ant gliomas, the most common form of primary brain tumour.

6 comprise the most common malignant childhood brain tumour.

7 oblastoma is the most frequent and malignant brain tumour.

8 re absent in more than half of children with brain tumours.

9 are the main cause of death in children with brain tumours.

10 nificant neuroinflammation in TSC-associated brain tumours.

11 th an increased risk of radiation-associated brain tumours.

12 st mutated tumour suppressors, especially in brain tumours.

13 HFPL2 (function unknown) is overexpressed in brain tumours.

14 rse neurocognitive outcomes in patients with brain tumours.

15 on neurocognitive outcomes in patients with brain tumours.

16 mprove the design of trials in patients with brain tumours.

17 e design of clinical trials in patients with brain tumours.

18 ings improve classification and diagnosis of brain tumours.

19 of life in long-term survivors of paediatric brain tumours.

20 stroke and, less frequently, head injury and brain tumours.

21 135 of 176,587 patients were diagnosed with brain tumours.

22 ng new and old cerebrovascular accidents and brain tumours.

23 tations in the pathogenesis and phenotype of brain tumours.

24 or the treatment of patients with high-grade brain tumours.

25 mGy 0.036, 95% CI 0.005-0.120; p=0.0097) and brain tumours (0.023, 0.010-0.049; p<0.0001).

26 ents previously operated on for an embryonal brain tumour (13 patients prospectively diagnosed with p

27 mia began 2 years after the first CT and for brain tumours 5 years after the first CT.

28 ath-promoting gene bax in a transgenic mouse brain tumour, a model in which p53-mediated apoptosis at

29 ), and nausea and vomiting (19%) for central brain tumours; abnormal gait and coordination (78%), cra

30 rcinoma, soft tissue sarcomas, osteosarcoma, brain tumours, adrenocortical carcinoma, Wilms' tumour a

31 d to assess the excess risk of leukaemia and brain tumours after CT scans in a cohort of children and

32 Rhabdoid brain tumours, also called atypical teratoid rhabdoid tu

33 The 8-year cumulative incidence of brain tumour among children with defective versus wild-t

34 The incidence of brain tumours among irradiated children (six of 52, 12.8

35 In children, stroke is as common as brain tumour and causes substantial mortality and long-t

36 liomas are the most common primary malignant brain tumours and are classified into four clinical grad

37 ours provides excellent anatomical detail of brain tumours and can also reveal the biology, cellular

38 rotron-generated X-rays for the treatment of brain tumours and drug-resistant epilepsies.

39 amyotrophic lateral sclerosis (ALS), stroke, brain tumours and epilepsy.

40 ent of disease progression in low back pain, brain tumours and primary epilepsy; (2) enhancing clinic

41 plinary structures of care for patients with brain tumours and structured processes of diagnostic and

42 eas tissues and interfaces between xenograft brain tumours and the surrounding healthy brain matter.

43 of neurocognitive sequelae in children with brain tumours, and discuss various strategies to integra

44 g and genetic associations for patients with brain tumours, and emphasise the need for future researc

45 routine in-situ clinical assessment of human brain tumours, and its use was later extended for examin

46 increased risk for meningioma and childhood brain tumours, and possibly bladder cancer, melanoma, an

47 ar factor NF-kappaB, and that ING4 regulates brain tumour angiogenesis through transcriptional repres

48 In this review the latest advances in MRI of brain tumours are discussed and their clinical applicati

49 The incidence of secondary malignant brain tumour at 7 years was 2.3% (0-5.6) and brainstem n

50 treated for cancer (including leukaemia and brain tumours) at the Edinburgh Children's Cancer Centre

51 We compared the cumulative incidence of brain tumours between subgroups, and with that of 421 ch

52 stoblast (CB) and this fate is stabilised by Brain tumour (Brat) and Pumilio (Pum)-mediated post-tran

53 fluctuate in time and follow the changes in brain tumour burden providing biomarkers to monitor brai

54 d assessed excess incidence of leukaemia and brain tumours cancer with Poisson relative risk models.

55 y in immunocompromised mice, label-retaining brain tumour cells display elevated tumour-initiation pr

56 gether, these findings confirm dye-retaining brain tumour cells exhibit tumour-initiation ability and

57 is a deadly and therapy resistant malignant brain tumour, characterized by an aggressive and diffuse

58 In children treated for brain tumours, chronic neurocognitive effects are especi

59 t diagnosis, especially of breast cancer and brain tumours, compared with families carrying protein t

60 Medulloblastoma is a malignant childhood brain tumour comprising four discrete subgroups.

61 lloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of sur

62 peaks, from a widely tested SV 1H-MRS human brain tumour database.

63 The WHO classification of brain tumours describes 15 subtypes of meningioma.

64 in suppressing tumour cell proliferation and brain tumour development depends on TRIM33-promoted beta

65 role in cytokinesis, cell proliferation and brain tumour development.

66 epth view of the molecular routes leading to brain tumour development.

67 EGFR-promoted tumour cell proliferation and brain tumour development.

68 However, patients with brain tumours do not present with or present with low am

69 ion, in view of the low incidence of primary brain tumours--draws attention to the need to improve th

70 scular disease, other acquired brain injury, brain tumour, drug or alcohol misuse, or dementia were n

71 Here, we review recent advances in brain tumour genomics and highlight how these findings i

72 ular mechanisms underlying the regulation of brain tumour growth and angiogenesis remain unresolved.

73 ressor gene, ING4, is involved in regulating brain tumour growth and angiogenesis.

74 An association with brain tumours has also been demonstrated.

75 Most children who have survived brain tumours have required surgical resection and focal

76 a rapidly expanding sphere of investigation, brain-tumour imaging is producing great excitement.

77 edulloblastoma, a highly malignant childhood brain tumour, impose debilitating effects on the develop

78 However, in many other types of brain tumour in both adults and children, the effect of

79 tases are the most common cause of malignant brain tumours in adults.

80 mours, whereas mature astrocytes do not form brain tumours in adults.

81 or about 30% of all newly diagnosed cases of brain tumours in children.

82 dulloblastomas are the most common malignant brain tumours in children.

83 ake of PEGylated-CH1055 dye were observed in brain tumours in mice, suggesting that the dye was detec

84 own to lead to an elevated risk of malignant brain tumours in patients with inborn errors of 2HG meta

85 rategy improves the sensitivity when imaging brain tumours in whole mice.

86 lastomas are molecularly distinct from other brain tumours including primitive neuroectodermal tumour

87 stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.

88 Silencing or inhibition of NHE9 in brain tumour-initiating cells attenuates tumoursphere fo

89 gh understanding of the biology of malignant brain tumours is likely to provide the background for th

90 ion of mature astrocytes to the formation of brain tumours is still not understood.

91 clinically challenging, malignant childhood brain tumour, is no exception.

92 d with severe neurological disorders such as brain tumours, it is important to understand how astrocy

93 o measure the concentrations of this drug in brain tumour lesions of lung cancer patients, as penetra

94 th Darcy's law is applied to a 3-D realistic brain tumour model that is extracted from magnetic reson

95 h and have already yielded new insights into brain tumours, multiple sclerosis, acute neurological in

96 b group were unknown (n=2), a second primary brain tumour (n=1), and acute myeloid leukaemia (n=1), a

97 tworks in control subjects and patients with brain tumours (n = 22).

98 ingioma (n=7; 12.0 [4.8-24.8]) and childhood brain tumours (n=3; 10.3 [2.1-30.1]), and for cancers of

99 , for example, are the most common malignant brain tumour of childhood, but their pathogenesis is unk

100 lloblastoma is a highly malignant paediatric brain tumour, often inflicting devastating consequences

101 er any clear evidence of an association with brain tumours or other malignancies.

102 y from the usual treatment of either primary brain tumours or systemic non-Hodgkin lymphoma.

103 It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor ce

104 tactic radiosurgery (SRS) for the control of brain-tumours outweighs the potential neurocognitive ris

105 y motor area (SMA) is frequently involved by brain tumours (particularly WHO grade II gliomas).

106 indicate that ING4 has an important role in brain tumour pathogenesis.

107 ggests an important role for this pathway in brain tumour pathogenesis.

108 cal tract involvement in childhood embryonal brain tumour patients who developed posterior fossa synd

109 ess case of leukaemia and one excess case of brain tumour per 10,000 head CT scans is estimated to oc

110 Here, we have identified a dye-retaining brain tumour population that displays all the hallmarks

111 Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with dist

112 Magnetic resonance imaging (MRI) of brain tumours provides excellent anatomical detail of br

113 Brain tumours rarely occur in survivors of childhood acu

114 cancers, and represent the leading cause of brain tumour-related death in both children and adults.

115 An unusually high frequency of brain tumours seen among children enrolled in one of our

116 a, allowing the identification of actionable brain tumour somatic mutations.

117 s in survival in patients with some types of brain tumours such as medulloblastoma.

118 els of JHDM1B expression found in aggressive brain tumours, suggest a role for JHDM1B in cancer devel

119 er patient are lost as the result of primary brain tumours than any other form of cancer.

120 ely characterizes the genomic alterations of brain tumours than plasma, allowing the identification o

121 oblastoma (MB) is the most common paediatric brain tumour that arises from cerebellar precursor cells

122 astoma multiforme (GBM) is a highly invasive brain tumour that is unvaryingly fatal in humans despite

123 Medulloblastoma is the most common malignant brain tumour that occurs during childhood.

124 Glioblastoma are highly aggressive brain tumours that are associated with an extremely poor

125 rs (IGCTs) are a group of rare heterogeneous brain tumours that are clinically and histologically sim

126 stic oligodendroglioma (AO) are rare primary brain tumours that are generally incurable, with heterog

127 Motor weakness in subjects with brain tumours that do not involve primary motor structur

128 Ependymomas are common childhood brain tumours that occur throughout the nervous system,

129 These are well differentiated primary brain tumours that typically develop in young adults.

130 alise on scientific and clinical advances in brain tumour treatment in neuro-oncology to accelerate a

131 sed in clinical studies of discrimination of brain tumour types and follow-up of patients bearing abn

132 supervised methods for the discrimination of brain tumour types, as it accounts for their increasingl

133 lastoma (the most common malignant childhood brain tumour), using scant/low-quality samples remaining

134 severe weakness following surgery for their brain tumours were followed longitudinally, and the subj

135 ontine Gliomas (DIPGs) are deadly paediatric brain tumours where needle biopsies help guide diagnosis

136 ns for chemoresistant cancers, especially of brain tumours where the use of temozolomide is frequentl

137 echanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form bra

138 s (GBM) are aggressive and therapy-resistant brain tumours, which contain a subpopulation of tumour-p

139 lso occur in other diseases, like metastatic brain tumours, which we describe in this case report.

140 Ependymomas are chemotherapy-resistant brain tumours, which, despite genomic sequencing, lack e

141 astoma multiforme is an aggressive, invasive brain tumour with a poor survival rate.

142 Glioblastomas (GBMs) are highly lethal brain tumours with current therapies limited to palliati

143 DNA repair gene and p53 efficiently induces brain tumours with hallmark characteristics of human pro

144 tiforme is the most common primary malignant brain tumour, with a median survival of about one year.

145 Meningiomas are mostly benign brain tumours, with a potential for becoming atypical or