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)

We have used radioiodination (125I) and two-dimensional polyacrylamide gel electrophoresis to determine that small- (oat) cell lung carcinoma (SCC)--a tumor with neuroendocrine features--possesses a surface protein pattern distinct from the other types of lung cancer cells (squamous, adeno-, and large-cell undifferentiated carcinoma). Twelve distinguishing proteins, 40 to 70 kilodaltons (kDal), characterized four separate lines of SCC; three of these, designated E (60 kDal; pI = 7.3), S (30 kDal; pI = 6.0), and U (57 kDal; pI = 5.6), may be unique SCC gene products and were identified only in [35S]methionine labeling of SCC and not in non-SCC or human fibroblasts. Two lines of adeno-, one of squamous, and one of undifferentiated large-cell lung carcinoma exhibited similar surface protein patterns to one another. Nine distinguishing proteins (40 to 100 kDal) and at least five large proteins (greater than 100 kDal) were unique to these lines. The surface protein phenotypes for SCC and non-SCC were distinct from those for human lymphoblastoid cells and fibroblasts. However, the neuroendocrine features of SCC were further substantiated because 6 of the 12 distinguishing SCC surface proteins, including E and U, were identified on human neuroblastoma cells. The proteins identified should (i) help define differentiation steps for normal and neoplastic bronchial epithelial cells, (ii) prove useful in better classifying lung cancers, and (iii) be instrumental in tracing formation of neuroendocrine cells.
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PMID:A unique cell-surface protein phenotype distinguishes human small-cell from non-small-cell lung cancer. 628 11

Serum levels of nervous system-specific enolase (alpha gamma form plus gamma gamma form) were determined in 18 patients with neuroblastoma and in 40 control infants by means of a sandwich enzyme immunoassay method specific to the gamma subunit (or 14-3-2 protein) of enolase isozymes. Levels in patients with neuroblastoma were elevated (mean, 70.3; range, 6.2 to 330.0 ng/mL) when compared with those of control subjects (4.3 +/- 1.7 ng/mL). Most of the patients (6/7), whose serum nervous system-specific enolase level increased more than 100 ng/mL, died within 1 month. Serial measurements in patients with neuroblastoma receiving various therapies have revealed that there was a good correlation between serum nervous system-specific enolase levels and the course of the disease. These results indicate that the nervous system-specific enolase in serum may be a valuable marker for therapeutic monitoring of patients with neuroblastoma, as reported recently in patients with small-cell carcinoma of the lung.
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PMID:Nervous system-specific enolase in serum as a marker for neuroblastoma. 635 7

Monoclonal antibodies were produced by immunizing rats with human small cell lung carcinoma (SCLC) cell lines. Monoclonal antibodies 600D11 and 624A12 were found to be directed against the ceramide pentasaccharide that contains the lacto-N-fucopentaose III (LNFP III) sequence of sugars, an isomer of the Lewis A blood group antigen. LNFP III is an immunodominant antigen whose reactivity is maintained in formalin-fixed paraffin-embedded sections (PS). LNFP III has been recognized in a number of human tumors including: SCLC; adenocarcinomas of the breast, gastrointestinal tract, genitourinary tract, and lung; renal cell carcinoma; neuroblastoma; and myelogenous leukemia. We now report the normal adult and fetal tissue distribution of the LNFP III antigen by immunoperoxidase staining on PS utilizing 600D11 and 624A12. Binding was demonstrated in bronchial epithelium and bronchial glands; squamous epithelium of the esophagus; gastric crypts, duodenal enterocytes and Brunners glands; argentaffin cells; jejunal and colonic goblet cells; pancreatic acinar cells; salivary glands; endocervical and exocervical cells; skin epidermis; myelinated motor fibers; cells of the adrenal medulla and anterior pituitary gland; polymorphonuclear leukocytes (PMNs); tissue macrophages and renal proximal tubules and loops of Henle. Staining was localized to cell membranes and within the cytoplasm, with greatest intensity at the apical and basal portions of the cells. These staining patterns were noted in adult and neonatal tissues, and initial expression could be traced to approximately the second trimester of fetal development. Knowledge of the normal tissue distribution of this immunodominant antigenic determinant may offer insight into its structural and functional role in benign and malignant tissues.
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PMID:Immunohistochemical localization of the immunodominant differentiation antigen lacto-N-fucopentaose III in normal adult and fetal tissues. 637 43

Three distinct transforming genes present in human tumor cell lines are all related to the viral oncogenes of Harvey and Kirsten murine sarcoma viruses, designated v-H-ras and v-K-ras, respectively. The transforming gene of a bladder carcinoma cell line has been shown to be a human homolog to v-H-ras [Parada, L. F., Tabin, C. J., Shih, C. & Weinberg, R. A. (1982) Nature (London) 297, 474-478; Santos, E., Tronick, S. R., Aaronson, S. A., Pulciani, S. & Barbacid, M. (1982) Nature (London) 298, 343-347]. The transforming gene common to one colon (SK-CO-1) and two lung carcinoma (SK-LU-1 and Calu-1) cell lines is the same human homolog of v-K-ras as is the transforming gene previously identified in a lung carcinoma cell line Lx-1 [Der, C. J., Krontiris, T. G. & Cooper, G. M. (1982) Proc. Natl. Acad. Sci. USA 79, 3637-3640]. The transforming gene of SK-N-SH neuroblastoma cells is weakly homologous to both v-H-ras and v-K-ras. NIH 3T3 cells transformed with the SK-N-SH transforming gene contain increased levels of a protein serologically and structurally related to the protein products of the v-H-ras and v-K-ras genes. Therefore, it represents a third member of the ras gene family, which we have called N-ras. Based on the homology with the v-ras genes, we have established the orientation of transcription and approximate coding regions of the cloned human K-ras and N-ras genes.
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PMID:Three human transforming genes are related to the viral ras oncogenes. 657 64

A family of human transforming genes, previously shown to share homology with the ras family of viral oncogenes, maps to three different human chromosomes. A well-characterized mouse-human hybrid cell panel, combined with Southern blotting, was used in this study. The transforming gene of the T24 bladder carcinoma cell line maps to human chromosome 11. An oncogene isolated from the lung carcinoma cell line SK-Calu-1 maps to human chromosome 12. The third ras-related gene, cloned from SK-N-SH, a neuroblastoma cell line, maps to human chromosome 1.
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PMID:Chromosomal assignment of a family of human oncogenes. 657 47

A potential application of the human tumor stem cell colony assay is to guide Phase II clinical investigations by identifying classes of tumors (or individual patients) which are sensitive in vitro to a new antitumor compound. We have tested human tumor stem cells from 140 tumor biopsies representing 20 different tumor types for chemosensitivity to the Phase II drug 4'-(9-acridinylamino)methanesulfon-m-anisidide. In vitro sensitivity was defined as a reduction in the number of tumor colony-forming cells to 30% of the control or less after a 1-hr exposure to one-tenth of the pharmacologically achievable plasma concentration of 4'-(9-acridinylamino)methanesulfon-m-anisidide. In vitro sensitivity was found in 29 cases: non-Hodgkin's lymphoma (2 of 2); cervical carcinoma (1 of 1); sarcoma (3 of 6); neuroblastoma (1 of 2); acute myelogenous leukemia (6 of 16); chronic myelogenous leukemia (1 of 3); melanoma (8 of 34); uterine carcinoma (1 of 5); lung carcinoma (1 of 9); ovarian carcinoma (4 of 36); and breast carcinoma (1 of 11). Prospective in vitro-in vivo correlations in eight patients with various tumor types showed that three of three patients sensitive in vitro to 4'-(9-acridinylamino)methanesulfon-m-anisidide responded in vivo, while five of five patients resistant in vitro had no clinical response. The results provide support for further evaluation of the utility of the human tumor stem cell colony assay for targeting Phase II clinical trials.
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PMID:In vitro chemosensitivities of human tumor stem cells to the Phase II drug 4'-(9-acridinylamino)methanesulfon-m-anisidide and prospective in vivo correlations. 689 12

We have previously demonstrated that DNA of mouse fibroblasts transformed by 3-methylcholanthrene (3-MC) induced foci of transformed cells when applied to monolayer cultures of NIH3T3 cells, which indicates that at least a part of this phenotype is encoded in DNA sequences. However, our conclusions were confined to the effects of DNAs of 3-MC-transformed mouse fibroblasts on recipient NIH3T3 cells, also of mouse fibroblast origin. To elucidate this phenomenon further, we have prepared DNAs from a series of mouse and non-mouse tumour lines of non-fibroblastic origin and investigated whether tumour transforming genes can act across tissue and species barriers to transform NIH3T3 cells. We find that DNAs obtained from human, rabbit and mouse bladder carcinoma lines, a lung carcinoma line and rat neuroblastoma and mouse glioma lines, are able to induce transformation of NIH3T3 cells on transfection.
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PMID:Transforming genes of carcinomas and neuroblastomas introduced into mouse fibroblasts. 720 18

Eighteen hundred and eighty-four cases of human solid tumours and 833 samples of normal human tissues, formalin-fixed and paraffin-embedded, were examined immunohistochemically for expression of c-kit oncogene product using polyclonal antibody against synthesized c-kit peptide. Seminoma/dysgerminoma and small cell lung carcinoma (SCLC) show preferential c-kit expression at 92% and 36% frequency, respectively, whereas only sporadic cases of cervical carcinoma and non-SCLC lung carcinoma show c-kit positivity. A normal tissue counterpart positive for c-kit product is detected in the testis (spermatocyte) and ovary (oocyte) but not in the lung or the cervix. In contrast, normal epithelial cells of the breast, skin basal cells and tissue mast cells harbour c-kit product, but transformed cells of the former two are largely deficient in the c-kit protein. One hundred and thirty-nine neuroendocrine tumours and 39 non-pulmonary small cell carcinomas were all negative, except for two cases of neuroblastoma. This indicates a distinct character for SCLC in c-kit expression. The c-kit product may be a useful marker in diagnostic pathology of seminoma/dysgerminoma and SCLC among human solid tumours, and in distinction of SCLC from non-pulmonary small cell carcinoma.
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PMID:Preferential localization of c-kit product in tissue mast cells, basal cells of skin, epithelial cells of breast, small cell lung carcinoma and seminoma/dysgerminoma in human: immunohistochemical study on formalin-fixed, paraffin-embedded tissues. 751 77

A review was made of the clinical data of 28 patients with metastatic orbital disease diagnosed in our clinic between 1972 and 1993. Fifteen were men and 13 were women. The average age at diagnosis was 58.7 years. The right orbit was involved in 12 and the left orbit in 14 cases. Two cases had bilateral orbital involvement. Breast carcinoma was the most frequent tumor (8 of 28, 28.6%) followed by neuroblastoma (7 of 28, 25.0%), lung carcinoma (6 of 28, 21.4%), prostate carcinoma (3 of 28, 10.7%), gastrointestinal carcinoma (2 of 28, 7.1%), renal cell carcinoma and thyroid carcinoma (1 of 28, 3.6% each). Proptosis (67.9%), motility disturbance (57.1%) and mass (50.0%) were the three most common presenting signs. Enophthalmos was noted in two cases with breast carcinoma. Nine cases presented with ophthalmic signs and metastatic tumor was recognized later. In the remaining 19 cases, the diagnosis of the primary tumor preceded the onset of orbital metastasis. The time interval between the detection of the primary malignancy and metastatic orbital tumor was shortest for lung carcinoma (mean: 2 months) and longest for breast carcinoma (mean: 34 months). Radiotherapy and chemotherapy were applied in 12 cases. Improvement in orbital signs and visual acuity was noted in 5 cases. Radiotherapy, chemotherapy and hormonal therapy were used in 8 patients and improvement in orbital signs was noted in 4 of these patients. Four of 28 patients (2 with breast carcinomas, one with prostate carcinoma and one with thyroid carcinoma) survived longer than 5 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metastatic orbital tumors. 764 86

The reactivity of a mAb (M16) raised against a small cell lung carcinoma line is described. M16 identifies a surface antigen expressed on cells of neuroectodermal origin following activation, as well as neoplastic transformation. M16 antigen expression is increased on retinoblastoma and neuroblastoma cell lines upon 'in vitro' stimulation and it is induced 'in vivo' on glial cells activated following brain injury. Furthermore, glial tumors show levels of M16 molecule expression increasing with the degree of malignancy, and in a retinoblastoma cell line, the expression of M16 was inversely related to the level of HLA-Class I and N-CAM antigens. The M16 antigen may represent a marker of both activation and neoplastic progression for neuroectodermal cells.
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PMID:Biochemical characterization and membrane expression of an antigen shared by activated and neoplastic cells of neuroectodermal origin. 770 33


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