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)

Sera from 30 patients with astrocytoma were tested for antibody reacting with cell surface antigens of cultured autologous astrocytoma cells. Ten percent of the patients had antibody detectable by mixed hemadsorption assays, approximately 50% by immune adherence and protein A assays, and 100% by anti-C3-mixed hemadsorption assays. Absorption analysis of reactive sera with autologous, allogeneic, and xenogeneic cells permitted the definition of three classes of astrocytoma cell surface antigens. Class I antigens showed an absolute restriction to autologous astrocytoma cells. Class II antigens were shared by all astrocytomas tested and could be detected also on neuroblastoma, sarcoma, and some (but not all) melanoma cell lines; these antigens were not found on cell lines derived from carcinomas or normal tissues. Class III antigens were widely distributed on cultured normal and malignant cells of human and animal origin. In this series, sera from 2 patients recognized class I antigens, 4 patients' serum recognized class II antigens, and 13 patients' sera recognized class III antigens. Absorption tests have shown that the AJ (class II) antigen of astrocytoma is serologically related to the previously described AH (class II) antigen of melanoma; in tests of nine melanoma cell lines, there was a correspondence between the AJ and AH phenotypes. This method of autologous typing provides a way to classify the cell surface antigens of astrocytomas and to assess the clinical significance of humoral immunity to these antigens.
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PMID:Serological analysis of cell surface antigens of malignant human brain tumors. 28 20

It is well known that there are many independent and inter-related clinical and pathologic factors which influence the prognosis of patients with benign and malignant conditions. Lymphocyte level is an index of cell-mediated immunity which is important in host defense against cancer. But it is surprising that a simple test such as peripheral lymphocyte count could be correlated with clinical stages and survival results in patients with Hodgkin's disease, non-Hodgkin's lymphoma and non-lymphomatous solid tumors. Regarding the latter, lymphocyte count had prognostic values in patients with cancer of the bone, Ewing's sarcoma; breast; colon; kidney, neuroblastoma; uterine cervix, and other sites. In general, higher lymphocyte counts before therapy correlated with longer survival. Using newer immunologic techniques, T and B lymphocytes can be identified and the different subtypes of leukemia, immunodeficiency and lymphoproliferative diseases have been studied intensively. Chronic lymphocytic leukemia represents a proliferation of B cells, while the Sezary syndrome represents that of T lymphocytes. There is a qualitative and quantitative disturbance of Blymphocytes in patients with multiple myeloma. In Hodgkin's disease, there is hyperactivity of the B cells and functional defect of the T cells. Finally, the nodular non-Hodgkin's lymphoma resulted from neoplastic transformation of the B lymphocytes. In several nonmalignant autoimmune conditions, abnormality of T-cell or B-cell counts has been reported. For example, T cells were reported to be decreased in patients with ulcerative or granulomatous colitis and in patients with rheumatoid arthritis, However, it needs to be pointed out that, in 1973, Farid and associates (44) reported a significant increase in T and a proportionate reduction of B rosette in 17 patients with untreated Grave's disease and 16 with Hashimoto's thyroiditis as compared with 24 normal and eight goiter controls. In 1975, six publications later, they (143) had to announce a retraction because further studies by them and by other investigators could not repeat the earlier results. Despite variations and lack of standardization of the test systems, some consistent deviations of T-lymphocyte and B-lymphocyte counts have been reported. T lymphocytes were quantitatively decreased in patients with carcinoma of the brain, breast, head and neck, liver, lung and urologic organs and with malignant melanoma. In general, there is a marked decrease of T cells with increasing stage of disease and a return of T cells to normal level after successful therapy. Cellular immunity is depressed, often lasting for years after localized radiation therapy, whether or not the thymus is included in the treatment field...
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PMID:Peripheral lymphocyte count and suppopulations of T and B lymphocytes in benign and malignant diseases. 30 Jan 79

Leukocyte adherence inhibition (LAI) is an easily carried out in vitro test for tumor reactivity which is based on the prevention of adherence of leukocytes incubated with antigen to which the donor is immune. In this study a comparison is made with dermal response to tumor antigen. A total of 234 patients were tested, 74 of whom had melanoma, 111 of whom had squamous cell carcinoma of the head and neck, 18 of whom had neuroblastoma and 31 of whom had other tumors. Forty-two persons without tumors acted as controls for the LAI test. A high degree of correlation was found between LAI and dermal response. Furthermore, LAI exhibited marked tumor specificity and showed a ten-fold greater sensitivity than dermal response. LAI may be used to monitor serial changes in tumor reactivity in cancer patients.
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PMID:Changes in tumor immunity during therapy determined by leukocyte adherence inhibition and dermal testing. 34 88

Two human melanoma lines, RPMI-7931 and HS-294, respond to mitogenic stimulation by PHA. A dose-response curve for these lines can be demonstrated with maximal stimulation at 16 and 32 micrograms per ml and inhibition at 75 to 250 micrograms per ml PHA. The mitogenic effects of PHA were inhibited by N-acetyl-D-galactosamine. Neuroblastoma cells also exhibits a similar but less important dose-response to PHA. These data indicate that human melanomas and neuroblastomas may have PHA receptors or mechanisms for mitogenic stimulation which are analogous to those observed with normal lymphocytes.
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PMID:Phytohemagglutinin effects on cultured human neural crest tumors. 51 Dec 4

5-Bromodeoxyuridine (BrdUrd) injected into the muscular tissue of fish bearing melanoma or neuroblastoma induces the production of virus-like particles in these tumors. The particles in the melanoma are morphologically similar to papovaviruses of polyoma-type, those in the neuroblastoma resemble oncornaviruses of B- and C-type.
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PMID:Virus-like particles induced by bromodeoxyuridine in melanoma and neuroblastoma of Xiphophorus. 52 65

L-Dopa has has been shown to demonstrate enhanced toxicity toward melanoma cells in vitro. Since melanocytes arise from the neural crest embryologically, the effect of L-dopa methyl ester, a soluble analog, on the murine C1300 neuroblastoma was studied. There was significant antitumor activity against the neuroblastoma, which was enhanced by combination with a dopa decarboxylase inhibitor, Ro4-4602. In vitro studies suggested inhibition of DNA synthesis as the principal site of action. A mechanism involving sulfhydryl compound scavenging is postulated.
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PMID:L-Dopa methyl ester: prolongation of survival of neuroblastoma-bearing mice after treatment. 62 65

If the study of tumor immunology is to have a profound impact on clinical medicine, certain hypotheses must be proven to be valid. First and foremost, it must be demonstrated that malignant tissue possesses antigenic substances (probably protein moieties) that are unique to that particular malignant process. In addition, these antigenic substances must be very similar in histologically similar tumors. Second, the host defense mechanisms must be capable of reacting to these tumor-associated antigens. The reaction is, of course, necessary in order to develop both diagnostic and therapeutic routes of application. The reaction of the immunologic system to these tumor-associated antigens could be monitored as an early serodiagnostic tool for subclinical cancer, and the cytotoxic reaction holds great promise as an immunotherapeutic tool. The essence of tumor immunologic research can thus be stated in the form of the following questions: 1. Do histologically similar cancers from identical primary sites share common tumor-associated antigens? 2. Does the immunologic system react to these antigens? 3. Can this reaction be assayed on one hand for serodiagnosis and augmented on the other for immunotherapy? Specific antigens have been found in animal tumors and have been divided into two classes: the viral induced tumors, which share common antigens when caused by the same viral agent, and carcinogen-induced tumors, which appear to have unique antigenic determinants for each tumor. In recent years a great many human tumors have been found to have tumor-associated antigens; these include colonic carcinoma, neuroblastoma, melanoma, soft tissue and osteogenic sarcoma, bladder carcinoma and Burkitt's lymphoma. This report includes evidence for the existence of such antigens in adenocarcinoma of the ovary and squamous cell carcinoma of the cervix. The laboratory evidence that has been presented would suggest that there are both a cell-mediated response and humoral response to the antigenic determinants of these two gynecologic cancers. It would appear that the mediated (lymphocyte) effect is considerably more cytotoxic and definitive than the humoral factors measured. In addition, the allogenic experiments would suggest strongly that indeed (at least with regard to these two cancers) histologically similar cancers from the same organ share common antigenic determinants. The identification and isolation of these tumor-associated antigens appears complex. The complexity is increased when one studies patients afflicted with these cancers for plasma carcinoembryonic antigens. This antigen, which was thought to be specific for adenocarcinoma of the colon, is found in the blood of a significant number of patients with adenocarcinoma of the ovary and squamous cell carcinoma of the cervix.
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PMID:Tumor-associated antigens in gynecologic cancer. 76 38

A few years ago Everson and I assembled all the examples of spontaneous regression in the world medical literature from 1900 to 1960 and added numerous cases from expriences of our friends. Our figure was 176. We excluded squamous cell carcinoma of the skin, leukemia, Hodgkin's disease, and a large number of cases that did not fulfill the prerequisites of confirmed diagnosis and no significant treatment. The four most common examples of regression were carcinoma of the kidney (31), neuroblastoma (29), malignant melanoma (19), and choriocarcinoma (19); these constituted more than half the group. We did not require that the regression be permanent because it appeared that the explanation of temporary regression would be just as important as the cause of permanent regression. There was no proven specific cause of the regression, but the following mechanisms had a possible relationship: immunologic action, elimination of carcinogens, trauma (altering the antigen-antibody relationship), hormones, irradiation, infection and/or fever, and drugs or chemicals. The most applicable of these is elimination of the carcinogen. Immunologic reactions seem to offer the best explanation, and the potential of humoral immunity is more impressive than that of cellular immunity.
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PMID:Spontaneous regression of cancer and the importance of finding its cause. 79 60

The resistance that many cancer patients show to the progress of their disease, attested to by well documented cases of spontaneous regressions as in neuroblastoma, hypernephroma, choriocarcinoma and malignant melanoma, and the long-term dormancy of multiple metastases seen particularly after removal of a primary mass, can be explained only by host defense mechanisms. Attemps at immunotherapy over the years are reviewed and new directions are presented.
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PMID:Immunologic approach to cancer therapy. 111 68

Ultrastructural features of neoplastic cells can provide clues for correct diagnosis when light microscopy fails. Secretory granules are characteristic in the following tumors: mucin granules in poorly differentiated adenocarcinomas, zymogen granules in acinic cell carcinomas, lysosomal granules in prostatic carcinomas, melanin granules in malignant melanoma, carcinoid, islet cell tumors, pheochromocytoma, and neuroblastoma granules in the corresponding neoplasms. Among cytoplasmic organelles, rough surfaced endoplasmic reticulum characterizes adrenocortical, ovarian, and hepatocellular carcinomas and plasmacytomas. Tonofibrils are characteristic of squamous cell carcinomas. Glycogen deposits distinguish Ewing's sarcoma from lymphoreticular neoplasms. Intercellular relationships and membrane specialization are important features in the differential diagnosis of various undifferentiated tumors. The frequent resolution of difficult diagnostic problems by electron microscopy outweighs the disadvantages of this technique, such as the expense and time required.
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PMID:The usefulness of electron microscopy in the diagnosis of human tumors. 115 Feb 21


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