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)

Nineteen primary intracranial sarcomas out of a total of about 25,000 brain tumour biopsies are reported. Subtypes included malignant fibrous histiocytoma (6 cases), leiomyosarcoma (3), rhabdomyosarcoma (2), angiosarcoma (2), and one case each of fibrosarcoma, low-grade fibromyxoid sarcoma, malignant ectomesenchymoma, mesenchymal chondrosarcoma, differentiated chondrosarcoma and Ewing's sarcoma. Histological and immunohistochemical features corresponded to those of extracranial sarcomas. Nests of pleomorphic astrocytes mimicking glioma were detected in the five storiform-pleomorphic malignant fibrous histiocytomas. Our results indicate that intracranial sarcomas can be classified like their extracranial counterparts. The low incidence compared with earlier series is related to changes in classification and progress in histogenetic clarification.
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PMID:Primary intracranial sarcomas: histopathological features of 19 cases. 171 39

Multiplanar capability and superior tissue contrast differentiation render magnetic resonance (MR) imaging the preferred method for examining patients with pituitary axis dysfunction or visual field deficits. In a review of 131 sellar or juxtasellar abnormalities, 76% were common lesions with distinctive features that helped establish their diagnosis: macroadenoma (n = 51), microadenoma (n = 20), meningioma (n = 14), craniopharyngioma (n = 10), and aneurysm (n = 5). On T1-weighted images, microadenomas were usually hypointense relative to normal pituitary gland, and macroadenomas and meningiomas were isointense relative to gray matter. Both microadenomas and meningiomas were more conspicuous immediately after contrast material administration. Craniopharyngiomas were the most heterogeneous of all the sellar lesions due to their cystic and solid components. MR images of aneurysms showed flow void and heterogeneous increased signal intensity in areas of slower turbulent flow. Other characteristics such as extrasellar versus intrasellar location, nature of contrast material enhancement, the presence of cystic components, and clinical findings permitted differentiation among less common lesions, including granulomatous disease, metastases, chiasmatic glioma, arachnoid cyst, hypothalamic glioma, schwannoma, germinoma, epidermoid, Rathke cyst, chordoma, chondrosarcoma, colloid cyst, and hamartoma.
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PMID:MR imaging of the sellar and juxtasellar regions. 194 11

The current case report deals with a 14-year-old girl with an intracerebral mesenchymal chondrosarcoma which has been recognized in two males and two females varying from 25 to 59 years of age. Three of the five patients had an associated malignant glioma. The present girl died eight years after her initial neurologic deficits and never received any definitive treatment for her deep seated neoplasm. These unique sarcomas may be confused with vascular lesions and have not been found to spread through the neuraxis. This unusual primary intracerebral mesenchymal chondrosarcoma appears to represent a field phenomenon with cartilaginous differentiation of glial and mesenchymal elements in the central nervous system.
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PMID:Intracerebral mesenchymal chondrosarcoma. 260 77

Twenty-seven cases of chronic isolated abduction deficit, seen in 25 years of neuro-ophthalmology consultation, were reviewed. "Isolated" was defined as the lack of any other neurologic or ophthalmologic findings for at least six months. Cases were further subdivided into the categories of true and pseudo-abducens paresis. The origin, diagnosis, and management of long-standing abducens palsies were determined. Cases of pontine glioma, chordoma, chondrosarcoma, and meningioma that presented as an isolated abducens palsy and remained undiagnosed for at least six months were reviewed.
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PMID:Chronic isolated sixth nerve palsies. 291 Feb 66

Murine embryonal carcinoma tumors were induced to differentiate in vivo by administration of retinoic acid. Six long-term surviving animals had seven slowly growing tumors which were transplanted s.c. into strain 129 mice. Untreated embryonal carcinomas were transplanted as controls. All of the 16 control transplants grew rapidly and killed their hosts within 25 days. All of the 24 transplants of retinoic acid-differentiated tumor survived. Sixteen experimental transplants originating from five original tumors showed no or slow growth for up to 16 weeks and were found to be histologically benign cystic teratomas. Two original tumors gave rise to eight relatively rapidly growing transplants. One tumor resulted in four histologically similar solid tumors which resembled chondrosarcomas, and the second tumor gave rise to four histologically similar solid tumors which proved to be a mixture of glioma and chondrosarcoma. Examination of the tumor sources of these latter transplants showed benign cystic teratomas with focal solid, mitotically active cellular areas which were histologically similar to the transplants. These data confirm that retinoic acid-induced differentiation of murine embryonal carcinoma cells results in altered biological potential of these cells and usually the formation of a benign teratoma. Rarely (about 1 per 2 X 10(8], the resulting differentiated cells will give rise to rapidly growing, histologically malignant tumors. One can predict such biological propensity when solid, mitotically active areas in the original tumor are found.
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PMID:Chemically induced differentiation of murine embryonal carcinoma in vivo: transplantation of differentiated tumors. 620 Dec 66

An unusual primary intracerebral tumor with combined features of chondrosarcoma and glioblastoma multiforme is presented. Glial elements showing a spectrum of hyperplastic and neoplastic changes were intermingled with sarcomatous areas, similar to that recently described by Lalitha and Rubinstein as "sarcoglioma." Many vessels in the gliomatous regions contained proliferating endothelial cells with marked cytologic abnormalities. Although no direct extension out of the vessel wall was conclusively identified, the possibility of sarcomatous change could not be completely excluded. We conclude that, in this case, we could not establish whether the sarcoma was primary and the glioma secondary ("sarcoglioma") or vice versa ("gliosarcoma"), nor could we rule out that the two components originated from the same ancestral pluripotential cells.
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PMID:Primary intracerebral tumor with mixed chondrosarcoma and glioblastoma--gliosarcoma or sarcoglioma? 624 92

Murine embryonal carcinoma tumors were induced to differentiate in vivo using retinoic acid. Six mice bearing seven tumors survived more than 100 days after treatment. Histological samples of these tumors showed no residual embryonal carcinoma cells, and, for the most part, they were benign cystic teratomas. Three tumors, in addition to the benign tissue, had solid, mitotically active areas. Two of these tumors upon transplantation gave rise to progressively growing, potentially lethal tumors which have proven to be permanently transplantable cell lines. Using techniques of light and electron microscopy, immunohistochemistry, flow microfluorometry, and cytogenetics, we have characterized these lines. One is a chondrosarcoma, and one is a glioma:chondrosarcoma mixture. Both are chromosomally different from the parent embryonal carcinoma stem cell line, but both were clearly derived from it.
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PMID:Malignant neoplasms of differentiated cells occurring after retinoic acid treatment of murine embryonal carcinomas in vivo. 671 3

N-Phosphonacetyl-L-aspartic acid (PALA) is new synthetic antimetabolite which inhibits de novo pyrimidine biosynthesis. Its significant activity against Lewis lung carcinoma, B16 melanoma, and glioma 26 suggested that it might be useful in the treatment of human solid tumors. Phase I trials revealed that dose-limiting toxicity included skin reactions, diarrhea, and stomatitis. Pharmacologic studies demonstrated rapid renal excretion of more than 70% of the unmetabolized drug in 24 h. Peak plasma levels correlated with dose of PALA administered. Partial responses to PALA were seen in one patient with melanoma, one with chondrosarcoma, and one with colon carcinoma. The potential for PALA's use in combination chemotherapy, particularly with 5-fluorouracil, is discussed.
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PMID:An overview of the clinical pharmacology of N-phosphonacetyl-L-aspartate (PALA), a new antimetabolite. 744 50

We provided evidence previously that bikunin, a Kunitz-type protease inhibitor, can disrupt dimerization of CD44 proteins, which may result in suppression of receptor-mediated MAP kinase signaling. However, to what extent dimerization may alter ligand-induced signaling has not been documented. Given the recent recognition that some growth factor receptors can form heterodimers with CD44, the present study was undertaken to determine whether the CD44 and growth factor receptors (e.g., EGFR, FGFR, HGFR, VEGFR, TGF-betaRI, or TGF-betaRII) can form heterodimers in cancer cells and, if so, to investigate the potential functional consequences of such heterodimerization. We also examined whether bikunin can abrogate these heterodimerizations and inhibit CD44/growth factor-dependent signaling. Here, we show direct evidence for heterodimerization of CD44-FGFR and CD44-TGF-betaRI in human chondrosarcoma HCS-2/8 cells, CD44-EGFR complex in human glioma U87MG cells, and CD44-TGF-betaRI heterodimer in human ovarian cancer HRA cells. Coupling of CD44 and growth factor receptor may be selective, depending on a cell type. Bikunin does not alter the ligand binding, whereas functionally reduces heterodimerization between CD44 and growth factor receptors. The disruption of heterodimerization substantially reduces receptor-induced tyrosine phosphorylation and ERK1/2 activation. Taken together, our data suggest that bikunin-mediated suppression of heterodimerization between CD44 and growth factors may inhibit the agonist-promoted activation of the signaling pathway.
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PMID:Bikunin down-regulates heterodimerization between CD44 and growth factor receptors and subsequently suppresses agonist-mediated signaling. 1559 42

Hedgehog (HH) signalling is important for specific developmental processes, and aberrant, increased activity has been described in various tumours. Disturbed HH signalling has also been implicated in the hereditary syndrome, Multiple Osteochondromas. Indian Hedgehog (IHH), together with parathyroid hormone-like hormone (PTHLH), participates in the organization of growth plates in long bones. PTHLH signalling is absent in osteochondromas, benign tumours arising adjacent to the growth plate, but is reactivated when these tumours undergo malignant transformation towards secondary peripheral chondrosarcoma. We describe a gradual decrease in the expression of Patched (PTCH) and glioma-associated oncogene homologue 1 (GLI1) (both transcribed upon IHH activity), and GLI2 with increasing malignancy, suggesting that IHH signalling is inactive and PTHLH signalling is IHH independent in secondary peripheral chondrosarcomas. cDNA expression profiling and immunohistochemical studies suggest that transforming growth factor-beta (TGF-beta)-mediated proliferative signalling is active in high-grade chondrosarcomas since TGF-beta downstream targets were upregulated in these tumours. This is accompanied by downregulation of energy metabolism-related genes and upregulation of the proto-oncogene jun B. Thus, the tight regulation of growth plate organization by IHH signalling is still seen in osteochondroma, but gradually lost during malignant transformation to secondary peripheral chondrosarcoma and subsequent progression. TGF-beta signalling is stimulated during secondary peripheral chondrosarcoma progression and could potentially regulate the retained activity of PTHLH.
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PMID:Peripheral chondrosarcoma progression is accompanied by decreased Indian Hedgehog signalling. 1675 18


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