Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferons are currently the most widely used biological response modifiers. They are of high clinical value in haematological malignancies (chronic myelogenous leukaemia, multiple myeloma, non-Hodgkin lymphoma), in solid tumours (malignant melanoma, hypernephroma, pancreas neoplasms, carcinoid tumours, Kaposi's sarcoma, glioma, in ovarium, cervix and bladder carcinoma, and in basalioma) and in infectious diseases (chronic hepatitis B, chronic non-A/non-B hepatitis, chronic delta hepatitis, AIDS, Papova virus and Rhinovirus infections, leishmaniasis, leprosy) and some other conditions. Although the mechanism of action of interferons has not been explained in every detail these agents are promising therapeutic means in a number of diseases.
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PMID:Role of interferon in clinical practice. 172 32

We have applied restriction fragment length polymorphism analysis to a 30-member panel of primary glioma DNAs, which had been previously examined for loss of genetic information (C. D. James, E. Carlbom, J. P. Dumanski, M. Hansen, M. Nordenskjold, V. P. Collins, and W. K. Cavenee, Cancer Res., 48:5546-5551, 1988), to determine the frequency and sublocalization of loss of genetic information from chromosome 9. We have also utilized scanning densitometry for dosage determination of the 9p-localized interferon alpha and interferon beta-1 genes among these same tumors. Our results reveal the following: (a) for those cases in which loss has occurred, the region of common loss lies on the short (p) arm of the chromosome; (b) loss of genetic information from the short arm of chromosome 9 occurs frequently in glial tumors of intermediate (anaplastic, grade III) and high (glioblastoma, grade IV) histological malignancy (10 of 20 cases) but not in tumors of low (grade II) histological malignancy (0 of 10 cases); (c) tumors with 9p deletions are hemi- or nullizygous for interferon beta-1 and the interferon alpha gene cluster; (d) cases of interferon nullizygosity occur exclusively among tumors of highest histological malignancy (glioblastoma). These data, especially the determination of a region of nullizygosity, suggest proximity to or residence within a gene(s) whose function(s) is (are) critical to the suppression of the malignant evolution of glial tumors.
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PMID:Chromosome 9 deletion mapping reveals interferon alpha and interferon beta-1 gene deletions in human glial tumors. 199 58

Comparison of constitutional and tumor genotypes at chromosomal loci defined by restriction fragment length alleles has proven useful in determining the genomic position and tissue specificity of recessive mutations that predispose to cancer (Hansen, M.F., and Cavenee, W.K. Cancer Res., 47:5518-5527, 1987). Here we have applied this approach to 53 unrelated patients with glial tumors of varying histological malignancy grade. Loss of constitutional heterozygosity for loci on chromosome 10 was observed in 28 of 29 tumors histologically classified as glioblastoma (malignancy grade IV) whereas no similar losses were observed in any of 22 gliomas of lower malignancy grade. Examination of restriction fragment length alleles on other chromosomes revealed that loss of sequences on chromosomes 13, 17, or 22 had occurred at nonrandom frequencies and in at least one instance of each malignancy grade of adult glioma. The tumors in which loss of constitutional heterozygosity was observed were composed of one or a mixture of glial cell subtypes displaying astrocytic, oligodendrocytic, and/or ependymal differentiation. These results demonstrate a close association of the loss of chromosome 10 sequences with the most malignant histological stage of glioma and that glioblastoma arises as the clonal expansion of an earlier staged precursor. Furthermore they suggest that glioblastoma is a common phenotypic and malignancy terminus for glial tumors of various cellular subtypes which is reached through a common molecular pathway. This approach which involves the identification of malignancy stage specific somatic losses of heterozygosity provides a genotypic, rather than phenotypic, analysis of tumor progression.
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PMID:Clonal genomic alterations in glioma malignancy stages. 290 Dec 88

Leprosy has a predilection for peripheral nerves and is not considered to involve the CNS. The idea that the CNS is exempt from Mycobacterium leprae bacilli has been suspected from a clinical perspective or CSF study in leprosy patients. However, there has been no direct evidence for CNS involvement by leprosy in a living patient. To the best of the authors' knowledge, the present case is the first report providing histopathological and molecular evidence for CNS involvement by leprosy in a living patient. Brain MRI revealed a 2-cm cystic lesion in the right frontal lobe of the patient. The medical history revealed that the patient had been receiving multidrug therapy for borderline lepromatous leprosy. Neuronavigation-guided craniotomy and lesion removal were performed due to a presumptive diagnosis of low-grade glioma. The brain specimen demonstrated variably thickened blood vessels and densely scattered foamy macrophages in the perivascular spaces and parenchymal stroma. Fite acid-fast stain displayed red granular inclusions that were suggestive for fragmented M. leprae. M. leprae-specific nested polymerase chain reaction amplification showed positive bands, and DNA sequencing also demonstrated homology with the M. leprae genome. This case supports the notion that M. leprae can involve the cerebral cortex regardless of cranial nerve engagement.
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PMID:Brain involvement by leprosy presenting as a frontal cystic lesion. 2452 21