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Abramson Cancer CenterNCI CANCERLIT® Search: Neuroblastoma - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Activation of vascular endothelial growth factor A transcription in tumorigenic glioblastoma cell lines by an enhancer with cell
- Primary neuroblastoma of the maxillary sinus.
- Oxidative stress modulates tyrosine kinase receptor A and p75 receptor (low-affinity nerve growth factor receptor) expression in SHSY5Y
- Redox status-dependent regulation of cyclooxygenases mediates the capsaicin-induced apoptosis in human neuroblastoma cells.
- Correspondence re: J. Mora et al., Neuroblastic and Schwannian stromal cells of neuroblastoma are derived from a tumoral progenitor cell.
- Correspondence re: J. Mora et al., Neuroblastic and Schwannian stromal cells of neuroblastoma are derived from a tumoral progenitor cell.
- Metaiodobenzylguanidine total-body scintigraphy required for revealing occult neuroblastoma in opsoclonus-myoclonus syndrome.
- Tissue transglutaminase differentially modulates apoptosis in a stimuli-dependent manner.
- Radiology of neuroblastoma in children.
- Estrogen receptor ligands affect mitochondrial activity in SH-SY5Y human neuroblastoma cells.
- Only amyloidogenic intermediates of transthyretin induce apoptosis.
- Organophosphorus compounds alter intracellular F-actin content in SH-SY5Y human neuroblastoma cells.
- [Nursing care planning in a child with neuroblastoma]
- Ca(2+)-independent caspase-3 but not Ca(2+)-dependent caspase-2 activation induced by oxidative stress leads to SH-SY5Y human
- Neuroblastoma: a challenge for pediatric oncology of the third millennium.
- Amplified MYCN in human neuroblastoma: paradigm for the translation of molecular genetics to clinical oncology.
- Linkage analysis in families with recurrent neuroblastoma.
- Elevated expression of galanin receptors in childhood neuroblastic tumors.
- N-Myc and Bcl-2 coexpression induces MMP-2 secretion and activation in human neuroblastoma cells.
- RAS, the magician.
- Protective effects of puerariaeflos against ethanol-induced apoptosis on human neuroblastoma cell line SK-N-MC.
- Neuroblastoma in a dysmorphic girl with a partial duplication of 2p caused by an unbalanced translocation.
- Clinical trials referral resource. Current clinical trials in neuroblastoma.
- Two regions of deletion in 9p22- p24 in neuroblastoma are frequently observed in favorable tumors.
- [Esthesioneuroblastoma of nasal cavity and ethmoid sinus]
- Micronuclei and apoptosis in glioma and neuroblastoma cell lines and role of other lesions in the reconstruction of cellular
- Flavopiridol inhibits vascular endothelial growth factor production induced by hypoxia or picolinic acid in human neuroblastoma.
- [Discovery of a neuroblastoma producing cardiogenic shock in a 2-month-old child]
- Expression of DeltaNp73 is a molecular marker for adverse outcome in neuroblastoma patients.
- Pain and suffering in an adolescent with neuroblastoma.
- Topotecan combined with myeloablative doses of thiotepa and carboplatin for neuroblastoma, brain tumors, and other poor-risk solid tumors in
- Neuroblastoma in monozygotic twins--a case of probable twin-to-twin metastasis.
- Quantitation of GD2 synthase mRNA by real-time reverse transcription-polymerase chain reaction: utility in bone marrow purging
- Reply to Langer et al. Expression of vascular endothelial growth factor (VEGF) and VEGF receptors in human neuroblastomas.
Table of Contents
1
UI - 11912213
AU - Liang Y; Li XY; Rebar EJ; Li P; Zhou Y; Chen B; Wolffe AP; Case CC
TI -
Activation of vascular endothelial growth factor A transcription in
tumorigenic glioblastoma cell lines by an enhancer with cell
type-specific DNase I accessibility.
SO - J Biol Chem 2002 May 31;277(22):20087-94
AD - Sangamo BioSciences Incorporated, Richmond, California 94804, USA.
Unregulated expression of vascular endothelial growth factor-A (VEGF-A)
plays an important role in tumor growth. We have identified a cell
type-specific enhancer, HS-1100, that contributes to VEGF-A
transcriptional activation in tumorigenic glioblastoma cell lines. This
enhancer exhibits increased accessibility to DNase I in glioblastoma
cell lines that express high levels of VEGF-A but not in several other
cell lines that express much lower levels of VEGF-A. HS-1100 contains a
number of sequence elements that are highly conserved among human,
mouse, and rat, including the hypoxia-response element (HRE). We show
that the HRE contributes significantly to the cell type-specific
enhancer activity of HS-1100 in U87MG glioblastoma cells. We use
chromatin immunoprecipitation assays to show that endothelial PAS domain
protein 1 (EPAS1) can efficiently bind to the endogenous HRE in U87MG
cells but not in HEK293 cells in which the chromosomal HS-1100 is not
accessible to DNase I. A dominant negative EPAS1 significantly reduces
HS-1100 enhancer activity and VEGF-A levels in U87MG cells. Our results
provide insight into the molecular mechanisms of VEGF-A up-regulation
during cancer development.
2
UI - 11955607
AU - Wei JL; Scheithauer BW; Smith JS; Jenkins RB; Passe SM; Arndt CA; Strome
TI -
SE
Primary neuroblastoma of the maxillary sinus.
SO - Int J Pediatr Otorhinolaryngol 2002 Apr 25;63(2):155-62
AD - Department of Otorhinolaryngology, c/o Section of Scientific
Publications, Mayo Clinic, Rochester, MN, USA.
Although neuroblastoma is the most common of extracranial solid tumors
of childhood and infancy, we report the first case of an isolated
neuroblastoma of a paranasal sinus. A 15-year-old girl with a right
maxillary sinus mass was asymptomatic except for persistent epiphora.
Computed tomography and magnetic resonance imaging scans showed that the
mass extended into the nasal cavity, encroached on the lamina papyracea,
and obstructed the nasofrontal duct. An extensive workup revealed no
evidence of systemic disease. The patient underwent right craniofacial
resection. Immunohistochemistry and electronmicroscopic findings were
consistent with conventional neuroblastoma. Fluorescence in situ
hybridization analysis was performed with probes selected to demonstrate
genetic alterations associated with neuroblastoma. Studies revealed
deletion of chromosome arm 1p, gain of chromosome 17, and normal N-myc
gene copy number. In summary, the tumor exhibited morphologic features
and genetic alterations more consistent with those of neuroblastoma than
with those of esthesioneuroblastoma.
3
UI - 12028822
AU - Olivieri G; Otten U; Meier F; Baysang G; Dimitriades-Schmutz B;
TI -
Muller-Spahn F; Savaskan E
Oxidative stress modulates tyrosine kinase receptor A and p75 receptor
(low-affinity nerve growth factor receptor) expression in SHSY5Y
neuroblastoma cells.
SO - Neurol Clin Neurophysiol 2002;2002(2):2-10
AD - Neurobiology Laboratory, Psychiatric University Hospital, Basel,
Switzerland. fianfranco.olivieri@pukbasel.ch
The interaction of neurotrophins and their tyrosine kinase receptors
(trks) is essential for differentiation and survival of brain cells. In
Alzheimer's disease (AD), the number of neurotrophins and receptors is
markedly decreased. The cause of this reduction is unclear, but the role
of beta-amyloid (Abeta) seems central in understanding the mechanisms
controlling neurotrophin and trk expression. In the study reported here,
we exposed SHSY5Y neuroblastoma cells to Abeta or hydrogen peroxide
(H(2)O(2)) and measured the expression of trk-A and p75 at the protein
and molecular levels. Both Abeta and H(2)O(2) induced oxidative stress
(measured by a decrease in cellular glutathione), which decreased trk-A
levels and increased p75 levels, decreased messenger RNA (mRNA) levels
of both receptors, and increased nerve growth factor (NGF) secretion.
Pretreatment of cells with the antioxidant melatonin returned levels of
protein expression, mRNA, and NGF secretion to normal. These results are
significant, as they can help in the planning and implementation of AD
treatment strategies involving neurotrophins.
4
UI - 12086397
AU - Lee YS; Kwon EJ; Jin da Q; Park SH; Kang YS; Huh K; Kim JA
TI -
Redox status-dependent regulation of cyclooxygenases mediates the
capsaicin-induced apoptosis in human neuroblastoma cells.
SO - J Environ Pathol Toxicol Oncol 2002;21(2):113-20
AD - Department of Physiology, College of Medicine, Kwandong University,
Kangnung, Korea.
Cyclooxygenases (COX) appear to be involved in the mechanism of
apoptosis in various cancer cells. In this study we investigated the
role of COX in the capsaicin (Cap)-induced apoptosis in SK-N-SH human
neuroblastoma cells. Cap induced decreased cell viability and apoptosis
in a dose-dependent manner. Cap also significantly reduced the basal
generation of reactive oxygen species (ROS) and lipid peroxidation in a
time-dependent fashion. Cap markedly suppressed the expression of COX-1
and COX-2. Pretreatment with NS-398, a selective COX-2 inhibitor, or
indomethacin, a nonselective COX inhibitor, significantly enhanced the
Cap-induced decreased cell viability and apoptosis. Exogenous
application of an oxidant, H2O2, significantly prevented the Cap-induced
apoptosis and suppressed the expression of COX isoforms. These results
suggest that redox status-dependent regulation of COX expression may
mediate apoptosis induced by Cap in human neuroblastoma cells.
5
UI - 12019183
AU - Ambros IM; Amann G; Ambros PF
TI -
Correspondence re: J. Mora et al., Neuroblastic and Schwannian stromal
cells of neuroblastoma are derived from a tumoral progenitor cell.
Cancer Res., 61: 6892-6898, 2001.
SO - Cancer Res 2002 May 15;62(10):2986-7; discussion 2988-9
6
UI - 12025836
AU - Shimada H
TI -
Correspondence re: J. Mora et al., Neuroblastic and Schwannian stromal
cells of neuroblastoma are derived from a tumoral progenitor cell.
Cancer Res., 61: 6892-6898, 2001.
SO - Cancer Res 2002 May 15;62(10):2987-8; discussion 2988-9
7
UI - 12012219
AU - Swart JF; de Kraker J; van der Lely N
TI -
Metaiodobenzylguanidine total-body scintigraphy required for revealing
occult neuroblastoma in opsoclonus-myoclonus syndrome.
SO - Eur J Pediatr 2002 May;161(5):255-8
AD - Reiner de Graaf Gasthuis, Department of Paediactrics, Delft, The
Netherlands. jf_swart@hotmail.com
A girl aged 13 months presented with clinical features of subacute
progressive ataxia leading to abasia, astasia, loss of unsupported
sitting and apraxia. In addition, an opsoclonus, myoclonia and introvert
behaviour developed. MRI of the brain, EEG, extensive tests of blood,
urine and CSF showed no abnormalities. Based on clinical symptoms only,
the diagnosis of opsoclonus-myoclonus syndrome (OMS) could be made.
Under the suspicion of a neuroblastoma, further investigations were
performed: a lateral and antero-posterior X-ray examination of the chest
showed no tumour; neither did ultrasound of the abdomen. Concentrations
of catecholamines and their metabolites in 24 h urine were normal and
none of five tested anti-neuronal antibodies were found. However, a
total-body scintigraphy with [I(123)] metaiodobenzylguanidine (MIBG)
revealed a paravertebral hot spot on the left side compatible with a
neural crest tumour. A MRI scan of the abdomen confirmed the
supraphrenic lesion. [I(123)]MIBG uptake was sufficient for [I(131)]MIBG
therapy. The response of the tumour to this therapy was favourable. The
neurological symptoms of the patient slightly improved under steroid
treatment. CONCLUSION: Opsoclonus-myoclonus syndrome is a serious
disease in infants, sometimes associated with occult neuroblastoma for
which a full oncological work-up, including metaiodobenzylguanidine
total-body scintigraphy is required.
8
UI - 12065637
AU - Tucholski J; Johnson GV
TI -
Tissue transglutaminase differentially modulates apoptosis in a
stimuli-dependent manner.
SO - J Neurochem 2002 May;81(4):780-91
AD - Department of Psychiatry and Behavioral Neurobiology, University of
Alabama at Birmingham, 1720 7th Avenue South, SC 1061, Birmingham, AL
35294-0017, USA.
Tissue transglutaminase is a unique member of the transglutaminase
family as it not only catalyzes a transamidating reaction, but also
binds and hydrolyzes GTP and ATP. Tissue transglutaminase has been
reported to be pro-apoptotic, however, conclusive evidence is still
lacking. To elucidate the role of tissue transglutaminase in the
apoptotic process human neuroblastoma SH-SY5Y cells were stably
transfected with vector only (SH/pcDNA), wild-type tissue
transglutaminase (SH/tTG) and tissue transglutaminase that has no
transamidating activity but retains its other functions (SH/C277S). In
these studies three different apoptotic stimuli were used osmotic
stress, staurosporine treatment and heat shock to delineate the role of
tissue transglutaminase as a transamidating enzyme in the apoptotic
process. In SH/tTG cells, osmotic stress and staurosporine treatments
resulted in significantly greater caspase-3 activation and apoptotic
nuclear changes then in SH/pcDNA or SH/C277S cells. This potentiation of
apoptosis in SH/tTG cells was concomitant with a significant increase in
the in situ transamidating activity of tissue transglutaminase. However,
in the heat shock paradigm, which did not result in any increase in the
transamidating activity in SH/tTG cells, there was a significant
attenuation of caspase-3 activity, LDH release and apoptotic chromatin
condensation in SH/tTG and SH/C277S cells compared with SH/pcDNA cells.
These findings indicate for the first time that the effect of tissue
transglutaminase on the apoptotic process is highly dependent on the
type of the stimuli and how the transamidating activity of the enzyme is
affected. Tissue transglutaminase facilitates apoptosis in response to
stressors that result in an increase in the transamidating activity of
the enzyme. However, when the stressors do not result in an increase in
the transamidating activity of tissue transglutaminase, than tissue
transglutaminase can ameliorate the apoptotic response through a
mechanism that is independent of its transamidating function. Further,
neither the phosphatidylinositol-3-kinase pathway nor the
extracellular-regulated kinase pathway is downstream of the modulatory
effects of wild-type tissue transglutaminase or C277S-tissue
transglutaminase in the apoptotic cascade.
9
UI - 11702143
AU - Hiorns MP; Owens CM
TI -
Radiology of neuroblastoma in children.
SO - Eur Radiol 2001;11(10):2071-81
AD - Department of Diagnostic Imaging, Hospital for Sick Children, Great
Ormond Street, London WC1N 3JH,UK.
The radiology of neuroblastoma reflects the diversity of the
manifestations of this condition. The current radiological practice for
imaging is outlined and illustrated with emphasis on cross-sectional and
radionuclide imaging.
10
UI - 12004198
AU - Simpson PB; Woollacott AJ; Moneer Z; Rand V; Seabrook GR
TI -
Estrogen receptor ligands affect mitochondrial activity in SH-SY5Y human
neuroblastoma cells.
SO - Neuroreport 2002 May 24;13(7):957-60
AD - Merck Sharp and Dohme Research Laboratories, Neuroscience Research
Centre, Terlings Park, Eastwick Road, Harlow, Essex CM20 2QR, UK.
We have studied the pharmacological regulation of mitochondrial activity
in a human neuroblastoma cell line. Cyclosporin A was found to directly
alter mitochondrial membrane potential and to decrease mitochondrial
permeability as measured using calcein. The estrogen receptor ligands
tamoxifen, nafoxidine and clomiphene were identified as agents which
affect mitochondrial membrane potential in a cyclosporin A-like manner.
Also when mitochondrial permeability was measured using calcein,
tamoxifen, nafoxidine and clomiphene were effective in inhibiting dye
loss from mitochondria. Nafoxidine and cyclosporin A inhibit effects of
mastoparan on SH-SY5Y mitochondria. These studies indicate that estrogen
receptor ligands appear to affect mitochondria in a cyclosporin A-like
manner in human neuroblastoma cells.
11
UI - 12051711
AU - Andersson K; Olofsson A; Nielsen EH; Svehag SE; Lundgren E
TI -
Only amyloidogenic intermediates of transthyretin induce apoptosis.
SO - Biochem Biophys Res Commun 2002 Jun 7;294(2):309-14
AD - Department of Cell and Molecular Biology, Umea University, S-901 87
Umea, Sweden.
In diseases like Alzheimer's disease and familial amyloidotic
polyneuropathy (FAP) amyloid deposits co-localize with areas of
neurodegeneration. FAP is associated with mutations of the plasma
protein transthyretin (TTR). We can here show an apoptotic effect of
amyloidogenic mutants of TTR on a human neuroblastoma cell line.
Toxicity could be blocked by catalase indicating a free oxygen radical
dependent mechanism. The toxic effect was dependent on the state of
aggregation and unexpectedly mature fibrils from FAP-patients who failed
to exert an apoptotic response. Morphological studies revealed a
correlation between toxicity and the presence of immature amyloid. Thus,
we can show that toxicity is associated with early stages of fibril
formation and propose that mature full-length fibrils represent an inert
end stage, which might serve as a rescue mechanism. (c) 2002 Elsevier
Science (USA).
12
UI - 11829415
AU - Carlson K; Ehrich M
TI -
Organophosphorus compounds alter intracellular F-actin content in
SH-SY5Y human neuroblastoma cells.
SO - Neurotoxicology 2001 Dec;22(6):819-27
AD - Laboratory of Neurotoxicity Studies, Virginia-Maryland Regional College
of Veterinary Medicine, Blacksburg, VA 24061, USA.
Cytoskeletal components, especially f-actin (filamentous actin), are
responsible for neurite extension and maintenance. Alterations in
neurite length and quality precede in vitro cell death induced by
organophosphorus (OP) compounds and implicate f-actin proteins in this
process. We, therefore, investigated changes in f-actin in SH-SY5Y human
neuroblastoma cells exposed to 0.1 and 1 mM paraoxon, parathion, phenyl
saligenin phosphate (PSP), tri-ortho-tolyl phosphate (TOTP), triphenyl
phosphite (TPPi), and di-isopropyl phosphorofluoridate (DFP) for 0-48 h.
The f-actin was measured by flow cytometry in cells labeled with Alexa
488 phalloidin. The relative amount off-actin was compared to total
protein levels as determined by spectrophotometry. The cellular content
of f-actin significantly decreasedfollowing exposure to PSP (0.1 mM, >30
min; 1 mM, >15 min), TOTP (0.1 mM, 16 h; 1 mM, >15 min), TPPi (1 mM, >4
h), paraoxon (1 mM, >24 h), and parathion (1 mM, 48 h). Exposure to DFP
(0.1 and 1 mM) did not significantly alter f-actin content at any time
point. Exposure to parathion (0.1 mM, 48 h) significantly increased the
amount of cellular f-actin. Total protein was significantly decreased
after exposure to PSP (0.1 and 1 mM, >8 h) and TPPi (1 mM, 48 h).
Significant increases in total protein were observed following exposure
to parathion (0.1 mM, >3 h). Consistent alterations in the protein
content of DFP-exposed samples were not observed. These results suggest
that the loss off-actin is an early event following OP compound exposure
and that this loss significantly precedes a loss of protein content for
some OP compounds (PSP, TPPi). Results also imply that under other
exposure conditions (TOTP, paraoxon, parathion) alterations in the
f-actin content are independent of protein content.
13
UI - 11995062
AU - Gabriel E
TI -
[Nursing care planning in a child with neuroblastoma]
SO - Osterr Krankenpflegez 2000 Oct;53(10):20-5
AD - St. Anna Kinderspital.
14
UI - 11992472
AU - Amoroso S; D'Alessio A; Sirabella R; Di Renzo G; Annunziato L
TI -
Ca(2+)-independent caspase-3 but not Ca(2+)-dependent caspase-2
activation induced by oxidative stress leads to SH-SY5Y human
neuroblastoma cell apoptosis.
SO - J Neurosci Res 2002 May 15;68(4):454-62
AD - Department of Pharmacology, School of Medicine, University of Ancona,
Ancona, Italy. amoroso@unina.it
Continuous and long-lasting exposure to tert-butylhydroperoxide (t-BOOH)
increased the number of apoptotic SH-SY5Y human neuroblastoma cells both
in the presence and in the absence of the intracellular Ca(2+) ion
chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
(BAPTA). In addition, t-BOOH exposure induced activation of CPP32, as
demonstrated by poly-(ADP-ribose) polymerase (PARP) cleavage, and of
ICH-1L caspases. Exposure to t-BOOH also induced a time-dependent
release of cytochrome c. Interestingly, in the presence of BAPTA, CPP32
activation still occurred, whereas ICH-1L activation was blocked.
Ac-DEVD-CHO, an inhibitor of CPP32 activity, prevented the appearance of
apoptotic cells, whereas the inhibitor of ICH-1L activity Z-VDVAD-FMK
did not. Collectively, these findings demonstrate that in SH-SY5Y
neuroblastoma cells exposure to continuous and long-lasting oxidative
stress induced activation of caspase-3 that was independent of
intracellular Ca(2+) ion concentration ([Ca(2+)](i)) elevation but led
to cell apoptosis. In contrast, caspase-2 activation was dependent on
[Ca(2+)](i) increase but did not result in apoptosis. Copyright 2002
Wiley-Liss, Inc.
15
UI - 12095929
AU - Massimo L
TI -
Neuroblastoma: a challenge for pediatric oncology of the third
millennium.
SO - Ann N Y Acad Sci 2002 Jun;963():59-62
AD - Director Emeritus, Department of Pediatric Hematology and Oncology, G.
Gaslini Scientific Children's Hospital, Genoa, Italy.
luisamassimo@yahoo.it
Neuroblastoma is the only cancer of childhood considered in this
conference on hormone-related tumors, because the percentage of deaths
in children with this rare type of cancer is still very high.
Pediatricians feel the need for help from basic researchers to better
understand the biological nature of this disease and to improve
protocols and the challenge of cure.
16
UI - 12095930
AU - Schwab M
TI -
Amplified MYCN in human neuroblastoma: paradigm for the translation of
molecular genetics to clinical oncology.
SO - Ann N Y Acad Sci 2002 Jun;963():63-73
AD - Division of Cytogenetics, Deutsches Krebsforschungszentrum, Im
Neuenheimer Feld 280, D-69120 Heidelberg, Germany. m.schwab@dkfz.de
Increase in the dosage of cellular oncogenes by DNA amplification is a
frequent genetic alteration of cancer cells. In neuroblastoma,
amplification of the gene MYCN has been associated with aggressively
growing cancers and is an indicator for poor prognosis. MYCN
amplification is of predictive value in identifying patients with
neuroblastoma who require specific therapeutic regimens and those who do
not benefit from chemotherapy.
17
UI - 12095931
AU - Perri P; Longo L; McConville C; Cusano R; Rees SA; Seri M; Conte M;
TI -
Romeo G; Devoto M; Tonini GP
Linkage analysis in families with recurrent neuroblastoma.
SO - Ann N Y Acad Sci 2002 Jun;963():74-84
AD - Laboratory of Neuroblastoma Research, Advanced Biotechnology Center,
Genoa, Italy. perri@cba.unige
Neuroblastoma is a neural crest-derived tumor of childhood with a
serious prognosis; only 20% of patients with stage 4 disease survive 5
years from diagnosis. Mechanisms involved in neuroblastoma development
are unclear, but the engagement of many neuroblastoma-related gene(s) is
suggested by specific chromosomal alterations. Most prominent among
these is the amplification of the MYCN oncogene and the deletion of the
1p36 region. Other genetic aberrations have been discovered over the
years such as deletions of 11q and 14q and gain of 17q. Although tumor
aggressiveness greatly depends on the most frequent genetic
abnormalities, to date no neuroblastoma-related gene has been
discovered. Neuroblastoma usually occurs sporadically, but 1.5% of all
diagnosed cases show familial recurrence with an autosomal dominant
inheritance and incomplete penetrance. A comparison between hereditary
and sporadic neuroblastomas led Knudson and Strong to gather that the
two-hit hypothesis, proposed for retinoblastoma, could be applied to
neuroblastoma. To determine if the 1p36 region harbors a predisposition
gene for familial neuroblastoma, we carried out linkage analysis at 1p36
loci in two families with recurrent neuroblastoma. Similarly, we
analyzed loci of chromosome 16, where a predisposition locus was
recently mapped. We also analyzed markers located close to several
candidate genes (RET, NF1, GDNF, GFRA1, EDNRB, and EDN3) involved to a
different extent in other neurocristopathies. Our findings indicate that
the candidate chromosomal regions and genes analyzed are not in linkage
with neuroblastoma.
18
UI - 11867941
AU - Berger A; Tuechler C; Almer D; Kogner P; Ratschek M; Kerbl R; Iismaa TP;
TI -
Jones N; Sperl W; Kofler B
Elevated expression of galanin receptors in childhood neuroblastic
tumors.
SO - Neuroendocrinology 2002 Feb;75(2):130-8
AD - Department of Pediatrics, General Hospital Salzburg, Salzburg, Austria.
The neuropeptide galanin (GAL) has been shown to be present in certain
brain tumors. In order to learn more about GAL and its receptors in
human tumors of the peripheral nervous system, we investigated the
expression of the GAL peptide and the GAL receptors in tumor tissue from
childhood neuroblastic tumors. GAL peptide concentrations up to 674 +/-
166 fmol/mg of tissue were detected by radioimmunoassay, but no
significant correlation with standard tumor markers or the prognosis of
the 14 patients investigated was observed. Ligand binding experiments
showed different levels of GAL binding in all 28 primary neuroblastomas
and 7 ganglioneuromas investigated. All three human GAL receptor
subtypes cloned to date could be detected, with the GALR1 receptor
subtype being expressed most prominently. GAL binding did not
significantly correlate with genetic markers such as unfavorable DNA
ploidy, amplification of the oncogene MYCN and allelic loss of
chromosome 1p. However, low galanin binding was significantly correlated
with survival (p = 0.021) in this limited analysis of neuroblastic tumor
samples. These results raise the possibility that the expression of GAL
binding sites may play a role in neuroblastic tumor biology and
behavior. Copyright 2002 S. Karger AG, Basel
19
UI - 12085233
AU - Noujaim D; van Golen CM; van Golen KL; Grauman A; Feldman EL
TI -
N-Myc and Bcl-2 coexpression induces MMP-2 secretion and activation in
human neuroblastoma cells.
SO - Oncogene 2002 Jul 4;21(29):4549-57
AD - Department of Neurology, University of Michigan, Ann Arbor 48109, USA.
Neuroblastoma is a peripheral nervous system tumor that accounts for
8-10% of all solid childhood tumors. N-Myc is the most reliable
prognostic indicator for neuroblastoma. Bcl-2 is detected in 40-60% of
primary neuroblastoma tumors and demonstrates anti-apoptotic action by
conferring resistance to chemotherapy and radiation treatment. In
neuroblastoma cell lines, the coexpression of N-Myc and Bcl-2 leads to
increased tumorigenic properties. Matrix metalloproteinases (MMPs) are
endopeptidases that degrade a wide range of basement membrane
components, a process important for tumor invasion. This study
investigates the effect of N-Myc and Bcl-2 on MMP expression and
activation. MMP-2 expression and secretion are increased in SHEP
neuroblastoma cells expressing Bcl-2 alone (SHEP/Bcl-2 cells) or both
N-Myc and Bcl-2 (SHEP/N-Myc/Bcl-2 cells). MMP-2 activity is increased in
the SHEP/N-Myc/Bcl-2 cells yet remains unchanged in SHEP/Bcl-2 cells.
TIMP-2 expression is high in SHEP/Bcl-2 cells, which likely inhibits
MMP-2 activity, and absent in SHEP/N-Myc/Bcl-2 cells, allowing MMP-2
activity. Invasion is increased in SHEP/N-Myc/Bcl-2 cells and prevented
by the use of a pharmacologic MMP-2 inhibitor. These data imply that
N-Myc and Bcl-2 cooperate to increase the expression, secretion, and
activation of MMP-2, which likely leads to a more tumorigenic phenotype
due to increased MMP-2 mediated invasion.
20
UI - 12001986
AU - Brooksbank C
TI -
RAS, the magician.
SO - Nat Rev Cancer 2002 Apr;2(4):249
21
UI - 11829154
AU - Jang MH; Shin MC; Kim YJ; Chung JH; Yim SV; Kim EH; Kim Y; Kim CJ
TI -
Protective effects of puerariaeflos against ethanol-induced apoptosis on
human neuroblastoma cell line SK-N-MC.
SO - Jpn J Pharmacol 2001 Dec;87(4):338-42
AD - Departments of Physiology, College of Medicine, Kyung Hee University,
Dongdaemun-gu, Seoul, Korea.
Puerariaeflos (PF) is an oriental medical herb for alcohol abuse. To
investigate whether PF possesses protective effects against ethanol
(EtOH)-induced cytotoxicity in the central nervous system,
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow
cytometric analysis, DNA fragmentation assay, and reverse
transcription-polymerase chain reaction were performed on SK-N-MC human
neuroblastoma cells. Cells treated with EtOH exhibited several apoptotic
features, while those pre-treated with PF prior to EtOH exposure showed
a decreased occurrence of apoptotic features. In addition, PF
pre-treatment inhibited the EtOH-induced increase in caspase-3 mRNA
expression. These results suggest that PF may exert protective effects
against EtOH-induced apoptosis in human neuroblastoma cells.
22
UI - 11822704
AU - Seven M; Karaman B; Hacihanefioglu S; Deviren A; Yuksel A; Basaran S
TI -
Neuroblastoma in a dysmorphic girl with a partial duplication of 2p
caused by an unbalanced translocation.
SO - Clin Dysmorphol 2002 Jan;11(1):39-42
AD - Genetic and Teratology Research Center (GETAM), Cerrahpas Medical
Faculty, Istanbul University, Turkey. mehseven@istanbul.edu.tr
A 1-year-old female child with multiple dysmorphic features including
microcephaly, hypertelorism, a short philtrum, low set ears, a narrow
high arched palate, micrognathia and growth retardation was found to
have a de novo chromosome abnormality including a partial duplication of
the short arm of chromosome 2 and a partial deletion of the long arm of
chromosome 17. The clinical features of the case shared many
similarities to previous reports of trisomy 2p. Three years later,
ecchymotic spots appeared around the left ocular region. Further
clinical and pathological examination confirmed the diagnosis of a
neuroblastoma. This is the first case of an unbalanced translocation,
46, XX, der (17), t (2; 17) (p23; q25), showing the development of a
neuroblastoma in addition to the dysmorphic features. We suggest that
trisomy 2p including the N-myc proto-oncogene may have predisposed the
patient to the development of a neuroblastoma.
23
UI - 11831613
AU - Anderson BD; Mason S; Cheson BD
TI -
Clinical trials referral resource. Current clinical trials in
neuroblastoma.
SO - Oncology (Huntingt) 2002 Jan;16(1):82-4, 86, 89
AD - National Cancer Institute, USA.
24
UI - 12072202
AU - Giordani L; Iolascon A; Servedio V; Mazzocco K; Longo L; Tonini GP
TI -
Two regions of deletion in 9p22- p24 in neuroblastoma are frequently
observed in favorable tumors.
SO - Cancer Genet Cytogenet 2002 May;135(1):42-7
AD - Department of Biomedicina dell'Eta Evolutiva, University of Bari, Bari,
Italy.
Neuroblastoma is a tumor of infancy that presents several chromosomal
abnormalities. Nonrandom deletion of chromosome arm 9p has been
identified in primary neuroblastoma suggesting the presence of a tumor
suppressor gene located on this chromosome. In previous work, we showed
that CDKN2A and CDKN2B genes, mapped at 9p21, were not deleted in
neuroblastoma cells. In the present article, we refine the deleted
region of 9p using polymerase chain reaction-based analysis of highly
polymorphic simple sequence repeats and a two color fluorescence in situ
hybridization technique on interphase nuclei. We analyzed 71 primary
tumors of patients at the onset of the disease. We found loss of
heterozygosity (LOH) in 16 of 71 (23%) cases; the frequency of LOH for
9p was higher (28%) in favorable stages 1, 2, and 4s than in unfavorable
stages 3 and 4 (14%). Our results identify two regions of frequent
allelic loss: the first at the locus D9S1849 and the second at the locus
D9S157. These regions appear to be distant from CDKN2A and CDKN2B loci
suggesting that other genes may be involved in 9p deletion. Finally, our
data show that 9p deletion is more frequent in tumors of patients with a
favorable prognosis, indicating that deleted genes may not be crucial
for tumor progression.
25
UI - 12094652
AU - Popko E; Popko M; Famulski W
TI -
[Esthesioneuroblastoma of nasal cavity and ethmoid sinus]
SO - Otolaryngol Pol 2002;56(2):235-7
AD - Katedra i Klinika Otolaryngologii AM w Bialymstoku.
This paper presents a rarely occurring tumor of nasal cavity and ethmoid
sinus (esthesioneuroblastoma--2nd grade of the pathological grading
system proposed by Hyams). It was observed in a woman aged 68. Moreover,
there were described surgical therapy and repair of cerebral spinal
fluid leaks using composite bone/mucosal graft of the lower turbinate as
a donor material. The treatment was successful.
26
UI - 11820738
AU - Akudugu JM; Bohm L
TI -
Micronuclei and apoptosis in glioma and neuroblastoma cell lines and
role of other lesions in the reconstruction of cellular
radiosensitivity.
SO - Radiat Environ Biophys 2001 Dec;40(4):295-300
AD - Department of Radiation Oncology, Faculty of Medical Sciences and
Tygerberg Hospital, University of Stellenbosch, South Africa.
It is now well established that micronuclei frequency does not always
rank cell lines according to radiosensitivity. There is, however, a
growing interest in reconstructing cellular radiosensitivity (measured
by colony assay) from concurrent micronucleus and apoptosis data. Using
a variety of radiosensitive and radioresistant cell lines, we have
derived a missing parameter--Poe, the probability of cell death by other
events such as small deletions, chromosome aberrations, late apoptosis
and necrosis which are undetectable by micronucleus and apoptosis assays
performed at a single time point. In the radioresistant glioma cell
lines G120, G60, G28, G44 and G62 (SF2 > or =0.59), a characteristic
threshold dose exists above which cell loss due to undetectable lesions
occurs. In the radiosensitive SK-N-SH and KELLY cell lines (SF2 < or
=0.43), the Poe parameter is positive at very low doses, reaches a
maximum and declines at higher doses. In the radiation resistant G28
cells, Poe was found to be below zero for doses up to 6 Gy. In the G62,
G44 and G120 cell lines, the threshold doses to induce Poe events were
0.87, 3.04 and 3.85 Gy, respectively. Cell death by undetectable lesions
is a cell-specific and time-dependent variable. Micronucleus and
apoptosis assays performed concurrently and at a specific time point
miss cell death due to other events and this may be the reason why
reconstruction of cellular radiosensitivity from micronucleus and
apoptosis data fails.
27
UI - 12115498
AU - Rapella A; Negrioli A; Melillo G; Pastorino S; Varesio L; Bosco MC
TI -
Flavopiridol inhibits vascular endothelial growth factor production
induced by hypoxia or picolinic acid in human neuroblastoma.
SO - Int J Cancer 2002 Jun 10;99(5):658-64
AD - Laboratory of Molecular Biology, G. Gaslini Institute, Genoa, Italy.
Human neuroblastoma (NB) tumors elaborate angiogenic peptides, and
enhanced angiogenesis correlates with their aggressive behavior,
metastatic spread and poor clinical outcome. Hence, inhibition of
angiogenic factor production may represent a potential therapeutic
target for NB treatment. There is currently little information regarding
the stimuli that control NB production of angiogenic mediators. In this
study, we analyzed the effects of hypoxia, a common feature of solid
tumors and a major drive to tumor angiogenesis, and of PA, a tryptophan
catabolite produced under inflammatory conditions and endowed with
several biologic properties, on the production of the angiogenic
activator VEGF by advanced-stage human NB cell lines. We demonstrate
that both stimuli are potent inducers of VEGF expression and secretion.
VEGF upregulation by PA involved iron chelation because iron sulfate
prevented this effect whereas the iron-chelating agent DFX induced VEGF
production. Conversely, the CDK inhibitor Flp completely blocked VEGF
induction by hypoxia. This effect occurred as early as 3 hr after
stimulation and did not require de novo protein synthesis. Moreover, Flp
exerted similar inhibitory activity on VEGF induction by PA or DFX,
suggesting that this compound targets an essential step in the signaling
pathway that leads to VEGF expression. Our findings demonstrate that PA
can modulate angiogenic factor production by tumor cells and establish
the importance of Flp as an inhibitor of VEGF production by human NB.
Copyright 2002 Wiley-Liss, Inc.
28
UI - 12108315
AU - Chauty A; Raimondo G; Vergeron H; Branchereau S; Dessemme P; Devictor D;
TI -
Hartmann O
[Discovery of a neuroblastoma producing cardiogenic shock in a
2-month-old child]
SO - Arch Pediatr 2002 Jun;9(6):602-5
AD - Departement de pediatrie, institut Gustave-Roussy, 94805 Villejuif,
France.
CASE REPORT: A two-month-old male child presented a severe heart failure
associated with a malignant hypertension. Abdominal ultrasound revealed
a mass connected to the left adrenal gland. CT scan showed a tumor of 7
x 6 x 8 cm, forcing back both the left kidney and the aorta. A biopsy
allowed the diagnosis of neuroblastoma without MYCN oncogene
amplification. Intensive care stabilized the hemodynamic situation.
Under chemotherapy the tumor volume decreased significantly and complete
surgical excision became possible. Three years after diagnosis, the
patient remained in complete remission. CONCLUSION: Clinical
presentation of this neuroblastoma was extremely uncommon. The
catecholamines produced by the tumoral cells could induce an increase of
the myocardiac work following the left ventricule post charge increase.
Theses mechanisms could be synergistic for a myocardial exhaustion.
29
UI - 11859407
AU - Casciano I; Mazzocco K; Boni L; Pagnan G; Banelli B; Allemanni G;
TI -
Ponzoni M; Tonini GP; Romani M
Expression of DeltaNp73 is a molecular marker for adverse outcome in
neuroblastoma patients.
SO - Cell Death Differ 2002 Mar;9(3):246-51
AD - Laboratory of Population Genetics, Istituto Nazionale per la Ricerca sul
Cancro (IST), Largo Rosanna Benzi 10, 16132 Genova, Italy.
The p73 gene is a p53 homologue which induces apoptosis and inhibits
cell proliferation. Although p73 maps at 1p36.3 and is frequently
deleted in neuroblastoma (NB), it does not act as a classic
oncosuppressor gene. In developing sympathetic neurons of mice, p73 is
predominantly expressed as a truncated anti-apoptotic isoform
(DeltaNp73), which antagonizes both p53 and the full-length p73 protein
(TAp73). This suggests that p73 may be part of a complex tumor-control
mechanism. To determine the role of DeltaNp73 in NB we analyzed the
pattern of expression of this gene in vivo and evaluated the prognostic
significance of its expression. Our results indicate that DeltaNp73
expression is associated with reduced apoptosis in a NB tumor tissue.
Expression of this variant in NB patients significantly correlates with
age at diagnosis and VMA urinary excretion. Moreover it is strongly
associated with reduced survival (HR=7.93; P<0.001) and progression-free
survival (HR=5.3; P<0.001) and its role in predicting a poorer outcome
is independent from age, primary tumor site, stage and MYCN
amplification (OS: HR=5.24, P=0.012; PFS: HR=4.36, P=0.005). In
conclusion our data seem to indicate that DeltaNp73 is a crucial gene in
neuroblastoma pathogenesis.
30
UI - 12027962
AU - Paice JA
TI -
Pain and suffering in an adolescent with neuroblastoma.
SO - Cancer Pract 2002 May-Jun;10 Suppl 1():S4-8
AD - Northwestern University, Medical School, Division of
Hematology-Oncology, Northwestern Memorial Hospital, Chicago, Illinois,
USA.
31
UI - 11607767
AU - Kushner BH; Cheung NK; Kramer K; Dunkel IJ; Calleja E; Boulad F
TI -
Topotecan combined with myeloablative doses of thiotepa and carboplatin
for neuroblastoma, brain tumors, and other poor-risk solid tumors in
children and young adults.
SO - Bone Marrow Transplant 2001 Sep;28(6):551-6
AD - Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New
York, NY 10021, USA.
Topotecan appears to be relatively unaffected by the most common
multidrug resistance mechanisms, may potentiate cytotoxicity of
alkylators, has good penetration into the central nervous system, is
active against a variety of neoplasms, and has myelosuppression as its
paramount toxicity. We present our experience with a myeloablative
regimen that includes topotecan. Twenty-one patients with poor-prognosis
tumors and intact function of key organs received topotecan 2 mg/m2 by
30-min intravenous (i.v.) infusion on days -8, -7, -6, -5, -4; thiotepa
300 mg/m2 by 3 h i.v. infusion on days -8, -7, -6; and carboplatin by 4
h i.v. infusion on days -5, -4, -3 with a daily dose derived from the
pediatric Calvert formula, using a targeted area under the curve of
seven mg/ml* min ( approximately 500 mg/m2/day). Stem cell rescue was on
day 0. The patients were 1 to 29 (median 4) years old; 18 were in
complete remission (CR) and three in partial remission (PR). Early
toxicities were severe mucositis and erythema with superficial peeling
in all patients and a seizure, hypertension, and renal insufficiency
followed by veno-occlusive disease in one patient each. Post-transplant
treatment included radiotherapy alone (four patients) or plus biological
agents (11 patients with neuroblastoma). With a follow-up of 6+ to 32+
(median 11+) months, event-free survivors include 10/11 neuroblastoma
patients (first CR), 4/5 brain tumor patients (second PR or CR), 1/3
patients with metastatic Ewing's sarcoma (first or second CR), and a
patient transplanted for multiply recurrent immature ovarian teratoma; a
patient with desmoplastic small round-cell tumor (second PR) had
progressive disease at 8 months. Favorable results for disease control,
manageable toxicity, and the antitumor profiles of topotecan, thiotepa,
and carboplatin, support use of this three-drug regimen in the treatment
of neuroblastoma and brain tumors; applicability to other tumors is
still uncertain.
32
UI - 11506485
AU - Anderson J; Kempski H; Hill L; Rampling D; Gordon T; Michalski A
TI -
Neuroblastoma in monozygotic twins--a case of probable twin-to-twin
metastasis.
SO - Br J Cancer 2001 Aug 17;85(4):493-6
AD - Unit of Molecular Haematology, Institute of Child Health, Great Ormond
Street Hospital for Children NHS Trust, London, UK.
Concordance for neuroblastoma in monozygotic twins has been reported
only rarely, and the cause of the shared pathology has not been
established. We describe a case of infant monozygotic twins developing
tumours that were morphologically, clinically and molecularly
indistinguishable, but with a delay of 6 months between times of
presentation. Both tumours were metastatic and had amplification of MYCN
and deletion at 1p36. Twin 1, who developed neuroblastoma first, had
constitutional karyotype abnormalities in at least 5% of peripheral
blood mononuclear cells involving 1p and 3p, and a deletion of 1q44 in
21% of cells. Twin 2 had a normal constitutional karyotype and lacked
rearrangement or deletion of these regions. We propose an acquired
neuroblastoma predisposition specific for twin 1, and in utero
metastatic spread of tumour cells to twin 2 via the shared placental
circulation. Copyright 2001 Cancer Research Campaign.
33
UI - 12115395
AU - Cheung IY; Lo Piccolo MS; Collins N; Kushner BH; Cheung NK
TI -
Quantitation of GD2 synthase mRNA by real-time reverse
transcription-polymerase chain reaction: utility in bone marrow purging
of neuroblastoma by anti-GD2 antibody 3F8.
SO - Cancer 2002 Jun 1;94(11):3042-8
AD - Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New
York, New York 10021, USA. cheungi@mskcc.org
BACKGROUND: Antigen ganglioside GD2 is expressed abundantly on
neuroblastoma (NB) cells. Anti-GD2 monoclonal antibody (MoAb) 3F8 kills
NB cells by complement-dependent cytotoxicity and antibody-dependent
cellular cytotoxicity. Its utility in bone marrow (BM) purging is
evaluated by a real-time reverse transcription-polymerase chain reaction
(RT-PCR) assay to quantify the mRNA of GD2 synthase, the key enzyme in
GD2 synthesis. METHODS: From 1990 to 1993, 10 patients with
relapsed/refractory Stage 4 NB participated in a pilot study. In these
patients, MoAb 3F8 was used to purge tumor cells from harvested BM that
had 5% or less tumor content by immunofluorescence (IF). Subsequently,
31 Stage 4 NB patients who underwent treatment on the N7 protocol
(1994-1999) had their BM, which was in remission, purged by 3F8 before
(131)I-3F8 myeloablative radioimmunotherapy. GD2-positive tumor cells
before and after purging were quantified by real-time quantitative
RT-PCR of GD2 synthase. RESULTS: GD2 positivity by IF was found before
purging in six of eight patients in the pilot study. Five of six
patients became negative postpurging. Of 31 patients on the N7 protocol,
the more sensitive real-time quantitative RT-PCR detected GD2 synthase
mRNA in the BM samples of 7 patients even though the prepurge BM samples
were negative by histology and IF. Six of the seven BM samples became
negative after 3F8 purging. Marker positivity before purging was
statistically significant in predicting overall survival (P = 0.04), but
not progression-free survival (P = 0.1). In vitro hematopoietic stem
cell recovery and the median time to engraftment were acceptable.
CONCLUSION: Tumor cell depletion quantified by real-time RT-PCR
demonstrated efficacy of MoAb 3F8 in BM purging. Copyright 2002 American
Cancer Society.
34
UI - 12116069
AU - Crazzolara R; Abrederis K; Kreczy A; Meister B
TI -
Reply to Langer et al. Expression of vascular endothelial growth factor
(VEGF) and VEGF receptors in human neuroblastomas.
SO - Med Pediatr Oncol 2002 Aug;39(2):146
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