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

The Quebec Neuroblastoma Screening Project was initiated to assess the clinical and biological aspects of screening infants for the presence of neuroblastoma in North America. All children born in the province of Quebec from May 1, 1989 to April 30, 1994 are eligible for participation. This report provides results from 22 months' accrual of infants who were screened using urine-saturated filter paper for determination of the catecholamine metabolites vanillylmandelic acid (VMA) and homovanillic acid (HVA). More than 157,000 infants have been screened to date at 3 weeks of age, representing 92% of the entire birth population of Quebec. Over 98,000 infants have been screened a second time at 6 months of age, which made up 76% of the Quebec birth cohort. After a two-stage initial screening, 340 (0.13%) infants (182 at 3 weeks and 158 at 6 months) required second laboratory examinations because of elevated levels of urinary VMA, HVA, or both. Twenty infants from the 3-week screening (0.01%) and nine from the 6-month screening (0.01%) were subsequently referred to one of four Quebec pediatric oncology centers for neuroblastoma evaluation. Seven of 20 children from the 3-week screening and two of nine children from the 6-month screening have been identified as having neuroblastoma. During the same period, 14 additional children in the birth cohort were diagnosed clinically with neuroblastoma; eight were diagnosed prior to screening at 3 weeks of age, three children had negative results at 3 weeks of age, two had negative results at 3 weeks and at 6 months of age, and one had never been screened.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Screening for neuroblastoma in North America. 2-year results from the Quebec Project. 145 96

Halothane exposure over the cultured cells (100 and 1,000 ppm) caused a disruption of the pattern of actin distribution in both fibroblasts and neuroblastoma cells. Neuroblastoma cells exposed to halothane also lost microspikes; however, neurite elongation was not affected by halothane. The present study suggests that halothane induces the functional disruption of actin, resulting in an interference of normal neural development in vivo.
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PMID:The effect of halothane on cultured fibroblasts and neuroblastoma cells. 146 63

Neuroblastoma x glioma hybrid NG108-15 cells and mouse neuroblastoma N18TG-2 and N1E-115 cells were transiently transfected with the sense cDNA coding for rat choline acetyltransferase (ChAT). All transfected cell lines showed a high level of ChAT activity. ACh secretion was monitored by recording miniature end-plate potentials (MEPPs) in striated muscle cells that had been co-cultured with transfected cells. The number of muscle cells with synaptic responses and the MEPP frequency were higher in co-culture with transfected NG108-15 cells than with control or mock cells. No synaptic response was detected in muscle cells co-cultured with transfected N18TG-2 or N1E-115 cells. The results show that ACh secretion into the synaptic cleft was enhanced due to ChAT overexpression in NG108-15 hybrid cells but not in neuroblastoma cells.
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PMID:Enhanced acetylcholine secretion in neuroblastoma x glioma hybrid NG108-15 cells transfected with rat choline acetyltransferase cDNA. 146 77

Neuroblastoma is one of the childhood malignancies that frustrates both the clinical and scientist. Clearly, some forms of the disease are relatively benign and the patient can expect to be cured. However, even today, Stage 4 neuroblastoma is one of the childhood malignancies where the overall prognosis remains very poor. Despite extensive investigations into the biology of the disease, little has been gleaned about the underlying causes of the tumour and what truly separates good and poor risk disease. Fortunately, patients under the age of one with neuroblastoma often fall into the good risk group. Many people now believe that neuroblastoma is not just one disease, but several. Some forms of the tumours may, in fact, not be truly malignant. The data that has led to this conclusion and the biological characteristics that are associated with the different forms of the neuroblastoma will be reviewed. In addition, a brief outline of new studies which may identify some of the factors associated with the neuroblasts ability to metastasise will be discussed.
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PMID:Neuroblastoma in the very young child: biological considerations. 150 19

Neuroblastoma is one of the most common solid tumours of childhood and is unique amongst paediatric cancers in that it results in the urinary excretion of catecholamine metabolites which are easily measured in spot urine samples and so is a condition for which screening may be considered. The continuing poor prognosis associated with late stage disease has stimulated great interest in this proposition. The Japanese have been undertaking pioneering studies of such screening since 1974 and since 1985, all 6 months old babies have been offered screening. Preliminary data would appear to suggest that screening is effective in greatly improving the survival of children with neuroblastoma. However there are difficulties associated with the interpretation of survival data since screening undoubtedly results in the detection of cases which would otherwise have remained 'silent', and the well known problems of lead-time and length-time bias complicate matters still further. The time is not yet ready for universal implementation of screening and further investigation is required.
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PMID:Poor prognosis neuroblastoma: is screening the answer? 150 35

Using a cDNA library from bovine adrenal medulla, we have isolated cDNAs coding for a potassium channel. These cDNAs encode a 660-amino acid protein that has a molecular weight of 73,288 kDa and no amino-terminal signal peptide. We have called it BAK4. Analysis of its sequence reveals close similarity (94% homology) with a recently described potassium channel from rat brain (RCK4) and heart (RHK1). Neuroblastoma cells (Neuro-2a cell line) were stably transfected with BAK4 DNA. Expression of the DNA was under the control of a heat-shock promoter. Several clones, that were isolated by neomycin resistance selection, had integrated the plasmid DNA in a stable form. Upon heat induction, these cells produced BAK4 RNA and a potassium outward current, not present in control non-transfected cells. The current, which was transient and decayed markedly during the duration of 200 ms-pulses, can be described as a Ik(A) potassium current. The expression of these types of channels in brain (RCK4,RHK1), heart (RHK1) and adrenal medulla (BAK4) suggest their possible implication in important functions for the cell.
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PMID:Molecular cloning and permanent expression in a neuroblastoma cell line of a fast inactivating potassium channel from bovine adrenal medulla. 150 68

Radio-frequency electromagnetic radiation (RFR) at 915 and 147 MHz, when sinusoidally amplitude modulated (AM) at 16 Hz, has been shown to enhance release of calcium ions from neuroblastoma cells in culture. The dose-response relation is unusual, consisting of two power-density "windows" in which enhanced efflux occurs, separated by power-density regions in which no effect is observed. To explore the physiological importance of these findings, we have examined the impact of RFR exposure on a membrane-bound enzyme, acetylcholinesterase (AChE), which is intimately involved with the acetylcholine (ACh) neurotransmitter system. Neuroblastoma cells (NG108), exposed for 30 min to 147-MHz radiation, AM at 16 Hz, demonstrated enhanced AChE activity, as assayed by a procedure using 14C-labeled ACh. Enhanced activity was observed within a time window between 7.0 and 7.5 h after the cells were plated and only when the exposure occurred at power densities identified in a previous report as being effective for altering the release of calcium ions. Thus RFR affects both calcium-ion release and AChE activity in nervous system-derived cells in culture in a common dose-dependent manner.
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PMID:Dose dependence of acetylcholinesterase activity in neuroblastoma cells exposed to modulated radio-frequency electromagnetic radiation. 151 Jul 40

Neuroblastomas are malignant, embryonic tumors, and most are probably congenital in origin. Neuroblastoma is a heterogeneous neoplastic disease with respect to response to treatment and prognosis. Some of its clinical behavior is ascribed to the ability of the tumor to regress spontaneously. Spontaneous regression of neuroblastoma is occasionally observed in young infants, but occurs extremely rarely in older children. This feature is in accordance with the concept that tumors develop by a series of changes, progressing from a dependent state to an autonomous state. Spontaneous regression was documented in less than 2% of Danish neuroblastoma patients. However, the "true" incidence of regression may be higher. Epidemiological data suggest that, in recent decades, borderline lesions may be included among truly malignant neuroblastomas. The recent birth cohorts compiled in Denmark show that 1 in 7,000 live births will develop neuroblastoma before 15 years of age. If 65% of all childhood neuroblastomas could be detected at or before the age of 6 months, then the expected prevalence by screening would be 1/11,000. One can speculate that 1/18,000 live births might possibly benefit from screening at age 6 months, since 59% of these children had tumors in stages III and IV diagnosed after the age of 6 months. However, the proof that screening can only detect lesions that would have progressed to become malignant tumors depends on observing an appropriate fall in the incidence of the malignant tumors in older children and a decline in mortality. Therefore, it is of some concern that the incidence of neuroblastomas appears to actually increase with screening while mortality has been little effected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroblastoma: epidemiology and pattern of regression. Problems in interpreting results of mass screening. 153 Jan 15

Cultured human neuroblastoma cells can be classified morphologically into 3 types: neuroblastic (N), intermediate (I) and substrate adherent (S). Neuroblastoma cells of all types were found to attach and display distinct morphological characteristics on fibronectin, with S-type cells attaching better than N-type cells. Studies of the expression of integrin fibronectin receptors (alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1 and alpha V beta 1) were carried out using a total of 26 morphologically distinct cell lines and their subpopulations. Fluorescence-activated cell sorting (FACS) analysis and immunoprecipitation revealed that all S-type cells expressed abundant alpha 5 beta 1, while N-type cells barely expressed this molecule. Although alpha 3 beta 1 expression of S-type cells was also higher than that of N-type cells, some N-type cells had significantly increased levels of this molecule. alpha 4 beta 1 was found to be randomly expressed. All cell lines tested expressed alpha V beta 1. Human neuroblastoma cells, the majority of which are N-type cells with very low alpha 5 beta 1 expression, are also contrasted with other childhood cancer cells (rhabdomyosarcoma, Ewing's sarcoma, and glioma), all of which expressed high levels of alpha 5 beta 1. The characteristic expression of integrin fibronectin receptors may account for the clinically unique tumor behavior, and the immunohistochemical staining for integrins may become a useful alternative to conventional histology in differential diagnosis and a marker for prognosis in neuroblastoma.
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PMID:Unique expression of integrin fibronectin receptors in human neuroblastoma cell lines. 153 85

N-myc expression has been reported in neuroblastoma, retinoblastoma and small cell lung carcinoma. Increased expression associated with gene amplification in neuroblastoma correlates with disease stage and prognosis. N-myc expression has been observed in diverse murine tissues during early stages of development with loss of expression in later stages. Abelson murine leukemia virus (A-MuLV)-transformed pre-B cells express N-myc, whereas mature B cells do not. To determine whether human B-lymphocyte precursors also have increased N-myc expression, we extracted DNA and RNA from representative cell lines, prepared Southern and Northern blots and examined them with the N-myc probe, pNB-1. RNA from the following B-cell developmental stages were examined. One null, 1 pre-pre-B, 3 pre-B (including pre-B-lymphoblastic leukemia, a poor prognostic category) and 5 mature B. Neuroblastoma cells and tissues served as positive controls; negative controls included human muscle, placenta, epithelial cell lines, monocytic, promyelocytic, and T-cell lines. N-myc expression was detected in neuroblastoma cells, but in none of the mature human B or B-lymphocyte precursor cells. Additional immunocytochemical studies performed for N-myc nuclear protein likewise failed to detect this gene product. We conclude that human pre-B cells, unlike murine B-cell precursors, do not express increased levels of N-myc RNA. Expression of this oncogene in human neoplastic B cells does not appear to correlate with developmental stage or prognostic group.
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PMID:Human B-lymphocyte precursors do not express the N-myc gene. 157 Oct 96


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