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51. Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1 mutations.

52. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy.

53. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy

55. White matter compromise predicts poor intellectual outcome in survivors of pediatric low-grade glioma

58. BI-21 * BRAF MUTATION AND CDKN2A DELETIONS DEFINE A CLINICALLY DISTINCT SUBGROUP OF CHILDHOOD SECONDARY HIGH GRADE GLIOMA

60. THOR METHYLATION PROVIDES INSIGHT INTO THE TELOMERE MAINTENANCE LANDSCAPE OF MALIGNANT GLIOMAS

61. NEUROPSYCHOLOGY

62. EPENDYMOMA

63. RADIOLOGY

64. MEDULLOBLASTOMA

65. HIGH GRADE GLIOMAS AND DIPG

66. TERT promoter mutations are highly recurrent in SHH subgroup medulloblastoma

67. TERT promoter mutations are highly recurrent in SHH subgroup medulloblastoma

69. CONTRIBUTION OF DNA COPY-NUMBER VARIATION (CNV) TO CANCER SUSCEPTIBILITY AND LARGE-SCALE GENOME ALTERATIONS IN OSTEOSARCOMA (OS)

70. PEDIATRICS CLINICAL RESEARCH

72. EPENDYMOMA

73. BIOLOGY

74. HIGH GRADE GLIOMAS

75. NEUROPSYCHOLOGY

76. RARE TUMORS

77. EPIDEMIOLOGY

78. CLINICAL TRIALS

79. Visual outcomes in children with neurofibromatosis type 1-associated optic pathway glioma following chemotherapy: a multicenter retrospective analysis

81. Neuro-cognitive

84. Duplication of 7q34 is specific to juvenile pilocytic astrocytomas and a hallmark of cerebellar and optic pathway tumours

93. Short Report Detection of RAG mutations and prenatal diagnosis in families presenting with either T–B– severe combined immunodeficiency or Omenn's syndrome.

96. BI-21BRAF MUTATION AND CDKN2A DELETIONS DEFINE A CLINICALLY DISTINCT SUBGROUP OF CHILDHOOD SECONDARY HIGH GRADE GLIOMA

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