Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle-specific actin (MSA) and desmin are considered to be sensitive and specific markers for muscle differentiation. The authors compared staining patterns for these markers in 576 samples of normal, reactive, and neoplastic tissues. The standard avidin-biotin-peroxidase complex technique was performed with the use of two commercial antibodies against MSA (HHF35; Enzo Biochemical, Inc., New York, NY) and desmin (DER11; DAKO Corporation, Santa Barbara, CA), respectively, on consecutive paraffin-embedded tissue sections from these cases. Both MSA and desmin were found in all 80 normal muscle samples. Although MSA appeared diffusely in all vascular smooth muscle samples, desmin was demonstrated focally in vascular smooth muscle cells in 100 of 196 samples. MSA but not desmin always was found in myoepithelial cells (25 samples), pericytes (286 samples), and decidual cells (7 samples). Among 76 cases of myofibroblast-containing lesions, 14 and 54 were found to have desmin and MSA, respectively. MSA and desmin were found in 4 of 4 cardiac rhabdomyomas, 34 of 34 rhabdomyosarcomas, and 5 of 6 leiomyomas. Among 22 leiomyosarcomas, 7 displayed either MSA or desmin and 7 showed both markers. In general, more tumor cells showed staining for MSA than desmin, but the reverse was true in some cases. Tissue fixed in Zenker's solution seemed to show a significant decrease in MSA immunoreactivity, but no significant change for desmin staining was observed. None of the 154 normal tissues and 22 benign nonmyogenic tumors expressed MSA or desmin. Among 133 malignant nonmyogenic tumors, positive staining for both desmin and MSA was found in 3 of 8 cases of glioblastoma multiforme, 1 of 10 malignant schwannomas, and 1 of 14 malignant fibrous histiocytomas; staining for only MSA was found in 3 of 14 malignant fibrous histiocytomas, 1 of 10 malignant schwannomas, 6 of 6 fibromatoses, 1 of 1 mammary myofibroblastoma, and 1 of 7 malignant mesotheliomas; and staining for desmin only was seen in 1 of 7 malignant mesotheliomas.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparative immunohistochemical staining for desmin and muscle-specific actin. A study of 576 cases. 137 4

The authors report malignant glioma occurring in two sibling cases. The elder brother presented with right hemiparesis and hemihypesthesia at 14-year-old. Computed tomographic (CT) scanning demonstrated a low-density area in the left frontoparietal lobe. The tumor was partially removed. Histologic diagnosis was glioblastoma multiforme. Radiation therapy was given postoperatively, but he died due to tumor recurrence 15 months after onset. The younger sister was admitted comatose due to intratumoral bleeding at 19-year-old. CT scans showed a high-density area in the right temporal lobe. The tumor was excised subtotally. Histological diagnosis was malignant astrocytoma (grade III). Radiation therapy, chemotherapy (ACNU), and immunotherapy (interferon) were given postoperatively, but she died due to recurrence 34 months after onset.
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PMID:Siblings with malignant glioma--report of two cases. 171 48

Glioblastoma multiforme, the most malignant astroglial-derived tumor, grows as an adherent mass and locally invades normal brain. An examination of adult cerebral glioblastoma biopsy material for the expression of adhesive proteins that might potentiate adhesion and invasion demonstrated tumor cell-associated vitronectin (5/5). In contrast, vitronectin was not detected associated with glial cells in low grade astroglial tumors (0/4), reactive astrogliosis (0/4), or in normal adult cortex and cerebral white matter (0/5). Also, a wide variety of other adhesive ligands were absent from the glioblastoma tumor parenchyma. The alpha v beta 3 integrin was the only vitronectin receptor identified in glioblastoma tumors in situ, and was also not expressed on low grade astroglial-derived tumors, reactive astrogliosis, or on glia or neurons in normal adult cortex and cerebral white matter. In a cell attachment assay, cultured glioblastoma cells attached to the parenchyma of glioblastoma tumor cryostat sections at the sites of vitronectin expression, but failed to attach to normal brain. This adhesion was inhibited by antibodies directed against vitronectin, the alpha v beta 3 integrin, and with an Arg-Gly-Asp-containing peptide. These data provide evidence for a cell adhesion mechanism in glioblastoma tumors that might potentiate glioblastoma cell invasion of normal brain.
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PMID:Glioblastoma expression of vitronectin and the alpha v beta 3 integrin. Adhesion mechanism for transformed glial cells. 172 25

Intraoperative radiation therapy (IORT) was used as part of the initial therapy for malignant glioma in 32 of 73 patients with histologically verified anaplastic astrocytoma (grade III astrocytoma) and glioblastoma multiforme. The initial treatment for all cases was subtotal or total tumor resection combined with external irradiation and chemotherapy. IORT was performed 1 week after tumor resection, with doses of 10-50 Gy (mean 26.7 Gy) in one session. Fourteen of 32 cases had IORT two times because of tumor recurrence. The IORT patients had survival rates at 24 and 36 months after initial treatment of 57.1 and 33.5% (median survival 26.2 months). The other 41 patients had 23.6 and 13.1% survivals (median survival 20.7 months), which were significantly lower (p less than 0.01). Tumor recurrence within the original lesion site was suspected because of clinical condition, computed tomography, and magnetic resonance imaging studies in 65.6% of the IORT group (21 cases) 12 months after initial treatment. Twenty cases of death in the IORT group, including five autopsy cases, demonstrated regional tumor recurrence with a high incidence of intraventricular tumor invasion. The authors consider IORT is beneficial for selected malignant glioma patients, including tumor recurrence, because of prolonged survival.
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PMID:Intraoperative radiation therapy for malignant glioma. 172 57

A 65-year-old male was admitted with memory and gait disturbance. A computed tomography (CT) scan showed bilateral, diffuse, low-density areas with two round, slightly enhanced masses. T1-weighted magnetic resonance image revealed a low-intensity area in the left paraventricular region, which converted to increased signal intensity, extending to the right paraventricular region through the splenium, on T2-weighted images. The tumor was diagnosed as glioblastoma multiforme after needle biopsy and treated by irradiation and chemotherapy. Seven months after admission, a CT scan revealed subependymal infiltration of the tumor with spotty calcification. He died of respiratory complications 11 months after the onset of symptoms. The autopsy showed brain swelling with flattened gyri. Horizontal sections of the brain showed diffuse enlargement of the white matter and basal ganglia with scattered hemorrhage and necrosis. Microscopically, the lesion was far more extensive and diffuse than was suspected from gross examination. Wide glial tumor cell infiltration was observed in the cerebral hemispheres, basal ganglia, brainstem, cerebellum, and even the cervical spinal cord with minimum destruction of the pre-existing architecture. Calcification was found around the thrombosed vessels and necrotic lesions. The clinical diagnosis and histological features of gliomatosis cerebri are discussed with reference to reported cases.
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PMID:[Diffuse cerebrospinal gliomatosis. Case report]. 172 37

The bcl2 protooncogene was originally discovered because of its involvement in t(14;18) chromosomal translocations frequently found in non-Hodgkin's lymphomas. The expression of this gene is reported to be highly tissue specific, with bcl2 mRNAs being readily detectable only in hematolymphoid tissues and brain. To explore the possible involvement of bcl2 in neural tumors, we surveyed a variety of tumor cell lines for the presence of the p26-BCL2 protein by immunoprecipitation and immunoblotting methods. Very high levels of BCL2 protein were found in three of nine neuroblastoma (NB) cell lines examined; these levels of p26-BCL2 were comparable to lymphoma cell lines that contain a t(14;18). Despite the impressive relative amounts of BCL2 protein, however, no structural alterations or changes in the methylation status of bcl2 genes were detected in these NB cell lines by conventional Southern blotting. Of the other NB cell lines surveyed, three contained intermediate levels of BCL2 and another three cell lines had little or no detectable BCL2 protein, raising the possibility that determination of relative levels of BCL2 protein may help to segregate neuroblastomas into groups with different biological and clinical characteristics. BCL2 protein levels were not influenced by induction of neuronal differentiation with nerve growth factor in two of the two cell lines examined [SH-SY5Y (high BCL2); GICAN (low BCL2)] and did not correlate with N-MYC gene amplification or expression of nerve growth factor receptors. NB cell lines that contained little or no detectable BCL2 protein, however, tended to contain significant proportions of flat epithelioid cells, whereas bcl2-expressing cell lines were composed primarily of neuronal-like cells, suggesting that expression of this protooncogene correlates with the differentiation characteristics of these tumor cell lines. In addition to NBs, lower levels of BCL2 protein were also found in a variety of other neural crest-derived tumors and tumor cell lines, including some neuroepitheliomas, Ewing's sarcomas, neurofibromas, and melanomas. With regard to tumors of central nervous system origin, bcl2 expression was absent from most medulloblastomas but was detected at moderate to low levels in a retinoblastoma and some glioblastoma multiforme cell lines. Taken together, these findings imply that bcl2 protooncogene expression is differentially regulated within the various lineages of cells that give rise to the nervous system.
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PMID:Differential expression of bcl2 protooncogene in neuroblastoma and other human tumor cell lines of neural origin. 174 26

The present paper describes the analysis of immunostaining patterns of four antibodies, alpha-1-antitrypsin (alpha-AT), glial fibrillary acid protein (GFAP), S-100 protein (S-100), and vimentin in 31 human gliomas. The gliomas were 10 astrocytomas, 10 anaplastic astrocytomas, and 11 glioblastoma multiforme tumors. The immunoreactivity for vimentin and alpha-AT that is one of the main proteinase inhibitors changed in proportion to the degree of histological malignancy. As alpha-AT was localized mainly in the cytoplasm of tumor cells and partially in extracellular spaces, it was thought to have been derived from tumor cells. Preparations immunolabelled with anti-GFAP and anti-S-100 showed no increasing loss of immunoreactivity parallel with increasing malignancy.
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PMID:[Immunohistochemical expression of alpha-1-antitrypsin in human gliomas]. 176 54

Multiple genetic changes take place during tumor development and progression. These genetic changes result in inactivation of tumor suppressor genes and activation of proto-oncogenes. Frequent genetic changes observed in gliomas are losses of chromosomal regions on 9p, 10q, 13q, 17p and on 22. Loss of 10q is seen in more than 80% of the glioblastoma multiforme (GBM) tumors suggesting the presence of a gene critical for GBM formation on this chromosome. Amplification of epidermal growth factor receptor gene and expression of platelet derived growth factor and fibroblast growth factor genes are also common among gliomas. The most common genetic abnormality found in medulloblastomas is loss of 17p. The C-myc gene is amplified in a few primary tumors, but the incidence of amplification is higher in medulloblastoma derived cell lines. These findings suggest that the same two genetic processes, gene amplification and regional chromosomal loss, which characterize other primitive childhood neuroectodermal tumors such as retinoblastoma and neuroblastoma are also important in medulloblastomas.
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PMID:Genetic alterations in glioma and medulloblastoma. 178 30

The rate at which water-soluble chemotherapeutic drugs enter brain tumors can be extremely variable. The ability to measure or predict the rate of drug entry may have an important role in treatment. We have developed a method that uses information from contrast-enhanced computed tomographic scans to measure quantitatively the rate of transcapillary transport of iodinated compounds in brain tumors. In a group of 10 patients with brain tumors, we obtained serial measurements of tissue (Am) and arterial plasma (Cp) iodine concentration from timed computed tomographic scans done over 30 minutes, after intravenous infusion of meglumine iothalamate (Conray-60). These measurements were analyzed with a two-compartment pharmacokinetic model and nonlinear least-squares regression methods to obtain K1, a blood-to-tissue transfer constant; k2, a tissue-to-blood rate constant; and Vp, tissue plasma vascular volume. Images of K1, k2, and Vp were reconstructed after calculating these values for each 0.8 x 0.8 x 5-mm volume element of the original data. Mean whole tumor K1 values varied from 2.0 mu 1 gm-1 min-1 in a thalamic astrocytoma to 33.9 mu 1 gm-1 min-1 in a glioblastoma multiforme. The value of k2 varied from 0.034 to 0.108 min-1, and Vp varied from 2.4 to 7.9 ml 100 gm-1. In tumor-free brain, the K1 of meglumine iothalamate was 2.9 mu 1 gm-1 min-1; k2 was 0.058 min-1; and Vp was 2.1 ml 100 gm-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative measurements of capillary transport in human brain tumors by computed tomography. 178 85

Human glioma-associated markers can be exploited for the development of new diagnostic strategies and treatment modalities for these malignancies. A goat antiserum was first raised against human anaplastic astrocytoma (AC or AA) and glioblastoma multiforme (GB or GBM) extracts. Extensive sequential absorptions with normal brain tissue, normal serum, and human serum albumin (HSA) gave an antibody fraction specific for glioma. Balb/c mice were subsequently immunized with these glioma extracts. B-cell hybridomas from these mice were then cloned and subcloned by limiting dilution, yielding six monoclonal antibodies (MAbs) that were entirely specific for tumor tissues, and did not react with normal human serum or with normal human brain, liver, kidney, spleen, or muscle. Moreover, the murine MAbs did not cross-react with certain other human tumors, including melanoma. The fully absorbed antiserum and the murine MAbs both identify a polypeptide pattern possibly related to human glial fibrillary acidic protein (GFAP) or other intermediate filament proteins on immunoblots. These immunological reagents could serve as powerful tools for the diagnosis and possibly therapy of these uniformly fatal tumors.
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PMID:Preparation and characterization of antisera and of murine monoclonal antibodies to human glioma-associated antigen(s). 180 72


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