作者: H. Ohgaki , P. Kleihues , B. Schäuble , A. zur Hausen , K. von Ammon
DOI: 10.1007/BF00196514
关键词: Cancer research 、 Cytogenetics 、 Pathology 、 Astrocytoma 、 Germline mutation 、 Tumor suppressor gene 、 Neoplastic transformation 、 Anaplastic astrocytoma 、 Biology 、 Loss of heterozygosity 、 Glioma
摘要: Diffusely infiltrating low-grade astrocytomas (WHO grade II) have an intrinsic tendency for progression to anaplastic astrocytoma III) and glioblastoma IV). This change is due the sequential acquisition of genetic alterations, several which recently been identified. In astrocytomas, p53 mutations with or without loss heterozygosity on chromosome 17p are principal detectable change. Anaplastic contain at overall incidence 34% and, in addition, 19q frequent homozygous deletion p16 tumor suppressor (MTS-1) gene. The most malignant astrocytic neoplasms, glioblastoma, further shows 10 amplification epidermal growth factor receptor (EGF-R) gene incidences 66% 34%, respectively. type distribution brain tumours not suggestive specific environmental carcinogens operative their aetiology. Analysis 91 families germline reported date show that nervous system account 12% all neoplasms. Of a total 57 reported, 30 were classified histologically these, 73% origin. observation somatic sporadic largely restricted those origin also prevail among CNS neoplasms associated mutation strongly suggests, capable initiating neoplastic transformation astrocytes human system.