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 purpose of this study was to determine whether the neurula stage mouse embryo can regulate tumor formation of C-1300-3 neuroblastoma cells. Five neuroblastoma cells were injected into the second somite of neurula stage embryos, and their ability to form tumors was tested, 24 hr later, by transplanting the portion of the embryo containing the cancer cells into the testes of adult mice. Only one-third the number of tumors was obtained in comparison with controls in which (i) five neuroblastoma cells were injected into blocks of liver tissue that were then transplanted into the testes of adult animals or (ii) five C-1300-3 neuroblastoma cells were injected directly into the testes. When five C-1300-3 cells were injected into somites, which had been dissected from embryos, and the injected somites were placed in animals, significantly fewer tumors were obtained in relationship with controls. Although it is not known whether the neuroblastoma cells are induced to differentiate or are killed by the embryonic tissue, the effect appeared to be specific because the tumor-forming ability of L1210 leukemia, B-16 melanoma, embryonal carcinoma 247, and a parietal yolk sac carcinoma was unaffected by somites.
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PMID:The neurula stage mouse embryo in control of neuroblastoma. 659 4

A total of 114 children with solid tumors refractory to conventional therapy were evaluated for response and/or toxic effects after receiving cisplatin at doses of 3.0-4.5 mg/kg with aggressive hydration and mannitol diuresis every 3 weeks; a minimum of two courses was required for evaluation of response (110 patients). Objective responses were noted in 18 patients: rhabdomyosarcoma (three), Wilm's tumor (three), osteogenic sarcoma (three). Ewing's sarcoma (two), neuroblastoma (one), undifferentiated sarcoma (one), hepatoblastoma (one), ovarian teratoma (one), hepatocellular carcinoma (one), embryonal carcinoma of the mediastinum (one), and thymoma (one). Twenty-six patients had some evidence of renal toxicity. Asymptomatic hearing loss was commonly found when audiometry was performed (eight of 18 patients tested). Eight additional patients had symptomatic hearing problems--tinnitus or hearing loss. Myelosuppression was mild. Hypomagnesemia and/or hypocalcemia were common but only one patient had symptoms. Cisplatin, administered at a dose of 3.0 mg/kg with aggressive hydration and mannitol diuresis, is reasonably well-tolerated. Its role in the therapy for those tumors against which it shows activity remains to be determined.
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PMID:Phase II trail cisplatin in refractory childhood cancer: Children's Cancer Study Group Report. 694 56

Murine extra-embryonic endodermal cells derived from either teratocarcinomas or cultured mouse blastocysts contain two protein species of Mr = 55,000 and Mr = 50,000 endodermal cytoskeletal proteins A and B, respectively) that are insoluble in nonionic detergent and 1 M NaCl and are not found in abundance in embryonal carcinoma cells, the stem cells of teratocarcinomas. Antiserum raised against the electrophoretically purified endo B protein immunoprecipitated endo B from [35S]methionine-labeled cell lysates of three parietal endodermal cell lines, a presumptive visceral endodermal cell line, and a mouse hepatoma line. Immunoprecipitable endo B was not found in murine embryonal carcinoma cells, fibroblasts, myoblasts, keratinocytes, erythroleukemic or neuroblastoma cells. These results are consistent with the view that endo B is not tubulin, vimentin, desmin, or keratin. Amino acid composition data, partial peptide analysis of immunoprecipitated endo B, and immunoprecipitation analysis with antikeratin serum support the suggestion that endo B is not a keratin. Indirect immunofluorescent staining of parietal endodermal cells with the endo B antiserum resulted in the fluorescence of a fibrillar cytoskeletal network. The synthesis of endo B was increased dramatically when embryonal carcinoma cells were induced to differentiate by treatment with retinoic acid. Endo B appears to be a cytoskeletal protein that is synthesized when malignant embryonal carcinoma cells differentiate to benign extra-embryonic endoderm.
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PMID:Identification and immunoprecipitation of cytoskeletal proteins from murine extra-embryonic endodermal cells. 726 44

Here we report that protein tyrosine phosphatases (PTPases), like their enzymatic counterpart the protein tyrosine kinases, can play an important role in cell differentiation. Expression of the transmembrane PTPase receptor protein tyrosine phosphatase alpha (RPTP alpha) is transiently enhanced during neuronal differentiation of embryonal carcinoma (EC) and neuroblastoma cells. Retinoic acid induces wild type P19 cells to differentiate into endoderm- and mesoderm-like cells. By contrast, retinoic acid treatment leads to neuronal differentiation of P19 cells, ectopically expressing functional RPTP alpha, as illustrated by their ability to generate action potentials. Endogenous pp60c-src kinase activity is enhanced in the RPTP alpha-transfected cells, which may be due to direct dephosphorylation of the regulatory Tyr residue at position 527 in pp60c-src by RPTP alpha. Our results demonstrate that RPTP alpha is involved in neuronal differentiation and imply a role for pp60c-src in the differentiation process.
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PMID:Receptor protein tyrosine phosphatase alpha activates pp60c-src and is involved in neuronal differentiation. 769 97

The 14 tumors reported in Rubinstein-Taybi syndrome since 1989, when added to the 22 previously reported, are beginning to show a pattern of neural and developmental tumors, especially of the head, which is malformed in the syndrome. Among the neoplasms were 12 of the nervous system: 2 each of oligodendroglioma, medulloblastoma, neuroblastoma, and benign meningioma, a pheochromocytoma, and 3 other benign tumors; 2 of nasopharyngeal rhabdomyosarcoma; and 1 each of leiomyosarcoma, seminoma, and embryonal carcinoma. Among the other benign tumors were an odontoma, a choristoma, a dermoid cyst, and 2 pilomatrixomas.
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PMID:Tumors in Rubinstein-Taybi syndrome. 955 2

Mouse Hoxb-4 (Hox-2.6) is a homeobox gene that belongs to a family which also includes Hoxa-4, Hoxc-4, and Hoxd-4 and that is related to the Deformed gene in Drosophila melanogaster. We have determined the sequence of 1.2 kb of 5' flanking DNA of mouse Hoxb-4 and by nuclease S1 and primer extension experiments identified two transcription start sites, P1 and P2, 285 and 207 nucleotides upstream of the ATG initiator codon, respectively. We have shown that this region harbors two independent promoters which drive CAT expression in several different cell lines with various efficiencies, suggesting that they are subject to cell-type-specific regulation. Through detailed mutational analysis, we have identified several cis-regulatory elements, located upstream and downstream of the transcription start sites. They include two cell-type-specific negative regulatory elements, which are more active in F9 embryonal carcinoma cells than in neuroblastoma cells (regions a and d at -226 to -186 and +169 to +205, respectively). An additional negative regulatory element has been delimited (region b between +22 and +113). Positive regulation is achieved by binding of HoxTF, a previously unknown factor, to the sequence GCCATTGG (+148 to +155) that is essential for efficient Hoxb-4 expression. We have also defined the minimal promoter sequences and found that they include two 12-bp initiator elements centered around each transcription start site. The complex architecture of the Hoxb-4 promoter provides the framework for fine-tuned transcriptional regulation during embryonic development.
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PMID:Multiple positive and negative regulatory elements in the promoter of the mouse homeobox gene Hoxb-4. 796 51

In the developing mammalian central nervous system, neural precursor cells show a tightly regulated inverse relationship between cell proliferation and differentiation. The molecular mechanisms which control the inter-relationship between these two events are poorly understood. To approach this problem, we previously identified several novel genes which are most prominently expressed in the early embryonic brain. Further cloning and sequencing of one such gene, Nedd1, revealed that it can encode a protein with a M(r) of 71,000, the amino-terminal half of which shares significant structural similarity with the beta-subunit of heterotrimeric GTP-binding proteins. Nedd1 mRNA is strongly expressed in early embryonic brain, but it can be detected at low levels in a number of adult tissues as well as cell lines and is up-regulated in an embryonal carcinoma cell line upon retinoic acid-induced differentiation. Ectopic expression of Nedd1 gene by means of eukaryotic vectors in various cell lines resulted in varying degrees of growth suppression. The strongest effects were evident in differentiation-competent neuroblastoma-derived cell lines. Our results suggest that the Nedd1 gene may play a role in the differentiation-coupled growth arrest in neuronal cells.
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PMID:Molecular cloning and biological activity of a novel developmentally regulated gene encoding a protein with beta-transducin-like structure. 815 64

Telomerase, the enzyme that maintains the ends of linear eukaryotic chromosomes, is active in human germ cells and in a majority of tumor tissues and immortalized cell lines. In contrast, most mature somatic cells and tissues contain low or undetectable telomerase activity, implying a stringent negative regulatory control mechanism. We report here that telomerase activity is dramatically inhibited during the terminal differentiation of HL-60 human promyelocytic leukemia cells to monocytic and granulocytic lineages. A loss of telomerase activity was seen in response to three different inducers of differentiation, was independent of differentiation-induced apoptosis, and occurred in the presence of unaltered expression of the RNA component of telomerase. Reduction in telomerase activity was also observed during the differentiation of murine F9 teratocarcinoma and C2C12 myoblast cells. In contrast, induced differentiation of murine p19 embryonal carcinoma and Neuro 2a neuroblastoma cells did not result in a loss of telomerase activity. These results are therefore consistent with the absence of telomerase activity in human somatic cells and the presence of telomerase activity in many somatic murine cells and tissues.
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PMID:Selective inhibition of telomerase activity during terminal differentiation of immortal cell lines. 870 26

A novel member of the winged helix (formerly HNF-3/Forkhead) transcriptional regulatory family, termed Genesis, was isolated and characterized. Putative translation of the complete cDNA revealed the winged helix DNA binding domain to be centrally located within the protein, with regions on either side that contain known transcriptional regulatory motifs. Extensive Northern analysis of Genesis found that the message was exclusively expressed in embryonic stem cells or their malignant equivalent, embryonal carcinoma cells. The Genesis transcript was down-regulated when these cells were stimulated to differentiate. DNA sequences that Genesis protein would interact with were characterized and were found to contain a consensus similar to that found in an embryonic stem cell enhancer sequence. Co-transfection experiments revealed that Genesis is a transcriptional repressor. Genesis mapped to mouse chromosome 4 in a region syntenic with human chromosome 1p31, a site of nonrandom abnormalities in germ cell neoplasia, neuroblastoma, and acute lymphoblastic leukemia. Genesis is a candidate for regulating the phenotype of normal or malignant embryonic stem cells.
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PMID:Genesis, a winged helix transcriptional repressor with expression restricted to embryonic stem cells. 879 5

The mediastinum is the host for a number of relatively unusual primary neoplasms, as well as a frequent recipient of metastatic tumors. From the perspective of fine-needle aspiration cytomorphology, several distinct patterns are yielded. The polygonal (or epithelial-like) cell pattern may be seen with benign and malignant thymomas, germinomas, embryonal carcinoma, and many metastatic carcinomas. An intimate admixture of small lymphocytes with these epithelial cells may occur in this category. The small cell pattern may be produced by malignant non-Hodgkin's lymphomas, neuroblastoma, carcinoid tumors, and metastatic oat cell carcinoma. Uncommon morphologic forms of thymoma and carcinoid tumors, as well as benign mesenchymal lesions, may yield a picture of a spindle-cell proliferation. In addition to cytomorphology, the cytologist needs to integrate clinical, radiographic, immunocytochemical, and ultrastructural data to formulate a final diagnosis.
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PMID:Differential diagnostic considerations and potential pitfalls in fine-needle aspiration biopsies of the mediastinum. 883 18


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