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 previously reported on stimulation of clonal growth of cell lines from human solid tumors by recombinant human interleukin 3, recombinant human granulocyte-macrophage colony-stimulating factor, and recombinant human granulocyte colony-stimulating factor (W. E. Berdel et al., Blood, 73: 80-83, 1989; Exp. Hematol., 16: 510, 1988). Within an extensive screening program of hematopoietic growth factor activity on malignant cells, the effects of recombinant human interleukin 6 (rhIL-6) were tested on the growth (tritiated thymidine uptake and human tumor cloning assay) of 26 different human cell lines derived from a wide range of solid tumors (head and neck, 4; lung, 1; pancreatic, 1; gastric, 1; colorectal, 3; renal, 3; bladder, 1; prostate, 1; breast, 2; ovary, 2; choriocarcinoma, 1; sarcoma, 2; glioblastoma, 2; neuroblastoma, 2). rhIL-6 (dose range up to 10(4) IU/ml) caused no reproducible enhancement or inhibition of tritiated thymidine uptake by tumor cell lines from nonhematopoietic origin. Furthermore, 19 of the tumor cell lines were clonogenic in a capillary modification of the human tumor cloning assay. No reproducible stimulation of clonal growth by rhIL-6 was observed in any of the cells tested. Particularly, there was no sensitivity of those cell lines for rhIL-6, which were previously shown to be sensitive for recombinant human interleukin 3 and recombinant human granulocyte-macrophage colony-stimulating factor in this assay. On the other hand, there were no significant growth-inhibitory effects of rhIL-6 on the cell lines tested in this study. Further experiments showed no influence of neutralizing monoclonal anti-hIL-6 antibody on the growth of 3 kidney carcinoma cell lines, making autocrine growth-modulating loops for IL-6 in these lines unlikely. In conclusion, no major interactions between hIL-6 and the growth of the human malignant cell lines from nonhematopoietic origin tested were detected in this study.
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PMID:Studies on the interaction between interleukin 6 and human malignant nonhematopoietic cell lines. 185 4

The sarcomas, particularly those of soft-tissue origin, pose substantial diagnostic challenges for the clinician and pathologist. Several small round cell sarcomas, including Ewing's sarcoma, peripheral primitive neuroectodermal tumor, and alveolar rhabdomyosarcoma, can be difficult to distinguish from one another. These same sarcomas can be difficult to distinguish from other small round cell tumors, including non-Hodgkin's lymphoma and neuroblastoma. Spindle cell sarcomas, including malignant peripheral nerve sheath tumor, synovial sarcoma, and leiomyosarcoma, present similar diagnostic challenges. This review discusses 1) recent advances in immunohistochemistry, electron microscopy, and cytogenetics that enable a specific diagnosis in virtually all sarcoma cases; 2) cell biology and oncogenetic implications of novel morphologic and genetic findings in sarcomas; and 3) clinical implications of the recent characterization of several family cancer syndrome genes.
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PMID:Laboratory investigation, genetics, and experimental models in sarcomas. 193 25

The group of rounded small-cell tumors include different neoplasias involving different therapies; we can name neuroblastoma, Ewing' sarcoma, embrionary rhabdomyosarcoma, lymphoma and other pathology such as Askin's tumor or small cell tumor of the thorax area. Based on microscopic and immunohistochemistry findings, it is suggested that it originates from the neural crest or pluri-potential cells from the neuroectodermy. This has a very aggressive behaviour and is usually resistant to oncologic therapies.
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PMID:[Undifferentiated small cell tumor of the thoracopulmonary region]. 195 81

Two pleomorphic (anaplastic) neuroblastomas, from two children aged 1 and 6 years, were transplanted into nude mice. Two noteworthy observations were made. In one case, the transplanted tumor gave rise to a soft-tissue sarcoma. Moreover, in both cases hepatic metastases were associated with a striking modification of murine hepatocytes, resulting in hyperchromatic and dysplastic nuclei. The latter finding was particularly evident in the hepatic areas surrounding all metastases of pleomorphic (anaplastic) neuroblastoma cells.
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PMID:Pleomorphic (anaplastic) neuroblastoma in nude mice. 198 17

Molecular characterization of neuroendocrine (Merkel cell) carcinoma of the skin. Review of the literature and report of three cases. Although neuroendocrine carcinoma of the skin (NECS) is comparatively a rare clinical-histological entity, numerous morphological and ultrastructural studies have been carried out since the tumor was identificated by Toker (1972). Recently immunocytochemistry has allowed a better molecular characterization (immunophenotype) of this tumor and a more exact diagnosis. The main problem for the pathologist is the differential diagnosis between NECS and skin neoplasms--both primitive and metastatic--which require a more aggressive treatment. Often the classical morphological criteria do not distinguish NECS from non-Hodgkin's lymphoma, amelanotic melanomas, cutaneous metastases of lung small cell carcinoma or of neuroblastoma. The co-expression of cytokeratins and neurofilaments constantly found in NECS, is surely the best differential criterion from non-neuroendocrine carcinomas. Furthermore, the typical paranuclear location of both the intermediate filaments in NECS is a distinctive peculiarity as opposed to lung microcytoma, where cytokeratins and neurofilaments, when present, show widespread perinuclear positivity. Chromogranin A is found only in a small percentage of tumor cells, whilst synthesis of calcitonin, somatostatin, gastrin, ACTH, is very rare. Finally, the lack of common leukocyte antigen (CLA), S-100 protein and vimentin in NECS rules out the diagnoses of lymphoma, melanoma and sarcoma respectively.
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PMID:[Molecular characterization of cutaneous neuroendocrine (Merkel cell) carcinoma. Review of the literature and presentation of a caseload]. 209 Oct 10

We have examined expression of the smg p25A (a ras p21-like GTP-binding protein) gene in neural crest-derived tumor cell lines and neuroblastoma tissues. The human neuroblastoma cell lines GOTO, IMR-32, NB-1, and SK-N-SH expressed the 1.6-kilobase smg-25A mRNA. SH-SY5Y and SH-IN, variant cell lines with a neuronal phenotype derived from SK-N-SH, expressed much more smg-25A mRNA than did SH-EP1, a variant line with an epithelium-like phenotype also derived from SK-N-SH. The primitive neuroectodermal tumor cell lines SK-N-MC and KU-SN and the Ewing's sarcoma cell lines RD-ES and SK-ES expressed the smg-25A mRNA to a much smaller extent than did neuroblastoma cell lines. Of 15 human neuroblastoma specimens tested, 13 expressed the smg-25A mRNA to various extents. When the relative ratio of the smg-25A mRNA level to the glyceraldehyde-3-phosphate dehydrogenase mRNA level was compared among neuroblastoma tumor tissues, the value was significantly higher in tumors histologically diagnosed as ganglioneuroblastoma. The smg-25A mRNA was not detected in the tissues of Hodgkin's lymphoma, Wilms' tumor, Ewing's sarcoma, or undifferentiated sarcoma of the liver. These results suggest that the smg-25A mRNA level is closely related to the neuronal differentiation state of tumors derived from the neural crest.
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PMID:Expression of the smg p25A (a ras p21-like GTP-binding protein) gene in human neuroblastoma cell lines and tumor tissues. 212 31

In recent years there has been a significant improvement in the survival rate of children with malignant solid tumors. With Wilms' tumor, the survival rate has risen to 80%, but a subset of these patients with unfavorable histologies and therefore a higher rate of relapse need a different strategy. For those patients with soft tissue sarcoma, brain tumors, and bone tumors the combination of preoperative chemotherapy, surgery, and radiotherapy followed by maintenance multiagent chemotherapy has resulted in a survival rate of 45% to 70%. In the case of neuroblastoma, a similar aggressive approach has not resulted in an improved survival. A different approach that uses screening of infants by urinary testing for VMA and HVA to detect earlier and potentially less malignant tumors has begun in Japan and North America in the hope that preclinical detection will reduce mortality.
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PMID:Advances and management of solid tumors in children. 215 15

We describe a series of 28 fine needle aspiration biopsies (FNAB) of soft tissue from 22 patients. Four patients had two separate FNABs, and one had three aspiration procedures. The patient population was limited to children and young adults (age range, 2 months to 29 years; mean, 16 years) who were known to have diverse forms of cancer, and who subsequently developed a mass in the peripheral soft tissues (including breast). The interval between the time of diagnosis of the primary malignant neoplasm and FNAB ranged from 1 day to 17 years (mean, 39 months). All FNAB diagnoses were confirmed by subsequent surgical open biopsy or clinical follow-up greater than 1 year. No complications occurred from the procedure. The cytomorphology is presented in selected cases and correlated with the patient's original tissue histopathology. Twenty aspirates were diagnosed as cytologically malignant, one as suspicious for malignancy. Seven were considered benign. None were unsatisfactory. One false-positive and no false-negative cytologic diagnoses were obtained. The overall accuracy of FNAB diagnoses was 96%, while sensitivity was 100% and specificity 88%. Sites of aspiration included soft tissues of the head and neck (seven cases), trunk (eight cases), breast (four cases), and extremities (nine cases). Malignant cytologic diagnoses included sarcoma (thirteen), seminoma (two), lymphoma/leukemia (two), melanoma (one), undifferentiated neoplasm (one), and neuroblastoma (one). Electron microscopy of aspirated cells was used to confirm the diagnosis in two cases. Fine needle aspiration biopsy of soft tissue masses from children and young adults with cancer demonstrates a high diagnostic accuracy, and its use is justified in this population.
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PMID:Metachronous soft-tissue masses in children and young adults with cancer: correlation of histology and aspiration cytology. 219 Sep 11

Transcripts for the muscle regulatory gene MyoD1 are expressed during normal skeletal muscle myogenesis and in rhabdomyosarcomas but not in other tissues or in soft-tissue sarcomas. Here we report the distribution of MyoD1 protein, determined by reactivity with anti-MyoD1 polyclonal sera in normal tissues, rhabdomyosarcoma cell lines, and in a variety of pediatric solid tumors. The distribution of MyoD1 protein was highly restricted in normal tissues and was detected only in fetal skeletal muscle and more faintly in adult skeletal muscle. All six human rhabdomyosarcoma cell lines analyzed expressed MyoD1 mRNA transcripts as well as immunoreactive protein. The immunohistochemical expression of MyoD1 protein was then examined in 49 surgical specimens from a variety of pediatric solid tumors. Each of 16 rhabdomyosarcoma specimens was positive for MyoD1, including four that did not express the intermediate filament protein desmin. Two of five specimens originally designated sarcoma type indeterminate (STI) and two of three specimens originally designated extraosseous Ewing's sarcoma (EOE) were positive for MyoD1, suggesting commitment to myogenic differentiation. Three of eight Wilms' tumors, which also expressed desmin and had clearly evident myogenic elements, also were positive for MyoD1. Tumors that failed to express MyoD1 protein included neuroblastoma, primitive neuroectodermal tumor, non-Hodgkins lymphoma, embryonal sarcoma of the liver, malignant fibrous histiocytoma, malignant rhabdoid tumor, and Ewing's sarcoma of the bone. These results indicate that expression of MyoD1 protein is highly restricted in normal human tissues and that expression of this gene product in malignant tissue may be diagnostic for rhabdomyosarcoma. Furthermore MyoD1 staining may be a valuable adjunct in the classification of pediatric soft-tissue sarcomas.
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PMID:Myogenic regulatory protein (MyoD1) expression in childhood solid tumors: diagnostic utility in rhabdomyosarcoma. 226 Jun 21

An investigation of 749 deaths occurring among 4082 patients surviving at least five years after the diagnosis of childhood cancer in Britain before 1971 has been undertaken. Of the 738 with sufficient information the numbers of deaths attributable to the following causes were: recurrent tumour, 550 (74%), a second primary tumour, 61 (8%), a medical condition related to treatment of the tumour, 49 (7%), an traumatic death unrelated to the tumour or its treatment, 34 (5%), finally, any other cause unrelated to the tumour or its treatment, 44 (6%). Less than 10% of five year survivors of non-Hodgkin lymphomas, neuroblastoma, retinoblastoma, Wilms' tumour, or a soft tissue sarcoma died of recurrent tumour during the next 15 years, while more than 25% of five year survivors of Hodgkin's disease, ependymoma, medulloblastoma, and Ewing's tumour died of recurrent tumour during the corresponding period. Almost 50% of five year survivors of acute lymphoblastic leukaemia died of recurrent disease during the corresponding 15 years, a large proportion of deaths being due to central nervous system relapse in an era before central nervous system prophylaxis was routinely given. Comparison of the mortality observed with that expected from mortality rates in the general population indicated three times the expected number of deaths from non-neoplastic causes. Five times the expected number of deaths from cardiovascular causes were observed, these were predominantly myocardial infarction and cerebrovascular accidents. There was no evidence of an excess in the number of suicides observed, but there were three times the expected number of deaths from accidents observed after central nervous system tumours. Two groups of patients were identified whose deaths were potentially avoidable. Seven patients with craniopharyngioma and panhypopituitarism presented with addisonian crises during periods of stress not adequately covered by exogenous corticosteroids. In the other group were children who received radiotherapy and later developed problems related to radiation fibrosis. We emphasize that our investigation relates to patients diagnosed with childhood cancer before 1971. The pattern of mortality that will emerge after recent treatment regimens, in which chemotherapy is being used more extensively, is likely to be different from that observed in our study.
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PMID:Late deaths after treatment for childhood cancer. 227 Sep 44


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