作者: Yue Cheng , Ho-Keung Ng , Shang-Fu Zhang , Min Ding , Jesse Chung-Sean Pang
DOI: 10.1016/S0046-8177(99)90057-6
关键词: Loss of heterozygosity 、 Carcinogenesis 、 Anaplastic astrocytoma 、 Microsatellite instability 、 Immunohistochemistry 、 Cancer research 、 Biology 、 PTEN 、 Gene mutation 、 Tumor suppressor gene
摘要: Abstract High-grade astrocytomas are tumors that uncommon in children. Relatively few studies have been performed on their molecular properties and so it is not certain whether they follow different genetic pathways from those described adult diffuse astrocytomas. In this study, we evaluated 24 pediatric high-grade (11 anaplastic 13 glioblastomas) all of which were sporadic primary. We studied mutations p53 , phosphatase tensin homolog ( PTEN ), loss heterozygosity (LOH) chromosomes 17p13, 9p21 10q23–25, amplification epidermal growth factor receptor EGFR overexpression protein. addition, searched for microsatellite instability (MSI) by using MSI sensitive specific markers. found 38% (924) the brain stem except 2 (71%, 57) had mutations. 8% (224) However, no was any them. LOH at 17p13.1 50% (36 informative tumors), 83% (56 10q23–25 78% (79 tumors). Four showed MSI, them widespread regarded as with replication error (RER + ) phenotype. All 4 concurrent 10q23–25. Combining gene alterations, LOH, mutations, inactivation both alleles 57% (47 tumors) cases respectively. conclude development may primary or secondary paradigm glioblastomas. a subset these tumors, genomic also implicated.