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

Ribonucleic acid was isolated from a wide spectrum of central nervous system tumors to examine the expression of platelet-derived growth factors (PDGF) A and B, tumor growth factors (TGF-beta) 1 and 2, and ros messenger ribonucleic acid. Eight glioblastoma cell lines were examined as well as cell cultures from 22 tumor explants. The explants included 6 glioblastomas, 4 anaplastic astrocytomas, 5 astrocytomas, 3 ependymal tumors, 2 meningiomas, 1 medulloblastoma. and 1 ganglioglioma. For comparison, 2 nontumor glial cell cultures were included. The PDGF B-chain was expressed in 5 of 8 glioblastoma cell lines, 2 of 6 glioblastomas, and in 3 of 4 anaplastic astrocytoma explants. There was no PDGF B expression in 4 astrocytomas, 3 ependymomas of varying malignancy, in the remainder of the tumors, or in the nontumor glial cells. The PDGF A-chain was expressed in all of the tumors, with the exception of the malignant ependymoma and in both nontumor glial cell cultures. TGF-beta 1 was expressed in all of the tumors and in nontumor glial cells. The expression of TGF-beta 2 was expressed in many of the benign and malignant tumors and also in both nontumor glial cell cultures. The ros messenger ribonucleic acid was expressed in 1 of 5 glioblastoma cell lines and in 2 of 6 glioblastoma cell explants, but in none of the other tumors or in the nontumor glial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Expression of platelet-derived growth factors, transforming growth factors, and the ros gene in a variety of primary human brain tumors. 199 89

MR is generally known to be more sensitive but less specific than CT in the detection of brain lesions. In our opinion multiple echo sequences can markedly improve MR specificity in the diagnosis of tumors. We reviewed a series of 343 intracranial tumors studied with MR using multiple echo sequences and histologically verified. On the basis of the different signal patterns we divided brain tumors into 5 classes. Class 1: the signal intensity of the tumor increases progressively in T2 WI (100% of craniopharyngiomas, 21/21; 100% of epidermoid tumors, 12/12; 81% of astrocytomas (grades I to III), 64/79; 65% of neurinomas, 30/46). Class 2: the signal intensity of the lesion decreases progressively in T2 WI: A) the tumor has higher signal intensity than the parenchyma in all echoes (100% of medulloblastomas, 14/14; 53% of pituitary adenomas, 15/28); B) the tumor has the same signal intensity as the parenchyma in late echo acquisitions (100% of ependymal tumors, 12/12; 60% of meningiomas, 25/41). Class 3: the tumor has the same signal intensity as the parenchyma in all echoes (34% of meningiomas, 14/41). Class 4: glioblastoma model: one or more cysts of high signal intensity in T2 WI and slightly hyperintense nodules and/or rings and hyperintense peritumoral edema (73% of glioblastomas, 35/48; 72% of metastases, 18/25). Class 5: oligodendroglioma model: mixed hyper/hypointense pattern; cyst, calcifications and edema are very difficult to recognize within the lesion (95% of oligodendrogliomas, 18/19). The signal pattern was sometimes characteristic but never pathognomonic. Nevertheless, this classification proved to be an useful criterion to restrict the number of possible diagnoses. The study of T1 and T2 values seems to be less useful.
 ...
PMID:[Magnetic resonance in brain tumors: a classification based on signal behavior in multiple echo sequences]. 262 52

The gli gene was originally isolated from DNA amplified in double minutes in a glioblastoma (D259MG). Using a sensitive RNA-RNA hybridization, we tested a series of central nervous system tumors for expression of the gli gene. These included 8 glioblastoma cell lines, plus cell cultures of 5 glioblastomas, 4 anaplastic astrocytomas, 3 different ependymal tumors, a malignant meningioma, and a medulloblastoma. Two normal glial cell cultures were also examined. There was no gli expression in any of these specimens. In glioblastoma D259MG, approximately 130 molecules of gli mRNA per cell were present and the half-life of the mRNA was approximately 5 h. By reverse transcription and PCR, gli mRNA was observed in 4 cell lines and in normal human glial cells, but the level was estimated to be less than one five hundredth of that in the D259MG cell line. The results suggest that gli expression in central nervous system tumors is a rare event and mostly likely associated with amplification of the gene.
 ...
PMID:A search for gli expression in tumors of the central nervous system. 820 91

Protein (lectin)-carbohydrate interaction is supposed to be relevant for tumor cell behavior. The aims of the present work are to investigate whether galectin-1 modulates migration/invasion features in human gliomas in vitro, whether it can be detected in human gliomas immunohistochemically, and whether its expression is attributable to certain glioma subgroups with respect to invasion and prognosis. For this purpose, we quantitatively determined (by computer-assisted microscopy) the immunohistochemical expression of galectin-1 in 220 gliomas, including 151 astrocytic, 38 oligodendroglial, and 31 ependymal tumors obtained from surgical resection. We also xenografted three human glioblastoma cell lines (the H4, U87, and U373 models) into the brains of nude mice in order to characterize the in vivo galectin-1 expression pattern in relation to tumor invasion of the normal brain parenchyma. In addition, we characterized the role in vitro of galectin-1 in U373 tumor astrocyte migration and kinetics. Our data reveal expression of galectin-1 in all human glioma types with no striking differences between astrocytic, oligodendroglial, and ependymal tumors. The level of galectin-1 expression correlated with the grade in the group of astrocytic tumors only. Furthermore, immunopositivity of high-grade astrocytic tumors from patients with short-term survival periods was stronger than that of tumors from patients with long-term survivals. In human glioblastoma xenografts, galectin-1 was preferentially expressed in the more invasive parts of these xenografts. In vitro experiments revealed that galectin-1 stimulates migration of U373 astrocytes.
 ...
PMID:Galectin-1 is highly expressed in human gliomas with relevance for modulation of invasion of tumor astrocytes into the brain parenchyma. 1124 42

Gliosarcoma, a recognized subtype of glioblastoma, is a biphasic tumor exhibiting distinct glial and sarcomatous components. Ependymosarcomas are rarer, biphasic ependymal tumors exhibiting sarcomatous change. Genetic abnormalities associated with this curious phenotype are not well understood. We are presenting the first karyotype of ependymosarcoma with identification of a clonal t(1;19)(q12;p13). Fluorescence in situ hybridization (FISH) was performed with a probe set targeting 1q23 and 19p13.3. Although the tumor did not show evidence of t(1;19)(q23;p13.3) by FISH, increased ploidy was a feature of the sarcomatous component. On clinical followup the patient is doing well without evidence of recurrence 55 months after initial resection, and postoperative treatment with irradiation and temozolomide. The significance of the genetic alterations we describe associated with sarcomatoid change in ependymal neoplasms, and ultimately their prognostic relevance, merits further study.
 ...
PMID:Identification of t(1;19)(q12;p13) and ploidy changes in an ependymosarcoma: a cytogenetic evaluation. 2255 18

The present population-based study describes the survival of malignant central nervous system (CNS) tumors diagnosed during 15 years. Also, we obtained individual data regarding the use of temozolomide to analyze the impact of this drug on the survival of patients diagnosed with glioblastoma. From 1994 to 2008, a total of 679 incident cases of primary CNS tumors were reported by the Girona Cancer Registry after excluding 39 cases diagnosed by death certificate only. Number of cases and the corresponding proportion for each CNS histological subtype in the study population were: 25 oligodendroglial and oligoastrocytics (3.7%), 22 ependymal tumors (3.2%), 24 embryonal (3.5%), 372 astrocytic (54.8%), 1 choroid plexus (0.1%) and 235 without histological confirmation (34.6%). Observed survival after 5 years since diagnosis for the histological subtype were: 58.8%; 47.5%; 37.0%; 14.5% and 6.5%, respectively (p<0.001). Survival of patients diagnosed with glioblastoma according to temozolomide treatment (yes/no) was 60.8% vs. 13.6% and 5.9% vs. 2.5% after 1 and 5 years since diagnosis, respectively. Short-term survival was higher for patients diagnosed with glioblastoma and treated with temozolomide than patients not treated with temozolomide.
...
PMID:Population-based survival analyses of central nervous system tumors from 1994 to 2008. An up-dated study in the temozolomide-era. 2479 86

Gliomas form a heterogeneous group of tumors of the central nervous system (CNS) and are traditionally classified based on histologic type and malignancy grade. Most gliomas, the diffuse gliomas, show extensive infiltration in the CNS parenchyma. Diffuse gliomas can be further typed as astrocytic, oligodendroglial, or rare mixed oligodendroglial-astrocytic of World Health Organization (WHO) grade II (low grade), III (anaplastic), or IV (glioblastoma). Other gliomas generally have a more circumscribed growth pattern, with pilocytic astrocytomas (WHO grade I) and ependymal tumors (WHO grade I, II, or III) as the most frequent representatives. This chapter provides an overview of the histology of all glial neoplasms listed in the WHO 2016 classification, including the less frequent "nondiffuse" gliomas and mixed neuronal-glial tumors. For multiple decades the histologic diagnosis of these tumors formed a useful basis for assessment of prognosis and therapeutic management. However, it is now fully clear that information on the molecular underpinnings often allows for a more robust classification of (glial) neoplasms. Indeed, in the WHO 2016 classification, histologic and molecular findings are integrated in the definition of several gliomas. As such, this chapter and Chapter 6 are highly interrelated and neither should be considered in isolation.
...
PMID:Histologic classification of gliomas. 2694 49