ライフサイエンスコーパス: CNS tumor

1 CNS tumor or the cause of death listed as a CNS tumor.

2 h recipients of organs from donors without a CNS tumor.

3 nts of organs from 177 donors with a primary CNS tumor.

4 pediatric patients treated for leukemia or a CNS tumor.

5 ontemporary long-term survivors of pediatric CNS tumor.

6 agnosed between 1970 and 1986 with a primary CNS tumor.

7 radiation therapy are at risk for subsequent CNS tumors.

8 s grade I or II by the WHO classification of CNS tumors.

9 tumor donors when compared to donors with no CNS tumors.

10 re different from those elicited against non-CNS tumors.

11 transcriptional regulation of these genes in CNS tumors.

12 ncidence of both spontaneous and ENU-induced CNS tumors.

13 t of an ongoing prospective investigation of CNS tumors.

14 treatment of pediatric patients with primary CNS tumors.

15 etastases in pediatric patients with primary CNS tumors.

16 vaccines for the treatment of patients with CNS tumors.

17 rveillance for early detection of subsequent CNS tumors.

18 r patients affected by poorly differentiated CNS tumors.

19 an cancers and are associated primarily with CNS tumors.

20 World Health Organization classification of CNS tumors.

21 ite NRAS rarely being reported as mutated in CNS tumors.

22 tral nervous system (CNS) tumors and 494 non-CNS tumors.

23 med partial responses, both in patients with CNS tumors.

24 ed in children with recurrent or progressive CNS tumors.

25 h multifunctional effects in human embryonal CNS tumors.

26 of neural origin, has been detected in human CNS tumors.

27 history of or active central nervous system (CNS) tumor.

28 2.91) for childhood central nervous system (CNS) tumors.

29 are the survivors of central nervous system (CNS) tumors.

30 patients overall, including 10 patients with CNS tumors (38.5%).

31 sarcomas on strength testing (score +/- SD: CNS tumors, 76.5 +/- 4.7; sarcoma 67.1 +/- 7.2 v sibling

32 childhood cancer with and without subsequent CNS tumors (82 participants and 228 matched controls).

33 est scores were prevalent among survivors of CNS tumors and bone and soft tissue sarcomas on strength

34 ough good activity was also observed against CNS tumors and carcinomas of the breast and prostate.

35 recipients of organs taken from donors with CNS tumors and found no evidence of a difference in over

36 l number of long-term survivors of pediatric CNS tumors and is most influenced by the initial tumor h

37 sly published studies in adult-onset primary CNS tumors and replicated these in survivors of childhoo

38 survivors at high or low risk for subsequent CNS tumors and validated these models in an independent

39 ted IDH2 gene in 445 central nervous system (CNS) tumors and 494 non-CNS tumors.

40 eosarcomas, adrenocortical carcinomas (ACC), CNS tumors, and soft tissue sarcomas (STS) observed in 3

41 thy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we

42 The survival of children with CNS tumors approaches 70%, yet health-related quality of

43 Survivors of pediatric CNS tumors are at risk of severe neurocognitive impairme

44 lmost all data on the treatment of embryonal CNS tumors are derived from the pediatric population, si

45 of this review is to discuss the spectrum of CNS tumors arising in individuals with NF type 1 (NF1) a

46 ly useful for the treatment of MTX-sensitive CNS tumors, as it does not affect CSF MTX levels.

47 Lenalidomide was tolerable in children with CNS tumors at doses of 116 mg/m(2)/d during the initial

48 d augment antitumor immune responsiveness in CNS tumor-bearing mice treated with human gp100 + tyrosi

49 Continuous imiquimod administration in CNS tumor-bearing mice, however, was associated with the

50 between survivors diagnosed with leukemia or CNS tumor before 11 years old versus during later adoles

51 e nucleus of the nude rat resulted in lethal CNS tumor burden manifested by the onset of focal neurol

52 Organs from donors with CNS tumors can be used with a low risk of donor tumor tr

53 present study, we show that human embryonal CNS tumor cell lines and surgical tumor specimens expres

54 In parallel, we noted in CNS tumor cells that knockdown of BCL-xL (B-cell lymphom

55 our analyses to the central nervous system (CNS) tumor cells and to further define mechanisms of dru

56 In adults with advanced embryonal CNS tumors, conventional-dose intravenous cisplatin-base

57 In young children with CNS tumors, CSI and hemispheric location are associated

58 Despite 13,000 central nervous system (CNS) tumor deaths per year in the United States, CNS tum

59 tumor deaths per year in the United States, CNS tumor donors comprise only 1% of cadaveric donors re

60 e UK experience of transplanting organs from CNS tumor donors found no transmission in 448 recipients

61 There is a wide variation in the number of CNS tumor donors utilized by individual organ procuremen

62 CNS tumor donors were not used more often for either urg

63 ifference in patient survival of organs from CNS tumor donors when compared to donors with no CNS tum

64 focused on the treatment of the most common CNS tumors encountered in children and adults with NF1 a

65 fraction of CNS-PNETs, we identify four new CNS tumor entities, each associated with a recurrent gen

66 ble from those of various other well-defined CNS tumor entities, facilitating diagnosis and appropria

67 one of the transgenic mice formed detectable CNS tumors, even when aged.

68 iquimod resulted in synergistic reduction in CNS tumor growth compared with melanoma-associated Ag-pu

69 s into the causes and potential treatment of CNS tumors have come from discovering connections with g

70 Survivors of a CNS tumor, head and neck tumor, and leukemia are particu

71 By 60 years of age, 9%, 6%, and 5% of CNS tumor, head and neck tumor, and leukemia survivors,

72 ha knockout (KO) mice and studied their anti-CNS tumor immune responses.

73 llular interactions involved in NK cell anti-CNS tumor immunity are even less well understood.

74 sponse to chemotherapy of advanced embryonal CNS tumors in adults.

75 Gliomas are the most common CNS tumors in children and adolescents, and they show an

76 s and also for modified incidence of primary CNS tumors in rats treated with a single dose of the neu

77 POLD1], and rs11615 [ ERCC1]) and subsequent CNS tumors in survivors of childhood cancer.

78 ent innate antitumor immune response against CNS tumors in the absence of toxicity.

79 us tumorigenicity of central nervous system (CNS) tumors in the offspring of pregnant rats and also f

80 aited for a donor who did not have a primary CNS tumor, in addition to the life years gained by the t

81 Spontaneous CNS tumor incidence in control groups was 1.1-4.4% but s

82 The primary CNS tumors included medulloblastoma (n = 29), astrocytom

83 recently been associated with several human CNS tumors, including medulloblastomas and a broad range

84 Because of the difficulty in treating CNS tumors, innovative treatments and alternative delive

85 than 3 years with newly diagnosed embryonal CNS tumors is 14 mg.

86 points in clinical trials for patients with CNS tumors is in its infancy, so that long-term outcomes

87 d points in clinical trials of patients with CNS tumors is increasing.

88 The management of CNS tumors is limited by the blood-brain barrier (BBB),

89 Treatment of animals carrying orthotopic CNS tumor isolates with lapatinib- and obatoclax-prolong

90 Lapatinib and obatoclax killed multiple CNS tumor isolates.

91 fficking of tumor antigen-specific CTLs into CNS tumor lesions.

92 ss, immunotherapeutic targeting of malignant CNS tumors may be enhanced by the administration of the

93 We tested whether modulation of the CNS-tumor microenvironment by delivery of IFN-alpha-tran

94 donor with a primary central nervous system (CNS) tumor necessitates offsetting the risk of tumor tra

95 emangioblastomas are central nervous system (CNS) tumors of unknown histogenesis, which can occur spo

96 od cancer at high or low risk for subsequent CNS tumors on the basis of genetic and clinical informat

97 r donors of whom 397 had a past history of a CNS tumor or the cause of death listed as a CNS tumor.

98 especially those with a history of leukemia, CNS tumors, or neuroblastoma, may be at increased risk f

99 one-tailed; P < 0.16 two-tailed; ENU-induced CNS tumors, P < 0.08 one-tailed, P < 0.16 two-tailed), t

100 cance in the experiment overall (spontaneous CNS tumors, P < 0.08 one-tailed; P < 0.16 two-tailed; EN

101 In glioblastoma and non-CNS tumor panels, 806 was reactive with a high proportio

102 rapy may represent an effective modality for CNS tumors, particularly when combined with strategies t

103 e use of kidneys from a donor with a primary CNS tumor provides a further 8 years of life over someon

104 ndard for adjusting rates; underreporting of CNS tumor rates resulting from the exclusion of nonmalig

105 ) to induce glioma-specific type 1 CTLs with CNS tumor-relevant homing properties and the mechanism o

106 Development of novel therapies for CNS tumors requires reliable assessment of response and

107 eutic strategies for central nervous system (CNS) tumors requires a firm understanding of factors reg

108 development are illustrated by three common CNS tumors: retinoblastoma, glioblastoma, and medullobla

109 f cancer and leukemia but did not indicate a CNS tumor risk (incidence rate ratio = 1.03, 95% CI: 0.7

110 n most cancer registries; and information on CNS tumor risk factors, including concerns related to no

111 Survivors of central nervous system (CNS) tumors (SHR=4.6, 95% confidence interval, 4.3-5.0),

112 nitial diagnosis of leukemia (SMR = 15.5) or CNS tumor (SMR = 15.7).

113 The excess risk of cerebral infarction among CNS tumor survivors increases with attained age.

114 nd; P = .04 and .01, respectively) and among CNS tumor survivors on the TUG (score +/- SD: 5.1 +/- 0.

115 Beyond 60 years of age, every year, 0.4% of CNS tumor survivors were hospitalized for a cerebral inf

116 atosis type 2 (NF2) is an autosomal-dominant CNS tumor syndrome that affects 1:25,000 children and yo

117 malignant peripheral nerve sheath tumors and CNS tumors, the cancers traditionally associated with NF

118 ize the criteria that are used for different CNS tumors, the Response Assessment in Neuro-Oncology (R

119 n of HuR in 35 freshly resected and cultured CNS tumors to determine whether there was any correlatio

120 ecurrent, refractory, or progressive primary CNS tumors to estimate the maximum-tolerated dose (MTD)

121 omprised 643 pediatric patients with primary CNS tumor treated at St Jude Children's Research Hospita

122 s an appealing option to specifically target CNS tumors using the immune system.

123 Promising activity, particularly in CNS tumors, warrants phase II evaluation of this regimen

124 ncer at highest or lowest risk of subsequent CNS tumors was 87.5% and 83.5%, respectively.

125 B16/F10 murine melanoma (B16) as a model for CNS tumor, we show that vaccination with bone marrow-gen

126 ive vaccines against central nervous system (CNS) tumors, we evaluated the ability of vaccines with s

127 Results for CNS tumors were less consistent, but the most comprehens

128 vated in adolescents treated for leukemia or CNS tumors when compared with siblings.

129 Embryonal central nervous system (CNS) tumors, which comprise medulloblastoma, are the mos

130 generate tumor-specific immune responses to CNS tumors while the immuno-modulatory properties are be

131 Participants included 224 survivors of CNS tumors who were treated at St Jude Children's Resear

132 ss HRQOL rapidly and easily in children with CNS tumors, who have significantly worse HRQOL than heal