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)

Activin/EDG, a stimulator of the secretion of follicle stimulating hormone (FSH) from pituitary gland and an inducer of erythroid differentiation for Friend leukemia cells, has since been implicated in a variety of biological roles. Here, we show some novel effects of activin on murine embryonal carcinoma cells (EC cells). First, activin acts as a growth factor on undifferentiated P19 cells, a well characterized EC cell line for the study of mammalian development. Second, activin inhibits the retinoic acid (RA) induced differentiation of P19 cells to neurons and glial cells. The inhibitory effect of activin on neural differentiation, which has yet to be proved in other physiological peptides, is confirmed also on the differentiation of various neuroblastoma cell lines. Our results suggest a possible role of activin as a negative regulator of neural differentiation in mammalian development.
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PMID:Activin/EDF as an inhibitor of neural differentiation. 225 14

In 1986 we reported on the capacity of cis-diaminedichloroplatinum(II) (cisplatin, CDDP) to induce erythroid cellular differentiation in the K562 cell. To continue our study of the differentiating activity of cisplatin, we treated two human neuroblastoma cell lines with different doses of the drug in vitro. Both cell lines showed changes in morphology; however, only one achieved a fully differentiated neuronal phenotype (cisplatin concentration 1 micrograms/ml). The differentiated neuroblastoma cells exhibited extensive neurite outgrowth that reached maximal elongation after 5 days of culture, forming several interconnections. Cisplatin could induce neuronal differentiation, as did retinoic acid, a neuroblastoma-differentiating agent. The results show that cisplatin should be a candidate for further in vitro and in vivo studies of induced differentiation.
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PMID:Morphological change and cellular differentiation induced by cisplatin in human neuroblastoma cell lines. 259 98

The application of molecular biological techniques to the study of lympho-erythroid neoplasms, colo-rectal carcinoma and neuroblastoma has led to fundamental insights into the nature of cellular proliferation, transformation and immortalisation as well as providing prognostic information about the biological behaviour of certain tumours. The study of the molecular genetics of central nervous system tumours with particular reference to oncogenes is however in its infancy. Most of the current literature concerns studies of small numbers of glial tumours or of glial tumour cell lines. In this review the results of these studies are analysed and compared with relevant oncogene findings in experimental cerebral neoplasia, extracranial tumours and postulated mechanisms of oncogene activation. The role of proto-oncogenes in the development of the brain, and the clinical relevance of advances in molecular biology to central nervous system neoplasia are discussed.
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PMID:Oncogenes and neuro-oncology. 267 16

An acutely ill 6-month-old female infant presented with massive hepatomegaly, accompanied by severe anemia with peripheral normoblastemia and thrombocytopenia. Bone marrow examination revealed erythroid hyperplasia with gross erythroid dysplasia, reduced granulocytic precursors, and virtually absent megakaryocytes. The bone marrow also contained completely necrotic cells occurring in clumps as well as singly. The appearances suggested bone marrow involvement by neuroblastoma. Accordingly, combination chemotherapy was instituted and laparotomy was performed as soon as her clinical condition had improved. Left adrenalectomy was carried out, because a small adrenal nodule of ganglioneuroma was present. Liver biopsy showed expansion of portal tracts by loose fibrous connective tissue containing hemosiderin deposits and some degenerate cellular debris, consistent with areas of involuted metastatic neuroblastoma. Complete recovery followed, and subsequent bone marrow examination was entirely normal. It is thought that the dyserythropoiesis probably resulted from the release of toxic metabolites from regressing neuroblastoma.
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PMID:Transient dyserythropoiesis occurring during the involutionary phase of stage IV-S neuroblastoma. 271 38

Prion protein (PrP) forms the fibrils or prion rods isolated from scrapie-infected brain and has been proposed as the major component of the infectious agent of this slowly progressive spongiform encephalopathy. In previous Northern blot analyses PrP-specific mRNAs have been found in both normal and scrapie-infected brains but not in spleen, an organ which harbours large titres of infectivity. In the present study, mouse PrP DNA was used to probe for PrP mRNA in assorted tissues and cells. A reexamination of mouse and hamster spleens revealed that they contained low levels of PrP mRNA (approx. 0.8% of that in brain mRNA). No consistent differences were observed between normal and scrapie-infected tissues. Also positive for PrP mRNA under stringent hybridization conditions were mouse epithelial, neuroblastoma, erythroid, B-lymphocytic and embryo fibroblast tissue culture cell lines, a hamster ovary cell line, a rat glioma cell line, and human T lymphocytic and neuroblastoma cell lines. In contrast, no PrP mRNA was detected in two mouse myeloid cell lines and one T cell lymphoma. These results provide evidence that PrP is a protein common to numerous, but not all, cell types besides those of the brain.
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PMID:Detection of prion protein mRNA in normal and scrapie-infected tissues and cell lines. 289 63

Anthracyclines such as Adriamycin (ADR) and daunomycin markedly inhibit cell growth in vivo and in vitro. These studies demonstrate that 30 microM hemin, which induces hemoglobin synthesis in human and murine erythroleukemia cells in culture, markedly decreases the cytotoxicity of ADR in a variety of hemopoietic cell lines (K562, HEL-1, MEL-745, HL-60, and U937) and in erythroid burst-forming cells from normal human marrow. Hemin failed to protect four of the five nonhemopoietic cell lines tested, including MCF-, breast adenocarcinoma cells, C-205 colon carcinoma cells, mouse 3T3 fibroblasts, and mouse kidney VERO cells. Hemin did protect human neuroblastoma IMP-32 cells from ADR cytotoxicity; however, this nonhemopoietic cell line undergoes dendrite formation in response to hemin induction. Cytofluorographic analysis of cellular ADR content and labeling studies with [3H]daunomycin demonstrated that hemin decreases the intracellular accumulation of these anthracyclines by more than 50% in K562 erythroleukemia cells. These studies indicate that small doses of hemin prevent intracellular accumulation of anthracyclines and thereby markedly reduce anthracycline toxicity to cells. Since this protective effect is observed preferentially with hemopoietic cells, it is possible that this finding could be exploited to protect the bone marrow from the cytotoxic action of anthracyclines during therapy for nonhemopoietic tumors.
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PMID:Prevention of anthracycline-induced cytotoxicity in hemopoietic cells by hemin. 370 75

Murine erythropoiesis represents a favourable system in which to investigate the coordinate regulation of gene expression due to the availability of erythroid precursor cells at various stages of differentiation. In this report, we investigate the biosynthesis and cell specificity of two characteristic murine RBC membrane glycoproteins that resemble the human RBC glycophorins: a major component of apparent molecular mass 31 kD (glycophorin MA) and a minor 46 kD component (glycophorin MB). Both glycophorins bind to wheat germ lectin and share a common protein antigenic determinant recognised by a monoclonal antibody (GP 29.4), but they differ significantly in their carbohydrate components: whilst both glycophorins contain mainly O-linked sugars, glycophorin MA contains in addition at least one N-linked carbohydrate residue and terminal sialic acid residues. Pulse-chase in vivo labelling experiments combined with in vitro translations of glycophorin mRNAs show that the initial precursor to glycophorin MA is a 24.5 kD polypeptide which is subsequently processed and glycosylated to give the mature 31 kD molecule via a 21.5 kD polypeptide intermediate. Both glycophorins MA and MB are synthesized most actively in early to mid erythroblasts (e.g., Friend cells induced for 3 days with DMSO) but their synthesis is considerably reduced by the reticulocyte stage. However, of the other cell types tested (neuroblastoma, myeloma, fibroblasts, epithelial cells and T-lymphoma cells), none synthesizes glycophorin with the possible exception of a low level in thymus tissue. Thus murine glycophorins, in contrast to the RBC cytoskeletal proteins (spectrin, ankyrin, band 4.1) seem to be restricted to the erythroid cell lineage like human glycophorin.
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PMID:The cell specificity and biosynthesis of mouse glycophorins studied with monoclonal antibodies. 385 53

A 4 year-old child being treated for neuroblastoma developed erythroblastopenia. We used specific erythroid lineage markers (hemoglobin and spectrin) and in vitro erythroid colony assays to characterize this hematologic picture and discuss its relationships with the disease and its treatment.
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PMID:[Erythroblastopenia in a child during treatment of a neuroblastoma]. 391 40

Red blood cell differentiation involves the coordinate expression of a set of polypeptides some of which are erythroid-specific (the abundant globins as well as minor species such as glycophorin, carbonic anhydrase I and the RBC lipoxygenase) whereas others are found also in a subset of other cells, e.g. beta spectrin and a 19 kd polypeptide (ep 19) found in adult liver and kidney as well as erythroid cells. To investigate the genetic mechanisms involved in the regulation of these classes of genes, the expression of lipoxygenase, ep 19 and beta globin mRNAs was investigated in cell hybrids between mouse erythroid (Friend) cells and mouse T-lymphoma or neuroblastoma cells. All three mRNAs are expressed or repressed together in cell hybrids between the Friend cell and lymphoma or neuroblastoma cells respectively. Moreover, studies of the chromatin structure surrounding the genes reveal that erythroid cell-specific DNaseI hypersensitive sites within the ep 19 and beta major globin genes are lost in the Friend cell X neuroblastoma hybrids whereas they are retained in the Friend cell X lymphoma cell hybrids. This implies that the trans-acting mechanism responsible for regulating the RBC phenotype in these cell hybrids acts at the level of the early chromatin changes thought to reflect a pre-activation stage in gene expression.
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PMID:Analysis of chromatin changes associated with the expression of globin and non-globin genes in cell hybrids between erythroid and other cells. 392 31

A monoclonal antibody designated PI153/3, which reacts with neuroblastoma and fetal brain, is shown to identify also a cell surface determinant shared by pre-B and mature B cells and their corresponding leukemias including chronic lymphocytic leukemia, non-Hodgkin's lymphoma, B acute lymphoblastic leukemia, and hairy cell leukemia, but not plasmacytoma. Almost all non-T, non-B acute "lymphoid" leukemias bind PI153/3. The latter includes 71 of 74 common ALL tested, most but not all "unclassified" or "null" ALL and cases of both acute undifferentiated leukemia and Ph1 positive chronic myeloid leukemia in blast crisis with common ALL phenotypes. The antigen is absent or present at very low density on normal and leukemic T lymphocyte, myeloid and erythroid cells. The determinant appears to co-redistribute with cell surface immunoglobulin in B lymphocytes and segregates independently of other cell surface antigens associated with B cells and/or cALL including HLA-DR (Ia-like antigens) and the cALL (gp 100) antigen.
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PMID:A monoclonal antibody identifying a cell surface antigen shared by common acute lymphoblastic leukemias and B lineage cells. 696 98


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