Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0027819 (neuroblastoma)
27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of new morphologic methods in the diagnosis of bone tumors is demonstrated in a number of cases. In round cell malignancies (Ewing's sarcoma, malignant lymphoma, neuroblastoma, and anaplastic plasmacytoma) diagnostic accuracy can be improved by electron microscopic and immunohistochemical techniques. New methods are also of value in differentiating the metastatic carcinoma from malignant bone primaries. Electron microscopy may show epithelial cell features (ie, gland structures, desmosomes, and tonofilaments), while immunohistologic investigation of the cytoskeleton may facilitate differentiation of epithelial cells (positive for prekeratin) from mesenchymal cells (positive for vimentin). In the differential diagnosis of typical bone tumors, however, such as osteosarcoma, chondrosarcoma, and malignant fibrous histiocytoma, the value of enzyme histochemical, electron microscopic, and immunohistochemical methods appears somewhat restricted: alkaline phosphatase activity may be increased in both chondrosarcoma and osteosarcoma; collagen type II, the cartilage-specific collagen, is found not only in chondrosarcoma but in osteosarcoma as well. Moreover, osteosarcomas may contain a considerable number of macrophages and histiocytes, and so this feature is worthless in distinguishing osteosarcoma from malignant fibrous histiocytoma. A new approach for appraising the malignancy of bone tumors may be through flow cytometric investigation of nuclear DNA content. Osteosarcomas reveal DNA aneuploidies in more than 80% of cases, with a large proportion of cells in the S phase. These features may prove valuable for discerning osteosarcoma from myositis ossificans. In contrast to typical giant cell tumor of bone, a rare case of malignant giant cell tumor showed aneuploid cell lines indicating the malignant nature of the tumor.
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PMID:New cytomorphologic methods in the diagnosis of bone tumors: possibilities and limitations. 660 Jan 11

A simple method is described that permitted rapid isolation of plasma membranes from mouse N-18 neuroblastoma cells. The purified plasma membranes gave a 10-fold increase in the specific activity of incorporated [3H]fucose over that of the cell homogenate. The specific activities of two other membrane markers, 5'-nucleotidase and alkaline phosphatase, increased 11-fold and 15-fold, respectively. Metabolic labeling with [3H]fucose identified a major fucosyl glycoprotein with apparent molecular weight of 92 000. Three surface labeling methods together with SDS-polyacrylamide gel electrophoresis and fluorography were used to characterize and compare the surface glycoproteins of undifferentiated and differentiated N-18 cells. The galactose oxidase/NaB3H4 method labeled two major galactoproteins (Mr = 52 000, 42 000) in both undifferentiated and differentiated cells. The neuraminidase/galactose oxidase/NaB3H4 method revealed many sialylgalactoproteins. Among them, the 220-kdalton, 150-kdalton and 130-kdalton bands were at least 100% more prominently labeled in the differentiated cells whereas the 76-kdalton and 72-kdalton bands were less prominently labeled in the differentiated cells when compared to their undifferentiated counterparts. The prominently iodinated protein bands in the undifferentiated cells had apparent molecular weights of 130 000, 92 000, 76 000 and 72 000 as compared to 150-, 130-, 92- and 76-kdalton bands in the differentiated cells. The labeling data obtained will enable us to further study the changes of these identified surface glycoproteins, both quantitatively and topologically, during the differentiation of neuroblastoma cells.
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PMID:Identification of exposed surface glycoproteins in undifferentiated and differentiated mouse N-18 neuroblastoma cells. 705 92

Microtubule-associated protein 2 (MAP-2) is an abundant neuronal cytoskeletal protein that binds to tubulin and stabilizes microtubules. Using fusion protein constructs we have defined the epitopes of 10 monoclonal antibodies (mAbs) to discrete regions of human MAP-2. Proteins were expressed in pATH vectors. After electrophoresis, immunoblotting was performed. By western blot analysis five of the mAbs (AP-14, AP-20, AP-21, AP-23, and AP-25) share epitopes with only the high molecular weight isoforms (MAP-2a, MAP-2b); two of the mAbs (AP-18 and tau 46) recognize MAP-2a, MAP-2b, and MAP-2c. Although AP-18 immunoreactivity was detected within heat-stable protein homogenates isolated from a human neuroblastoma cell line MSN, fusion protein constructs encompassing human MAP-2 were negative, suggesting that the AP-18 epitope is phosphorylated. Furthermore, AP-18 immunoreactivity was lost after alkaline phosphatase treatment of heat-stable protein preparations from MSN cells. Four of the mAbs (322, 636, 635, and 39) recognize epitopes located within amino acids 169-219 of human MAP-2. AP-21 maps to a region between amino acids 553 and 645. AP-23 maps between amino acids 645 and 993, whereas AP-20, AP-14, and AP-25 map between amino acids 995 and 1332. Expression of the region of MAP-2 between amino acids 1787 and 1824 was positive to tau 46.
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PMID:Localization of specific epitopes on human microtubule-associated protein 2. 752 76

Human neuroblastoma cells, LAN, were used to study the phosphorylation and dephosphorylation of tau proteins. These cells contained mainly a form of tau comparable to fetal brain tau in molecular weight (55 kDa). Neuroblastoma tau reacted with antibodies that recognize epitopes spanning the whole tau molecule (E-1, Alz50, Tau-1, and Tau46), and antibodies (PHF-1, NP8, and T3P) that recognize hyperphosphorylated tau (PHF-tau) in Alzheimer's disease (AD) brains. Exposure of the cells to 45 degrees C heat stress resulted in dephosphorylation of the epitopes recognized by PHF-1, NP8, and T3P. Transfer of the heat-stressed cells to 37 degrees C led to rephosphorylation of the dephosphorylated epitopes. Cells that had been treated with okadaic acid (OA), regardless of whether they were subsequently subjected to heat stress or heat stress and recovery, all contained tau with a molecular weight similar to that of control cells. These tau proteins, similar to tau in control cells, also reacted with antibodies to phosphorylated epitopes. However, unlike the tau from control or heat-stressed cells, the OA-treated and heat-stressed tau had decreased reactivity with Tau-1. Alteration of Tau-1 immunoreactivity has been reported to be an early event in AD neurodegeneration. The reduction of Tau-1 immunoreactivity observed in OA-treated samples could be restored by incubation of electroblots of isolated tau with alkaline phosphatase, indicating an induction of the Tau-1 epitope phosphorylation by OA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversible heat stress-related loss of phosphorylated Alzheimer-type epitopes in Tau proteins of human neuroblastoma cells. 769 94

High-molecular-mass alkaline phosphatase (H-Mr AP) was detected in sera from children with solid tumors without liver metastases. H-Mr AP activities were determined by a liquid chromatographic and an electrophoretic method. In 5 out of 10 cases with solid tumors--Ewing sarcoma (n = 2), neuroblastoma (n = 2), and rhabdoid tumor (n = 1)--H-Mr AP activities ranged from 3.1-40.4 U/L and 3.1-16% of total serum AP activity. In sera of patients with leukemia (n = 18) H-Mr AP was not detectable. After the treatment of the sera with papain and phosphatidylinositol-specific phospholipase C, which release membrane-associated AP from membrane particles, H-Mr AP was no longer detectable. These results indicate that H-Mr AP in the sera of patients with solid tumors may derive from increasing cell shedding of the tumor cells with elevated levels of membrane fragments in serum, which is a well known phenomenon in liver tumors. H-Mr AP was not more detectable in the serum after successful tumor treatment. These data suggest that H-Mr AP was produced by the tumors and that this parameter may be a serological marker for some solid tumors even in the presence of normal total AP serum activity.
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PMID:High-molecular-mass or macromolecular alkaline phosphatase in sera of children with solid tumors. 815 5

Bone scintigraphy with 99mtechnetium-labelled polyphosphonates is the most sensitive test for early detection of skeletal metastases. Bone metastases are a major factor in prognosis and have a considerable influence on the therapy selected. In patients with prostate cancer, we recommend routine bone scintigraphy in the initial staging. Follow-up bone scans are indicated whenever a patient develops pain, an elevated level of acid phosphatase, or a rise in prostate specific antigen (PSA). Routine bone scans are not necessary for the initial staging of patients with renal cell carcinomas, bladder carcinomas and testicular tumours. Scans should be routinely performed, however, in patients with bone pain or elevated alkaline phosphatase or when radiological findings are inconclusive. Bone scanning is necessary in patients with neuroblastoma, both for the initial diagnosis and during follow-up in all cases with known skeletal involvement. In addition, bone scintigraphy should be performed in cases of recurrent or suspected malignant phaeochromocytoma as a complement to scintigraphy with iodine-123- or iodine-131-MIBG, respectively. Even though skeletal scintigraphy is a very sensitive test, it lacks specificity. This can be compensated, however, by careful interpretation of the scan in the light of the patient's history and the clinical findings. As a positive side-effect, bone scanning--especially in the form of multiphase scintigraphy--may detect renal abnormalities, concurrent diseases or complications in the upper or lower urinary tract. If scintigraphic findings are doubtful, plain film radiographs are required or, in selected cases, bone biopsy must be performed.
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PMID:[Nuclear medicine diagnosis and therapy in urology. Diagnosis of bone metastases]. 847 16

Addition of 400 microM AlCl3 to the culture medium for 72 h has been previously shown to induce perikaryal whorls of intermediate-sized filaments in intact mouse NB2a/d1 neuroblastoma cells. Immunoblot analyses demonstrated that in vivo treatment of cells with aluminum induced the de novo appearance of extensively phosphorylated NF-H isoforms in cytoskeletons of undifferentiated cells and increased levels of these isoforms in differentiated cells. Neurofilament subunits isolated from intact cells treated with aluminum were resistant to dephosphorylation in vitro by alkaline phosphatase and to in vitro degradation by endogenous calcium-dependent protease(s). These alterations were accompanied by a greater tendency of neurofilaments to form insoluble aggregates after isolation. These findings demonstrate direct effects of aluminum on neurofilament subunits within intact neuronal cells similar to those previously demonstrated following in vitro exposure of isolated neurofilaments to aluminum.
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PMID:Aluminum treatment of intact neuroblastoma cells alters neurofilament subunit phosphorylation, solubility, and proteolysis. 858 20

Protein phosphatase 2A is a heterotrimeric protein serine/threonine phosphatase consisting of a 36-kDa catalytic C subunit, a 65-kDa structural A subunit, and a variable regulatory B subunit. The B subunits determine the substrate specificity of the enzyme. There have been three families of cellular B subunits identified to date: B55, B56 (B'), and PR72/130. We have now cloned five genes encoding human B56 isoforms. Polypeptides encoded by all but one splice variant (B56gamma1) are phosphoproteins, as shown by mobility shift after treatment with alkaline phosphatase and metabolic labeling with [32P]phosphate. All labeled isoforms contain solely phosphoserine. Indirect immunofluorescence microscopy demonstrates distinct patterns of intracellular targeting by different B56 isoforms. Specifically, B56alpha, B56beta, and B56epsilon complexed with the protein phosphatase 2A A and C subunits localize to the cytoplasm, whereas B56delta, B56gamma1, and B56gamma3 are concentrated in the nucleus. Two isoforms (B56beta and B56delta) are highly expressed in adult brain; here we show that mRNA for these isoforms increases severalfold when neuroblastoma cell lines are induced to differentiate by retinoic acid treatment. These studies demonstrate an increasing diversity of regulatory mechanisms to control the activity of this key intracellular protein phosphatase and suggest distinct functions for isoforms targeted to different intracellular locations.
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PMID:The B56 family of protein phosphatase 2A (PP2A) regulatory subunits encodes differentiation-induced phosphoproteins that target PP2A to both nucleus and cytoplasm. 870 17

The diagnostic value of immunophenotyping (IP) as a first-line diagnostic method in diseases that infiltrate the childhood bone marrow (BM) or mimic infiltrated BM was examined. Two hundred and fifty unselected BM samples from 250 children suspected to have a malignancy infiltrating their BM were evaluated by means of IP and conventional morophological-cytochemical (MC) studies. We applied the alkaline phosphatase anti-alkaline phosphatase method for IP using a panel of monoclonal antibodies (Mabs) against leukocyte-associated antigens, neuroectodermal antigens, and intermediate filament antigens. Four cases of neuroblastoma, two cases of Ewing sarcoma, and one case of rhabdomyosarcoma were diagnosed by IP but not by MC studies. In nine cases of acute leukemia bone marrow blasts could not be ascribed to a specific lineage on the basis of blast morphology or histochemistry. Eight samples without morphological evidence of malignant infiltration revealed an increased percentage of immature B cell precursors (CD10+, TdT+) suggesting acute lymphoblastic leukemia. None of these children has developed malignant lymphoproliferative disease. Our data suggest that the immunological evaluation of BM in childhood is highly capable of discriminating between different malignant populations but it does not recognize malignancy and therefore supplements but cannot replace conventional methods for diagnosis.
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PMID:Differential diagnosis based on immunological-phenotyping in suspected malignant bone marrow involvement in childhood. 902 11

Peripheral stem cells were mobilized and collected in 20 children with stage 4 neuroblastoma. A total of 37 leukaphereses were performed in the 20 patients. The mean number of collected cells was 5.6 +/- 2.4 x 10(8)/kg (range 1.9-10.5), and the number of collected CD34+ progenitors was 6.1 +/- 6.3 x 10(6)/kg (range 0.75-21.7). CD34-positive selection was performed using the CellPro method. Of the adsorbed cells, 42 +/- 20% (range 4.3-76.6) stained positively for CD34, and the number of positively selected CD34+ cells was 2.0 +/- 1.9 x 10(6)/kg (range 0.09-7.1). The mean recovery of CD34+ cells was 36 +/- 20% (range 6-67). For detection of contaminating neuroblastoma cells before and after CD34-positive selection, a murine antidisialoganglioside GD2 antibody (14.G2a) was used, followed by the alkaline phosphatase antialkaline phosphatase (APAAP) method. Before the positive selection, various numbers of contaminating neuroblastoma cells were found in the leukaphereses of 7 patients. After positive selection, neuroblastoma cells were still detectable in all 7 patients, with a mean log depletion of tumor cells of 1.41 +/- 0.45 (range 0.69-2.13). In 1 patient, contaminating neuroblastoma cells were found only after CD34-positive selection. In 15 of the 20 patients, high-dose chemotherapy was performed, and positively selected CD34+ cells were reinfused in 12 patients. In 10 of these, the mean time to reach > 0.5 x 10(9)/L granulocytes was 12.3 +/- 1.7 days (range 10-16). One patient died at day 7 due to sepsis, and in 1 patient the backup was given at day 15. Because of the low number of collected CD34+ cells, 3 patients were grafted with a combination of unmanipulated PBSC and CD34+ progenitors. In summary, we have shown that positive selection of peripheral CD34+ progenitors is feasible in pediatric patients. However, strategies to improve the recovery of the CD34+ cells and the purging efficacy of this method (i.e., higher enrichment of CD34+ cells, combination of positive and negative selection methods) should be evaluated further.
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PMID:Positive selection and transplantation of peripheral CD34+ progenitor cells: feasibility and purging efficacy in pediatric patients with neuroblastoma. 923 78


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