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)

Human cDNA clones for NSCL-1 and NSCL-2, two basic domain helix-loop-helix (bHLH) genes expressed predominantly in the developing nervous system, were obtained from a fetal brain cDNA library. The full-length transcripts and the genomic structures were determined. The cDNAs for the two genes encode predicted proteins of similar size (133 and 135 amino acids for NSCL-1 and NSCL-2, respectively) and structure. The carboxyl-terminal 75 amino acids of the two proteins contain the bHLH motif and differ from each other by only three conservative amino acid changes, while the amino-terminal portions are markedly divergent from each other. In addition to the similar protein structure, the genes have a similar genomic organization, suggesting a close evolutionary relationship. The 5'-regulatory regions of the two genes share some features (i.e. potential TATA, CCAAT, and GATA binding sites) but also differ significantly in their G+C content. NSCL-1 is relatively G+C-rich (63%) in the sequences upstream of transcription initiation and has multiple potential binding sites for transcription factors that bind to G+C-rich sequences (e.g. AP-2). NSCL-2 is relatively A+T-rich (63%) in this region and has a potential binding site for AP1. Studies of expression in normal tissues demonstrated expression of NSCL-1 and NSCL-2 in the developing central and peripheral nervous system, most likely in developing neurons. Additional Northern analysis studies in cell lines revealed expression of these genes in some cell lines derived from tumors with neural or neuroendocrine features such as neuroblastoma, PNET, and small cell lung cancer. NSCL-1 is expressed in a larger number of these cell lines. The differences in expression may parallel differences in developmental regulation.
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PMID:A comparative structural characterization of the human NSCL-1 and NSCL-2 genes. Two basic helix-loop-helix genes expressed in the developing nervous system. 132 19

Teniposide and etoposide are third-generation semi-synthetic derivatives of epipodophyllotoxin. Following the initial clinical introduction of teniposide in the 1970s, investigations focused almost exclusively on its analogue, etoposide, because of its formulation, which was felt to have advantages in addition to oral administration. Despite consistently inadequate dosing and scheduling, early phase I and II trial results with teniposide were promising, and current trends encourage a second look. The substantial antitumor activity of teniposide is comparable with that of etoposide, and clinical interest was rekindled when it was shown to have considerable activity against small cell lung cancer (SCLC). In view of the inadequacy of early trials and the premature cessation of clinical study, it is recommended that teniposide be reevaluated for its activity against malignant lymphomas, Hodgkin's disease, leukemias, and SCLC, against all of which its early results were encouraging. In addition, consideration should be given to its activity against brain tumors, neuroblastomas and other childhood solid tumors, and ovarian cancer; its potential value against gastric, hepatocellular, breast, and bladder cancers also should be investigated. Other areas that warrant further study include elucidation of the exact mechanism of action of teniposide, its role in both single- and multiple-agent chemotherapeutic regimens, and resolution of its optimal dose and schedule. Finally, it is suggested that with new routes of administration and improved formulations, teniposide may be expected to play a significant role in the treatment of malignant lymphomas, SCLC, and pediatric lymphocytic leukemia and neuroblastoma.
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PMID:Teniposide in adult solid tumors: a historical perspective. 141 38

The N-myc oncogene has been implicated in the pathogenesis of a number of human tumors, including childhood neuroblastoma and adult small cell lung cancer. We have isolated and characterized complementary DNA clones derived from a transcription unit, N-cym, located on the opposite DNA strand to N-myc, with extensive overlap existing between the 5' ends of the two transcription units. The N-cym gene, which can encode a 109-amino acid protein, is expressed during fetal development, as well as in tumor cell lines containing amplified N-myc loci, where it is expressed at very high levels. Although other examples of overlapping, opposite-strand eukaryotic genes exist, N-myc and N-cym are unique in that they appear to be coregulated in tumor cell lines under basal growth conditions and in response to the differentiating agent retinoic acid. This coregulation suggests that their protein products may be functionally interrelated during normal development and oncogenesis.
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PMID:Isolation and characterization of complementary DNA for N-cym, a gene encoded by the DNA strand opposite to N-myc. 141 2

Monoclonal antibodies have been used to detect tumor cells in bone marrow of patients with neuroblastoma, breast cancer, small cell lung cancer, prostatic cancer and gastrointestinal carcinoma. By comparative analysis immunocytology proved to be more sensitive than conventional cytology and histology and had the additional advantage of specificity. A positive correlation exists between the presence of tumor cells in bone marrow and the extent of the primary tumor. The proliferative potential of the micrometastatic cells was assessed by characterization of EGF and transferrin receptors, tumorigenicity was shown by xenotransplantation experiments in nu/nu mice in a few instances. First follow-up studies indicate that the presence of disseminated tumor cells in bone marrow can be taken as predicting the subsequent development of overt metastasis.
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PMID:Detection, characterization and tumorigenicity of disseminated tumor cells in human bone marrow. 210 96

The immunomagnetic depletion method for removing tumor cells from bone marrow, previously refined using a Burkitt lymphoma model, was tested with neuroblastoma cells. The efficiency of depletion was quantified by immunofluorescence with a detection limit of 3.3 log of cell depletion corresponding to the elimination of 99.84% of an initial tumor cell content of 10%. A panel of five monoclonal antibodies (UJ13A; UJ127.11; UJ181.4; alpha-Thy1; H11) purged 2.8 log of SKNBE and LAN-1 cells, while two of these antibodies as single agents allowed only for a 1.7 log (UJ13A) and a 1.7 to 2.0 log (alpha-Thy1) depletion. This underlines the advantage of an antibody panel for neuroblastoma purging. The new antibody S-L 11.14, an IgG2a against small cell lung cancer which recognizes 90% of neuroblastoma cells purged 2.8 log.
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PMID:[Evaluation of a modified immunomagnetic procedure for the purging of neuroblastoma cells from bone marrow]. 219 50

Five hundred and fifty two bone marrow (BM) specimens (497 aspirates, 55 biopsies) from 518 patients with nonhaematological malignancies were examined to determine the frequency of metastatic deposits. BM involvement was highest in neuroblastoma (9/14), prostate cancer (2/4), retinoblastoma (3/7), Ewing's sarcoma (14/47), rhabdomyosarcoma (5/20) and small cell carcinoma of lung (3/18). BM aspiration smears were adequate in paediatric tumours (neuroblastoma, retinoblastoma, rhabdomyosarcoma) while BM biopsies were most useful in patients with Ewing's sarcoma, prostate cancer and small cell lung cancer. We conclude that BM is an easy investigation in the diagnosis and staging of nonhaematological cancers.
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PMID:Frequency of bone marrow involvement in non-haematological malignancies. 224 93

Three monoclonal antibodies (mAbs), NCC-LU-243, -244 and -246, detected three different epitopes on a 145-kDa cell membrane antigen, which had been designated as the cluster 1 antigen at the First International Workshop on Small Cell Lung Cancer (SCLC) Antigens. The distribution of the antigen in various tissues, cultured cells and sera was examined by immunohistochemistry and sandwich radioimmunoassay using these mAbs. The antigen is a normal differentiation antigen and is present in neuronal, neuroendocrine and cardiac muscle cells. The level of the antigen was highest in central nervous tissues, while it was undetectable in the liver, kidney and peripheral lung. Among tumor tissues, the antigen was detected only in SCLC, carcinoid tumor and neuroblastoma, indicating its usefulness as a marker for discriminating SCLC from non-SCLC. The level of the antigen varied among SCLC tissues and tended to be lower in variant-type cultured SCLC cells. Although an increase in the antigen level was observed in sera of some patients with advanced SCLC, the antigen did not possess any additional value over neuron-specific enolase as a serum tumor marker for monitoring SCLC patients.
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PMID:Quantitative distribution of cluster 1 small cell lung cancer antigen in cancerous and non-cancerous tissues, cultured cells and sera. 247 55

The soluble brain protein 14-3-2 first described by Moore and McGregor in 1965 is now known to be a cell specific isoenzyme of the glycolytic enzyme enolase (EC 4.2.1.11), designated neuron specific enolase (NSE). It is not only a marker for all types of neurons, but also for all neuroendocrine or paraneuronal cells. The appearance of NSE is a late event in neural differentiation, thus making NSE a useful index of neural maturation. The demonstration that tumors of the nervous system and of neuroendocrine origin contain NSE has promoted the study of NSE as a possible tumor marker. Immunocytochemistry has been used to identify NSE in cytologic preparations from several types of tumors, offering useful indications for differential diagnosis. NSE levels in serum from tumor patients are not useful in the diagnosis of early stage disease. However, serum NSE levels have been shown to be helpful in the identification of advanced small cell lung cancer, neuroblastoma and several other neoplasms. The main use of serum NSE is the monitoring of chemotherapy and the detection of a relapse in these cases.
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PMID:Clinical biochemistry of neuron specific enolase. 254 72

With the aid of a highly specific murine monoclonal antibody, F12, an immunofluorescence method was elaborated that allowed sensitive and specific detection of the ganglioside antigen fucosyl-GM1 (IV2FucII3NeuAcGgOse4Cer) in different types of human lung cancer and normal tissues. Nineteen of 21 cases of small cell lung cancer were positive with the F12 immunofluorescence method as compared to 2 of 10 squamous epithelial cell lung cancers and 1 of 5 large cell lung cancer specimens. Specimens of lung adenocarcinoma (8 cases) and bronchial carcinoid (3 cases) were all negative, as were 2 examined cases of neuroblastoma. No fucosyl-GM1 could be detected in normal lung and bronchus. However, in thymus, spleen, and lamina propria of the small intestine sparsely distributed clusters of small round cells were stained as well as intramural ganglionic cells of the small intestine and islet cells of the pancreas. All other normal tissues tested were negative. Results obtained with immunofluorescence closely agreed with immunochemical determination of fucosyl-GM1 in lipid extracts of tissues. Our findings suggest that fucosyl-GM1 is strongly associated with small cell cancer of the lung and demonstrate that this tumor-associated antigen can be detected with high sensitivity and specificity with an immunofluorescence method based on the use of the F12 monoclonal antibody.
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PMID:Immunohistological detection of fucosyl-GM1 ganglioside in human lung cancer and normal tissues with monoclonal antibodies. 264 49

A new monoclonal antibody (S-L 11.14) raised against small cell lung cancer reacted with all but one neuroblastoma tumor cell sample tested and was relatively specific for such cells within the bone marrow. The ability of S-L 11.14 to eliminate neuroblastoma cells from the bone marrow with an immunomagnetic purging method was evaluated in an experimental model using the LAN.1 and SKNBE neuroblastoma cell lines as targets. Residual malignant cells after the purging procedure were quantified by the Hoechst staining method. The use of S-L 11.14 as a single reagent resulted in a 3-log elimination of malignant cells, a depletion equal to that obtained with a cocktail of five monoclonal antibodies currently used in clinical trials. The addition of the S-L 11.14 antibody to this cocktail did not enhance depletion.
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PMID:S-L 11.14: a monoclonal antibody recognizing neuroectodermal tumors with possible value for bone marrow purging before autograft. 284 44


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