title: Oncogenes: cause or consequence in the development of glial tumors.
abstract: Recent developments in the field of oncogenes and growth stimulatory factors have provided limited but essential models in neuro-oncology. The observation in gliomas of platelet growth factor (PDGF)-like immunoreactivity fits with the autocrine secretion model, rising the possibility for the growth factor independence of the cancer cells. The discovery of the tumor suppressor genes, for which loss of function mutations are oncogenic as in the RB gene of the retinoblastoma and p53 gene, has introduced a new concept of oncogenesis which could be useful even in the cure of the neoplasms. Several oncogenes are amplified and/or expressed in brain tumors, some associated with polymorphism leading to abnormal protein products. Therefore, corresponding functions, such as production of deficient epidermal growth factor receptor (EGFR) encoded by erb-B, are impaired. Abnormal chromosomal patterns have been recognized in brain tumors and found mainly in chromosomes 7 and 22 on which oncogenes erb-B and sis are located, respectively. Location of proto-oncogenes, which are normally expressed in the brain, indicate that they share common distribution patterns mainly involving the cerebellum, hippocampus and olfactory bulbs. These proto-oncogenes may be regulated by physiological and pathological events. The concept of oncogene involvement in brain tumors must be extended to include the other factors such as G-proteins, growth factor receptors, membrane-associated and cytoplasmic protein kinases, which are all responsible for the control of the cell growth and their response to external signals including chemotherapeutic drigs.
authors.affiliation: Clinical Neurosurgery Section, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892.
authors.forename: A
authors.initials: A
authors.lastname: Akbasak
authors.forename: B
authors.initials: B
authors.lastname: Sunar-Akbasak
mesh_terms: D000818:Animals; D001254:Astrocytoma / Q000235:genetics / Q000473:pathology; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002869:Chromosome Aberrations; D004351:Drug Resistance / Q000235:genetics; D019204:GTP-Binding Proteins / Q000235:genetics / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D005909:Glioblastoma / Q000235:genetics / Q000473:pathology; D005910:Glioma / Q000235:genetics* / Q000473:pathology; D006133:Growth Substances / Q000235:genetics / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D015513:Oncogene Proteins / Q000235:genetics / Q000502:physiology; D009857:Oncogenes; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000502:physiology; D011519:Proto-Oncogenes; D011956:Receptors, Cell Surface / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology
chemical_list: D006133:Growth Substances; D015513:Oncogene Proteins; D011956:Receptors, Cell Surface; D014157:Transcription Factors; D011505:Protein-Tyrosine Kinases; D019204:GTP-Binding Proteins