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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroblastoma was first described in 1864 by Virchow. For the next 100 years, the primary approach to these patients was predominantly surgical resection. With the advent of multimodal adjuvant treatments using chemotherapy and irradiation in the 1950s and 1960s, coordination of multispecialty therapeutic interventions became important. By the late 1970s, effective neoadjuvant chemotherapeutic regimens enabled some inoperable tumors to be completely removed at the time of "second look" procedures. In the 1980s, advances in tumor biology and imaging gave new insight and novel prognostic indicators which helped determine the course of therapy. In the 1990s, treating poor risk patients with extremely high dose chemotherapy, irradiation, and allogeneic or autologous bone marrow rescue with or without surgical resection may finally improve the survival of these children.
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PMID:Recent developments in the management of neuroblastoma. 190 92

Neuroblastoma remains a common and deadly childhood tumor, resistant to both surgical and chemo/radiotherapeutic intervention in its advanced stages. The role of immunotherapy in such cancers has yet to be defined. In previous work, we found that the addition of interferon gamma (IFN-gamma) to 3-day in vitro tissue cultures of the murine neuroblastoma C1300, led not only to the tumor's increased cell surface expression of the immunologically important major histocompatibility complex (MHC) class I antigen, but also to an increased susceptibility of such modified tumor to subsequent lymphokine activated killer (LAK) cell lysis. In this study, we sought to determine the in vivo applicability of these findings. Initial dose-response studies helped define a regimen of rIFN-gamma's administration that upregulated MHC class I without activating host natural killer (NK) activity. A/J mice bearing 7-day-old subcutaneous C1300 were randomized to receive daily morning injections of either 0, 25,000, 50,000, or 100,000 U of rIFN-gamma intraperitoneally for 6 days. Animals were killed at days 3, 6, and 9 after initiation of rIFN-gamma therapy, and tumors were excised, digested, and stained for both MHC class I and II expression. At the time of sacrifice, splenocytes from each animal were tested for NK cytotoxicity toward YAC (an NK-sensitive lymphoma) and C1300. These studies defined 3 days of therapy with 25,000 U as a "priming" dose that increased expression of class I with minimal impact on NK activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-dose interferon gamma renders neuroblastoma more susceptible to interleukin-2 immunotherapy. 190 48

From 1970 to 1989, 121 children with mediastinal masses of various sorts were seen in the Department of Pathology, Royal Children's Hospital, Melbourne. The series is considered representative of the true incidence of these conditions in the state of Victoria, which had an average paediatric population during the time of this series of 900,000 children. The commonest cause of a mediastinal mass was NHL (36 cases). This was followed by HD (24 cases), then neuroblastoma and ganglioneuroma (16 and 9 cases respectively), duplication cysts (10 cases), teratomas (7 cases), neurofibroma (4 cases) and lymphangioma (3 cases). A great variety of rare conditions made up the remainder of the series and included mediastinal abscess, thymic cyst, pericardial cyst, accessory lobe of lung, plasma cell granuloma, fibromatosis, paravertebral Ewing's tumour, carcinoid tumour and neurofibrosarcoma. Presentation of the children with NHL was often acute with respiratory distress, while the child with HD was usually older and symptoms were more often systemic than local. The surgeon's role in diagnosis of these most frequently encountered mediastinal masses can be crucial and biopsy when indicated must be carried out with great care to produce material that is adequate for diagnosis and for the performance of cell marker studies and chromosome analysis. Neuroblastoma (NBL) and ganglioneuroma (GN) together were the third largest group. Children with neuroblastoma were usually young; 15 of the 18 cases were less than 2 years old. One-third of the infants with neuroblastoma presented with paraplegia and one-third with respiratory symptoms including wheeze, stridor and respiratory difficulty. Three children had Horner's syndrome. Prognosis of children with thoracic neuroblastoma is very good and contrasts with the poor outlook for those with abdominal neuroblastoma. Stage at presentation is probably the most important single prognostic variable. Ganglioneuroma presents at a later age than neuroblastoma and symptoms may be present for a long time or may be completely absent. Catecholamines, usually raised in neuroblastoma, are mostly normal in ganglioneuroma. Duplication cysts were the next most frequent group. Symptoms can often be acute and life threatening, although in three of our ten cases the cyst was an incidental finding on chest X-ray. However, only three of our patients had a normal respiratory examination. Teratomas were usually large and more often benign than malignant. Excision is the mandatory treatment and is usually curative. Although teratomas in young infants are often cellular and composed of many immature tissue types, their behaviour is benign.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mediastinal masses in childhood: a review from a paediatric pathologist's point of view. 190 92

The maturation of embryonal neural crest cells is thought to be regulated in part by the milieu into which these cells migrate. Neuroblastoma (NB) is a tumor of very early childhood that is thought to arise in association with the arrested differentiation of embryonal neural crest cells. In culture, neuroblastoma tumor cells differentiate in the presence of retinoic acid, which is also known to influence extracellular matrix protein synthesis. We have cultured neuroblastoma cells on laminin (LN) and fibronectin (FN) substrata to examine the role of extracellular matrix in retinoic acid (RA)-induced differentiation of these tumor cells. These proteins caused morphologic changes in NB cells indistinguishable from those caused by RA. Antiserum to each of these proteins blocked the effects induced by the corresponding protein, but neither antiserum affected the action of RA. Despite the induction of a neuronal morphologic change, matrix proteins did not alter the proliferation of NB cells. These results indicate that LN and FN modulate the differentiation of NB cells without inducing growth arrest and that RA-induced differentiation does not require these matrix proteins.
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PMID:Matrix proteins induce neuroblastoma cell differentiation without altering cell growth. 191 May 26

Neuroblastoma cells accumulate ascorbic acid and iron. It was hypothesized that these features could be exploited for sensitizing neuroblastoma cells for therapy in combination with reactive oxygen intermediates. In the present study the effects of 6-hydroxydopamine (6-OHDA) and H2O2 on metabolic parameters critical for cell survival were investigated in cells with low and high ferritin content in the presence and absence of ascorbate. Human neuroblastoma SK-N-SH cells were pretreated with 100 microM FeSO4 and 10 microM desferrioxamine, respectively, for 24 h yielding cells with different ferritin contents. The effects of 6-OHDA and H2O2 (25 microM-250 microM) in the absence and presence of 1 mM ascorbic acid on DNA strand break formation, activation of poly(ADP-ribose) polymerase, and finally decrease in NAD+ and ATP concentration were investigated. All these parameters were influenced by 6-OHDA and H2O2 in a concentration-dependent manner in a similar way. The effects were most pronounced in ferritin-rich cells and in the presence of ascorbic acid. Using isolated CCC PM2 DNA, 6-OHDA and ascorbic acid caused strand breaks that were prevented in the presence of mannitol or desferrithiocine. H2O2-mediated strand breaks were observed only in the presence of ascorbic acid. Based on these data and data published by others a model explaining the deleterious effects of ascorbic acid on neuroblastoma cells is presented. It is suggested that continuous application of a high dosage of ascorbic acid might be a useful approach in neuroblastoma therapy.
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PMID:Ascorbic acid enhances the effects of 6-hydroxydopamine and H2O2 on iron-dependent DNA strand breaks and related processes in the neuroblastoma cell line SK-N-SH. 193 70

The analysis of the N-myc gene in bone marrow specimens at the time of initial diagnosis and as well at the time of relapse from patients with Neuroblastoma stage IV and bone marrow infiltration could give some informations about the N-myc status of these patients. In stage IV neuroblastoma patients with bone marrow infiltration an estimation of the N-myc gene amplification should be attempted, if otherwise no information about the tumor content of the N-myc gene could be gathered. In our investigation we could demonstrate a Southern-blot-analysis of 27 bone marrow specimens with respect to the N-myc gene status which correlated qualitatively well to the N-myc amplification detected later on in the corresponding tumor tissue. In six cases the tumor infiltrated bone marrow showed a clear amplification of the N-myc gene. Because of the contamination by non malignant cells in bone marrow there was a quantitative difference in the calculated N-myc gene copies between the examined bone marrow specimens and corresponding tumor tissue.
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PMID:[N-myc status of neuroblastoma from bone marrow cells]. 194 39

Neuroblastoma is a tumor of postganglionic sympathetic origin, and nerve growth factor (NGF) is normally required for the survival and differentiation of sympathetic neuroblasts. Since the biological activity of NGF is mediated by the NGF receptor (NGFR), we hypothesized that defects in the NGF/NGFR pathway may play a role in maintenance of the undifferentiated state of neuroblastomas. To test this hypothesis, we examined the structure of the NGFR at the DNA, RNA, and protein levels in a panel of 10 neuroblastoma cell lines. In addition, we examined the function of the NGFR in these lines by analysis of NGF binding kinetics, as well as by the ability of NGF to induce c-fos expression and neurite outgrowth. Southern blot analysis showed that all 10 cell lines possess apparently normal NGFR genes. Northern blot and ligand binding/immunoprecipitation assays revealed four receptor-positive cell lines (NGP, NLF, SK-N-SH, and LA-N-6), with NGFR mRNA and protein of expected sizes (3.8 kilobases and Mr approximately 75,000, respectively). NGF binding assays and Scatchard analyses were performed on the four NGFR-positive lines. The NGP line possesses only low-affinity receptor (Kd approximately 3.5 x 10(-9)), whereas the other three lines express both low- and high-affinity forms (Kd approximately 10(-9) and Kd approximately 10(-11), respectively). However, none of the 10 lines exhibited a response to NGF treatment as assayed by c-fos mRNA induction and neurite extension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple defects of the nerve growth factor receptor in human neuroblastomas. 196 76

We have examined the hypothesis that nonhematopoietic malignancies may contain cells corresponding to those which occur during the differentiation of tissue precursors. Neuroblastoma, an embryonal tumor of the adrenal medulla, was studied because of its well described ability to differentiate both in vivo and in vitro. We examined the expression of four genes during development of the human adrenal medulla: tyrosine hydroxylase, chromagranin A, pG2, and beta-2-microglobulin. The sequential expression of these genes by adrenal neuroblasts marks successive stages during maturation of the chromaffin lineage. We also observed a population of neuroblasts during adrenal medullary development that did not express any of these four genes, suggestive of adrenal medullary cells differentiating along nonchromaffin lineage(s). We then evaluated 27 neuroblastoma cell lines for the expression of these genes and found that 24 expressed chromaffin markers, with 19 of these mimicking the pattern of gene expression found during development. Three cell lines did not express tyrosine hydroxylase, chromogranin A, or pG2, consistent with either a very undifferentiated neural crest cell or maturation along a nonchromaffin lineage. These data indicate that neuroblastoma tumor cells correspond to adrenal neuroblasts arrested during morphogenesis of the adrenal medulla and raise the possibility that malignant transformation of cells at different stages of tissue maturation may contribute to the diversity that characterizes tumors of solid tissues.
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PMID:Human neuroblastoma tumor cell lines correspond to the arrested differentiation of chromaffin adrenal medullary neuroblasts. 198 60

Neuroblastoma is a disease with wide spectrum clinically For the evaluation of the biological specificity of this tumor, we examined the expression of Ha-ras p21. The Ha-ras p21 detected in tumor cells showed a statistically significant association with the non-progressed tumor at the diagnosis and the favourable outcome of the patients. The association of Ha-ras p21 with their clinical outcome was closer than those of N-myc amplification. However, the complementary analyses of both Ha-ras p21 and N-myc gene seemed to provide more precise informations relating the patient's care.
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PMID:[Tumor markers--personal experience. Ha-ras P21 in neuroblastoma: a new marker associating to patient's prognosis]. 198 97

Neuroblastoma is an embryonal tumor that typically arises in cells of the developing adrenal medulla. IGF-II mRNA is expressed at high levels in the adrenal cortex before birth but it is not detectable until after birth in the adrenal medulla. Neuroblastoma cell lines corresponding to early adrenal medullary precursors did not express IGF-II, although all three cell lines we tested were growth stimulated by IGF-II. Cell lines corresponding to more mature adrenal medullary cells expressed IGF-II, and one, SK-N-AS, grows by an IGF-II autocrine mechanism (J. Clin. Invest. 84:829-839) El-Badry, Romanus, Helman, Cooper, Rechler, and Israel. 1989. An examination of human neuroblastoma tumor tissues for IGF-II gene expression using in situ hybridization histochemistry revealed that IGF-II is expressed by tumor cells in only 5 of 21 neuroblastomas, but is detectable in cells of nonmalignant tissues including adrenal cortical cells, stromal fibroblasts, and eosinophils in all 21 tumors. These findings indicate that IGF-II may function as an autocrine growth factor for some neuroblastomas and as a paracrine growth factor for others. They suggest that the growth regulatory pathways utilized by neuroblastoma mimic those used in the precursor cell type from which individual tumors arise.
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PMID:Insulin-like growth factor II-mediated proliferation of human neuroblastoma. 199 49


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