Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Loss of constitutional heterozygosity for specific chromosomal loci, when found consistently in a particular tumor type, suggests that a recessive oncogene important in the genesis of that tumor may be present within the involved chromosomal loci. DNA markers that detect restriction fragment length polymorphisms are powerful tools that have been used to detect loss of chromosomal loci in a growing number of human malignancies. The human brain tumor astrocytoma is usually malignant and virtually incurable. Two types of malignant astrocytomas are recognized histopathologically:anaplastic astrocytoma and glioblastoma multiforme. We carried out a restriction fragment length polymorphism analysis of tumors from 15 patients with anaplastic astrocytoma and 20 patients with glioblastoma using polymorphic DNA markers for loci on chromosome 17. Loss of constitutional heterozygosity for loci on chromosome 17 was found in both anaplastic astrocytoma and glioblastoma patients with equal frequency (40% of cases). Our mapping data revealed a region of loss on chromosome 17p between physical loci p11.2 and pter that was common to both patient groups. Taken together with the previously reported finding of loss of heterozygosity for loci on chromosome 10 in glioblastoma, these results indicate that tumorigenesis in the astrocyte lineage may involve recessive oncogenes on two different chromosomes.
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PMID:Loss of heterozygosity for loci on chromosome 17p in human malignant astrocytoma. 257 17

Information on pre-morbid height and weight from a national screening of tuberculosis between 1963 and 1975 was linked with the registrations in the population-based Norwegian Cancer Registry. For each case with a primary central nervous system (CNS) neoplasm, 10 matched controls were taken from the non-cases. Analyses were done by a Cox regression model for the total group of CNS neoplasms and the various histological groups. In the case of the total group, height emerged as a significant risk factor for both sexes. Within each sex, a similar trend was found for each histological group although statistical significance was retained only for glioblastoma among males and for other types of glioma (astrocytoma, oligodendroglioma, mixed glioma and ependymoma) for females. A significant negative association was revealed between Quetelet's index (weight/height squared) and 'other gliomas' in females. No association with body mass, as expressed by Quetelet's index, was found for patients with meningioma.
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PMID:Pre-morbid height and weight as risk factors for development of central nervous system neoplasms. 258 97

Expression of human LDL receptor mRNA and protein is induced in human glioblastoma-astrocytoma cells upon transfer into lipoprotein-deficient medium, a mode of induction likely to be physiological. The presence of cycloheximide (CHX) leads to up to 7.5-fold superinduction of LDL receptor mRNA within 4 hr and, upon removal of this inhibitor, to superinduction of LDL receptor protein as well. The extent of superinduction of LDL receptor mRNA reaches over 40-fold beyond the level expressed in medium containing regular serum. Despite its extensive superinduction, LDL receptor mRNA decays rapidly in the presence of CHX. Stabilization of LDL receptor mRNA is thus unlikely to account for the observed superinduction. These results show that normally the LDL receptor gene is expressed to only a small fraction of its full potential.
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PMID:Superinduction of the human gene encoding low density lipoprotein receptor. 259 46

Four cases of pleomorphic xanthoastrocytoma (PXA), a low-grade leptomeningeal glioma with a reported favorable prognosis affecting young patients, are reported together with a discussion and review of management and prognosis. A literature review has confirmed a favorable prognosis in at least 50% of patients with this disorder. Seventeen of 35 reported patients are still alive and often seizure-free for a mean period of 7.4 years (range 2 to 18 years) after diagnosis. Five patients have died within 2 years and four between 9 and 25 years after diagnosis of PXA. In some cases in which death followed shortly after diagnosis, there may have been histological confusion between PXA and a malignant glioma with heavily lipidized tumor cells. Nonetheless, transformation of PXA into a malignant astrocytoma or glioblastoma with eventual death may occur many years after initial diagnosis. From the currently reported cases it does not appear possible on clinicopathological grounds to predict which patients will have a favorable prognosis. Optimal management of PXA seems to be primary surgical resection with later surgery for residual or recurrent tumor. The role of radiotherapy in the management of PXA is at this time uncertain.
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PMID:Pleomorphic xanthoastrocytoma. Report of four cases. 264 2

The determination and comparison of genotypic combinations at genomic loci in constitutional and tumor tissues from patients with various types of cancer have defined the chromosomal locations of loci in which recessive mutations play a role in disease development. The predisposing nature of some of these mutant alleles is exemplified by studies of retinoblastoma and osteogenic sarcoma, two clinically associated diseases that share a pathogenetically causal predisposition mapping to 13q14. Genomic alteration of chromosome 10 is apparent in glioblastomas and mixed tumors of glioblastoma/astrocytoma grade III but not in homogeneous astrocytoma grades II or III; this suggests the definition of a locus involved in tumor progression and, perhaps, an approach to molecular genetic staging of tumors.
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PMID:Loss of heterozygosity in stages of malignancy. 266 35

Glioma are often histologically heterogenous. As many of these tumors are not removable in toto, due to their localisation, the most malignant part of the tumor may be missed and information for optimum therapeutic management is incomplete. Furthermore, low grade gliomas tend to become more malignant in their development; additional surgical intervention is often not possible. Non-invasive measurement of tumor glucose metabolism with (F-18)-2-fluoro-2-deoxyglucose (FDG) and positron-emission-tomography (PET) may be used to evaluate tumor malignancy. Malignant gliomas (astrocytoma III degree and glioblastoma) frequently showed increased peak metabolic rates (in comparison with normal white matter) and uncoupling of FDG transport and phosphorylation. Preliminary experiences with image-guided localized phosphorus-31 MR spectroscopy (P-31 MRS) demonstrated a decrease of phosphodiesters in malignant gliomas, whereas the phosphomonoesters showed an increase in several cases. The phosphocreatine peak was often reduced. A more active therapy of low grade gliomas might be indicated when signs of hypermetabolism in FDG-PET and alteration of energy-rich phosphates or membrane-phosphates in P-31 MRS are found.
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PMID:[Metabolic studies of gliomas with positron emission tomography and phosphorus 31 MR spectroscopy in diagnosis and treatment planning]. 268 95

Distribution of the epidermal growth factor (EGF) receptor in the surgical specimen of the human glioma was studied by immunohistochemical techniques using a monoclonal anti-EGF receptor antibody. Of 11 gliomas examined, EGF receptors were detected in nine glioblastomas and in one fibrillary astrocytoma. In the majority of cells, staining was observed over the cell membrane. Nuclear and cytoplasmic staining was also seen. In four glioblastomas, EGF receptor-positive cells were diffusely distributed in the tumor tissue. In one glioblastoma and one fibrillary astrocytoma, only a few positive cells were observed. These results imply the possible role of EGF receptors in the cellular proliferation of the human glioma.
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PMID:Epidermal growth factor receptor in human glioma. 271 19

Data were analysed from 4859 patients with different histological types of intracranial glioma registered by the Norwegian Cancer Registry between 1955 and 1984. Glioblastoma comprised 57.9% of all cases. The second most common primary brain tumour was astrocytoma (19.0%), then mixed glioma (9.2%), oligodendroglioma (7.9%), medulloblastoma (3.1%) and ependymoma (2.9%). A primary brain tumour in a child is approximately twice as likely to be an astrocytoma as a medulloblastoma. The age-specific incidence for glioblastoma increases with age, whereas the incidence of astrocytoma and oligodendroglioma peaks at middle age. Both glioblastoma and astrocytoma showed increased incidence rates over the study period and this was most pronounced in the age-group above 60 years. The prognosis for gliomas varied with age at time of diagnosis, generally being better the younger the patient. For oligodendroglioma patients, survival prospects were independent of age at time of diagnosis. The best prognosis was seen in patients up to 30 years with astrocytoma. Applied in epidemiology, the data indicate that astrocytoma, oligodendroglioma, mixed glioma and ependymoma may be treated as a group which should be separated from both glioblastoma and medulloblastoma.
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PMID:Neoplasms of the central nervous system in Norway. III. Epidemiological characteristics of intracranial gliomas according to histology. 273 7

The determination and comparison of genotypic combinations at genomic loci in normal and tumour tissues from patients with various types of cancer have defined the chromosomal locations of loci at which recessive mutations play a role in disease. The predisposing nature of some of these mutant alleles is exemplified in studies of retinoblastoma and osteogenic sarcoma. These two clinically associated diseases share a pathogenetically causal predisposition that maps to chromosome position 13q14. A similar mechanism at 11p15.5 is involved in the development of the embryonal variant of rhabdomyo-sarcoma, Wilms' tumour and hepatoblastoma. Finally, genomic alteration of chromosome 10 is apparent in glioblastomas and mixed tumours of glioblastoma/astrocytoma grade III but not in homogenous astrocytoma grades II or III, suggesting the definition of a locus involved in tumour progression and, perhaps, an approach to molecular genetic staging of tumours.
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PMID:Loss of genetic information in cancer. 274 36

Three-tiered system dividing supratentorial astrocytic neoplasms into the astrocytoma, anaplastic (malignant) astrocytoma and the glioblastoma multiforme has been widely used. However, the pathology of anaplastic astrocytoma is defined in different ways according to different classifications. A total of 42 biopsy specimens from 35 cases diagnosed as anaplastic astrocytoma were reviewed pathologically and their features were correlated with a follow-up clinical study to discuss the prognostic usefulness of the subdivision of anaplastic astrocytoma. In WHO classification, anaplastic astrocytoma is defined as "astrocytoma containing areas of anaplasia". Follow-up study of 7 cases with the histology as such revealed that 5 cases had survived more than one year and seven months. The other 28 cases showed a varied histology and were subclassified into an astrocytoma in which moderately anaplastic cells are found throughout the tumor, an astrocytoma formed by anaplastic fusiform cells, an astrocytoma composed of predominantly rounded anaplastic cells, and a pleomorphic astrocytoma with or without intracytoplasmic hyaline inclusions. A follow-up study of cases with these types of astrocytoma disclosed death in 15 cases within one year and 7 months following the first surgery and that three cases displayed typical histological features of glioblastoma at autopsy. It is considered that there would be a considerable overlap between the group of anaplastic astrocytoma and that of glioblastoma, if we use the term "anaplastic astrocytoma" in a broader category.
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PMID:[Problems entailed in the definition and pathology of anaplastic astrocytoma]. 281 Jul 69


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