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)

Radiolabeled antiferritin IgG will target ferritin-bearing tumors such as hepatoma, lung cancer, and neuroblastoma. In hepatoma 4 of 5 patients have had clinical remission of malignancy following intravenous doses up to 150 mCi of radiolabeled antiferritin IgG. The dosimetry of radiolabeled 131I-antiferritin reveals a 3-day effective half-life, low dose rate isotopic implant of tumors 5 rad/h, 2,000-3,000 rad to the tumor, and a tumor half-life of 7.7 days. The possibilities of this new cancer agent are discussed in regard to isotopes, greater antibody specificity, and methods of evaluation.
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PMID:Antiferritin IgG antibody for isotopic cancer therapy. 625 69

Monoclonal antibodies with selectivity for human lung cancer were produced by immunizing BALB/c mice with an established line of human small cell lung cancer (NCI-H69) and fusing the mouse spleen cells to mouse myeloma line X63-Ag8.653. The resulting hybrid cells were initially screened by immunoautoradiography for production of antibodies that would react with NCI-H69 and another small cell lung cancer line (NCI-H128) but not its autologous B-lymphoblastoid line (NCI-H128BL). Stable monoclonal antibody-producing lines were isolated by repeated cloning. Three independently derived monoclonal antibodies, designated 525A5, 534F8, and 538F12, were found to react with three of the major types of human lung cancer (small cell, adenocarcinoma, and squamous carcinoma). They did not react with bronchioloalveolar and large cell lung cancers, myeloma, lymphomas, leukemias, osteogeneic sarcoma, mesothelioma, hypernephroma, malignant melanoma, simian virus 40-transformed human fetal lung cells, skin fibroblast lines, human B-lymphoblastoid lines, human erythrocytes, and rodent cells. Interestingly, these antibodies also bound to three out of three human neuroblastomas and two out of three breast cancers but failed to react with mouse neuroblastoma and rat pheochromocytoma. The monoclonal antibodies reacted with human small cell lung cancer tumors obtained at autopsy, but had insignificant reactions with normal human lung, liver, spleen, and skeletal muscle. We conclude that monoclonal antibodies have been generated that react with common antigenic determinants expressed on several human lung cancer types, neuroblastoma, and some breast cancers, but are not detectable by our current assays on a variety of other human tumors or normal adult human tissues. Such antibodies are of potential clinical and biological importance.
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PMID:Monoclonal antibodies that demonstrate specificity for several types of human lung cancer. 627 Jun 85

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

Two murine IgG2Ak monoclonal antibodies (703D4, 704A 1) were produced and characterized after immunization with a human large cell lung cancer line (NCI-H 157). These antibodies detect different epitopes on 31 kilodalton [35S]methionine incorporating protein(s). Radiobinding and immunohistochemical studies show these antibodies bind to most (11/13) human non-small cell lung cancer (adenocarcinoma, epidermoid, and large cell), but not to small cell lung cancer (0/11) tumors tested. The epitopes these antibodies recognized are also expressed on human melanomas (7/8), two other tumors (osteogenic sarcoma, renal cell carcinoma), but not on many other human tumors (breast, colon, neuroblastoma, lymphoid), and not on a panel of normal adult human tissues. Because the antigen(s) are preserved after fixation and because of their ability to distinguish lung cancer types from each other and normal tissues, they should be of clinical, as well as of biologic interest.
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PMID:Monoclonal antibodies that distinguish non-small cell from small cell lung cancer. 630 2

The antigen expression of human small cell lung cancer (SCLC) was studied using a panel of 21 independent rat monoclonal antibodies. The panel was selected by isolating hybridomas producing antibodies reactive with two SCLC lines but not with autologous B-lymphoblastoid lines. The antibodies were then tested in radiobinding assays against a panel of 17 SCLC lines, 13 non-small cell lung cancer lines, 6 SCLC necropsy specimens, 13 neuroectodermal lines (melanomas, neuroblastomas, glioblastomas), 15 other human lines, the glycolipid extracts of SCLC, human meconium, and human red blood cells. Using immunohistochemical assays, 14 of the antibodies were tested against normal lung, liver, and kidney, and lung cancer biopsies and xenografts. These analyses revealed the following: (a) SCLC elicited predominantly immunoglobulin M antibodies despite hyperimmunization; (b) the 21 antibodies displayed distinct binding and immunohistochemical phenotypes, indicating that they recognized many different epitopes; (c) 14 of the 21 antibodies reacted with glycolipid determinants; (d) the 21 determinants were expressed on over 80% of SCLC cell lines, necropsy samples, and xenografts; (e) the determinants were also expressed on normal adult bronchial epithelium, proximal tubules of adult kidney, and in a few instances on other normal cell types; (f) the antigens were expressed less frequently on nonsmall cell lung cancer samples but did not clearly distinguish SCLC from non-small cell lung cancer; (g) biochemical and morphological variants of SCLC exhibiting more malignant and undifferentiated behavior and containing greatly amplified c-myconcogenes failed to express several determinants or expressed them at lower levels; (h) and finally, while many human cell lines failed to express the antigens including human melanoma and glioblastoma lines, human neuroblastoma lines frequently did express the SCLC antigens. These detailed studies utilizing a panel of distinct monoclonal antibodies define a series of antigens on the surface of the majority of SCLC undescribed previously.
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PMID:Analysis of human small cell lung cancer differentiation antigens using a panel of rat monoclonal antibodies. 671 99

The 28-amino-acid neuropeptide, vasoactive intestinal peptide (VIP), is a potent mitogen during embryonic development and plays a vital role in brain growth. VIP is also mitogenic for tumor cells, including the human neuroblastoma (NMB). Northern blot analysis has revealed VIP mRNA transcripts in NMB. We now report VIP-like immunoreactivity within these neuroblastoma cells that increased during logarithmic growth and decreased after attaining confluency. About 10(6) seeded cells secreted 5-40 pg of VIP-like immunoreactivity into the medium. These results suggest an autocrine role for VIP in the regulation of neuroblastoma growth. A VIP hybrid antagonist (neurotensin6-11 VIP7-28) that has been shown to inhibit lung cancer proliferation was now tested for inhibition of neuroblastoma growth. Receptor binding studies indicated that the hybrid antagonist displaced [125I]-VIP binding in the neuroblastoma cells (EC50 = 5 x 10(-6)M). Furthermore, as measured by thymidine incorporation and by cell counts, the potent VIP hybrid antagonist inhibited neuroblastoma multiplication in a dose-dependent manner. In conclusion, VIP may be an important regulator of growth of nerve cell progenitors and of tumors derived from neuronal origin and intervening with VIP function may lead to improved treatment of cancer.
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PMID:Inhibition of human neuroblastoma growth by a specific VIP antagonist. 757 66

Expression of the RCK gene, which is a target gene on 11q23 of the t(11;14) (q23;q32) translocation in the B-cell lymphoma cell line RC-K8, was studied by Northern and Western blot analyses. The RCK gene product is a member of the D-E-A-D box protein/RNA helicase family. With the use of Northern blot analysis, a 7.5-kb transcript of the RCK gene was shown to be expressed ubiquitously in human and mouse tissues. Polyclonal antibodies against the RCK gene product were raised, and the RCK gene expression pattern was examined in human and mouse tissues. Two different polyclonal anti-rck antibodies detected a specific 54-kilodalton product named rck/p54 in the majority of human and mouse tissues tested by Western blot analysis. However, rck/p54 was shown to be very low in the human brain and was not detectable in lumbar muscle and lung tissues, although RCK mRNA is abundantly present in these tissues. It is of interest that malignant transformed human cells arising from tissues with low or no expression of rck/p54, such as neuroblastoma, glioblastoma, rhabdomyosarcoma, and lung cancer cell lines, produced a moderate amount of rck/p54 protein, suggesting that rck/p54 plays a role in tumorigenesis. In addition, the rck/p54 protein was localized to cytoplasm by immunostaining with the use of laser microscopy and by subcellular fractionation.
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PMID:The rck/p54 candidate proto-oncogene product is a 54-kilodalton D-E-A-D box protein differentially expressed in human and mouse tissues. 761 84

Of the 2877 patients who underwent chest surgery at our department during the 20-year period between 1973 and 1992, 9 (0.3%) developed postoperative chylothorax. The underlying disease included primary lung cancer in 5 patients, pulmonary metastasis in 1, invasive thymoma in 2, and neuroblastoma of the posterior mediastinum in 1. For the treatment of chylothorax, the thoracic duct was ligated in 2 patients with a high volume of chylous leakage. In 6 patients treated conservatively, early pleurodesis was attained by injecting 1 to 5 doses (mean: 2.2 doses) of the streptoccal preparation OK-432 intrathoracically; favorable results were achieved. In 1 patient, the diagnosis of chylothorax was delayed because of postoperative pyothorax. This patient developed nutritional deficiency, compromised immunity, and disseminated intravascular coagulation (DIC), which led to death before the chylothorax could be treated. In principle, postoperative chylothorax should be treated conservatively. Favorable results can be expected with the intrathoracic injection of OK-432 beginning at the early postoperative period to achieve pleurodesis, combined with the prevention of nutritional deficiency, electrolyte imbalance, and infection.
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PMID:Treatment of postoperative chylothorax by pleurodesis with the streptococcal preparation OK-432. 782 62

One of the first oncogenes identified from human tumors was c-myc, which is frequently activated in Burkitt's lymphomas due to chromosomal translocations. Subsequently, members of the myc oncogene family were found to be amplified in neuroblastoma and small-cell lung cancer. In normal cells, Myc activity has been shown to be both necessary and sufficient for resting cells to enter the cell cycle. Interestingly, it appears that Myc not only drives the cell cycle, but also induces cell death by apoptosis in certain situations. Myc contains a transcriptional activation domain and a basic helix-loop-helix-leucine zipper DNA-binding and dimerization domain. As a heterodimer with a structurally related protein, Max, Myc can bind DNA in a sequence-specific manner. These results suggest that the Myc/Max heterodimer functions as a transcriptional activator of genes that are critical for the regulation of cell growth.
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PMID:Myc protein: partners and antagonists. 794 8

In the last decade, anti-neurons autoantibodies have been found in serum and cerebro spinal fluid of patients suffering from neurological paraneoplastic syndrome. This discovery has made possible to improve the knowledge of these syndromes as well as to characterize some proteins specific to the nervous system, unknown until now. Paraneoplastic encephalomyelitis can manifest together with an ataxic sensitive neuropathy, a limbic encephalitis, a brainstem or cerebellum syndrome. This encephalomyelitis is almost always associated with a small cells lung cancer and auto-antibodies, called anti-Hu, which recognize all the neurons of the nervous system. Patients with paraneoplastic cerebellar degeneration present an antibody, called anti-Yo, directed against Purkinje cells. In this case, the tumor is a gynecologic cancer. Patients presenting with an opso-myoclonus and a breast cancer have an antineurons anti-body, called anti-Ri, which is absent when the opso-myoclonus is associated with a lung cancer or a neuroblastoma. These three antibodies are the most frequently found and the best studied, but others, rarer, have been described. The genes coding for the proteins recognized by these three antibodies have been cloned. These proteins seem to play a major role in the neuronal maturation and homeostasis. These antibodies prove to be irreplaceable tools to study the phenomenons subtending the neuronal degeneration and the cellular proliferation.
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PMID:[Value of the detection of anti-nervous system autoantibodies in neurologic paraneoplastic syndromes]. 805 19


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