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Abramson Cancer CenterNCI CANCERLIT® Search: Neuroblastoma - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Pepper syndrome, truncus arteriosus communis and abnormal pulmonary venous return: an unusual association.
- Localization of the 17q breakpoint of a constitutional 1;17 translocation in a patient with neuroblastoma within a 25-kb segment
- Expression of the periostin mRNA level in neuroblastoma.
- Detection of N-myc amplification by FISH in immature areas of fixed neuroblastomas: more efficient than Southern blot/PCR.
- Comparison of the cell immunophenotype of metastatic and primary foci in stage IV-S neuroblastoma.
- GADD153 and 12-lipoxygenase mediate fenretinide-induced apoptosis of neuroblastoma.
- Detection procedures for neuroblastoma cells metastatic to blood and bone marrow: blinded comparison of chromogranin A heminested reverse
- Vanadate protects human neuroblastoma SH-SY5Y cells against peroxynitrite-induced cell death.
- Contribution of MAP kinase pathways to the activation of ATF-2 in human neuroblastoma cells.
- Infrequent mutations of the activating transcription factor-2 gene in human lung cancer, neuroblastoma and breast cancer.
- Esthesioneuroblastoma and cervical lymph node metastases: clinical and therapeutic implications.
- Molecular profiling of high-risk neuroblastoma by cDNA array.
- Hydroxyl free radicals induce cell differentiation in SK-N-MC neuroblastoma cells.
- Caspase 3 expression is altered in a coculture model of neuroblastoma.
- Primary paratesticular neuroblastoma.
- Glial cell line-derived neurotrophic factor up-regulates the expression of tyrosine hydroxylase gene in human neuroblastoma cell lines.
- Induced neuroblastoma cell differentiation, associated with transient HES-1 activity and reduced HASH-1 expression, is inhibited by Notch1.
- Retroperitoneoscopic adrenalectomy in a residual of neuroblastoma.
- Cholesterol-dependent modulation of the toxicity of HIV-1 coat protein gp120 in human neuroblastoma cells.
- Genetic parameters of neuroblastomas.
- Presenilin-1 mutations alter K+ currents in the human neuroblastoma cell line, SH-SY5Y.
- Ca(2+)-independent caspase-3 but not Ca(2+)-dependent caspase-2 activation induced by oxidative stress leads to SH-SY5Y human
- Antiproliferative effect of nitric oxide on epidermal growth factor-responsive human neuroblastoma cells.
- Progressive spinal lordosis after laminoplasty in a child with thoracic neuroblastoma.
- [Effect of interleukins and somatomedins on the production of neurotensin by cell line SH-SY5Y derived from human neuroblastoma]
- [Detection of Alzheimer type pathological epitopes on Tau proteins of neuroblastoma cells after treatment with okadaic acid]
- [Olfactory esthesioneuroblastoma with an ophtalmological presentation: a case report]
- Esthesioneuroblastoma: irradiation alone and surgery alone are not enough.
Table of Contents
1
UI - 11954746
AU - Nouet N; Doz F; Dessemme P; Lacaille F; Bonnet D
TI -
Pepper syndrome, truncus arteriosus communis and abnormal pulmonary
venous return: an unusual association.
SO - Eur J Pediatr 2002 Feb;161(2):114-5
2
UI - 12203774
AU - Van Roy N; Vandesompele J; Berx G; Staes K; Van Gele M; De Smet E; De
TI -
Paepe A; Laureys G; van der Drift P; Versteeg R; Van Roy F; Speleman F
Localization of the 17q breakpoint of a constitutional 1;17
translocation in a patient with neuroblastoma within a 25-kb segment
located between the ACCN1 and TLK2 genes and near the distal breakpoints
of two microdeletions in neurofibromatosis type 1 patients.
SO - Genes Chromosomes Cancer 2002 Oct;35(2):113-20
AD - Department of Medical Genetics, Ghent University Hospital, Ghent,
Belgium.
We have constructed a 1.4-Mb P1 artificial chromosome/bacterial
artificial chromosome (PAC/BAC) contig spanning the 17q breakpoint of a
constitutional translocation t(1;17)(p36.2;q11.2) in a patient with
neuroblastoma. Three 17q breakpoint-overlapping cosmids were identified
and sequenced. No coding sequences were found in the immediate proximity
of the 17q breakpoint. The PAC/BAC contig covers the region between the
proximally located ACCN1 gene and the distally located TLK2 gene and
SCYA chemokine gene cluster. The observation that the 17q breakpoint
region could not be detected in any of the screened yeast artificial
chromosome libraries and the localization of the 17q breakpoint in the
vicinity of the distal breakpoints of two microdeletions in patients
with neurofibromatosis type 1 suggest that this chromosomal region is
genetically unstable and prone to rearrangements. Copyright 2002
Wiley-Liss, Inc.
3
UI - 12194119
AU - Sasaki H; Sato Y; Kondo S; Fukai I; Kiriyama M; Yamakawa Y; Fuji Y
TI -
Expression of the periostin mRNA level in neuroblastoma.
SO - J Pediatr Surg 2002 Sep;37(9):1293-7
AD - Department of Surgery II, Nagoya City University Medical School, Nagoya,
Japan.
BACKGROUND: Neuroblastoma is the most common malignant solid tumor in
early childhood. Whether neuroblastoma is diagnosed by mass screening or
by clinical symptom, it has been reported to be correlated with
prognosis of the disease. The periostin protein shares structural and
sequence homology with fasciclin I, which is an insect adhesion
molecule. METHODS: Expression of periostin messenger RNAs were evaluated
by real-time reverse transcription polymerase chain reaction (RT-PCR)
assay in 24 tumor samples from neuroblastoma using LightCycler. The data
were analyzed in reference to clinicopathologic factors. RESULTS: There
was a tendency for higher periostin transcripts levels in the tumor
samples from stage IV when compared with the stage I (P =.0845). The
periostin mRNA level was higher in the group with disease diagnosed by
symptom than in the group with disease diagnosed by mass screening (P
=.0266). The periostin mRNA level also was higher in the group with
disease diagnosed after 1 year of age than in the group with disease
diagnosed before 1 year of age (P =.0059). CONCLUSION: Because the
groups with disease diagnosed by symptom or after 1 year of age were
reported to be the worse prognosis, the periostin mRNA expression levels
were correlated with tumor progression or prognosis of neuroblastoma.
Copyright 2002, Elsevier Science (USA). All rights reserved.
4
UI - 12210067
AU - Sartelet H; Grossi L; Pasquier D; Combaret V; Bouvier R; Ranchere D;
TI -
Plantaz D; Munzer M; Philip T; Birembaut P; Zahm JM; Bergeron C;
Gaillard D; Pasquier B
Detection of N-myc amplification by FISH in immature areas of fixed
neuroblastomas: more efficient than Southern blot/PCR.
SO - J Pathol 2002 Sep;198(1):83-91
AD - Department of Pathology, CHU de Grenoble, 38043 Grenoble Cedex 09,
France.
N-myc amplification is a major prognostic factor in neuroblastomas and
is systematically investigated by Southern blot or polymerase chain
reaction (PCR). A retrospective study of N -myc amplification has been
carried out using fluorescence in situ hybridization (FISH) in 97 fixed
neuroblastomas. For each tumour, FISH was performed on the area that
contained the most immature neuroblasts. Among these 97 neuroblastomas,
16 were amplified and 12 were not interpretable. FISH was not
interpretable in six cases. All neuroblastomas with N-myc amplification
detected by Southern blot/PCR were amplified with FISH, except three
that were not interpretable. Four tumours that were not interpretable in
Southern blot/PCR contained more than five copies of N-myc by FISH: one
was aneuploid and three were truly amplified, containing more than ten
copies of N-myc. Among these three patients, two died in a short time of
their tumours. Ten cases were not amplified by Southern blot/PCR and
showed more than five copies by FISH: four were aneuploid and two showed
heterogeneous amplification, with a few cells clearly amplified whereas
most were not. Four cases were amplified, of which two patients died of
their tumours. This study confirms that when applied to the most
immature areas of fixed neuroblastomas, FISH displayed a higher
sensitivity than molecular techniques (p < 0.001) and could detect
heterogeneous amplification. FISH could therefore become an important
complementary procedure in assessing prognosis in neuroblastomas.
Copyright 2002 John Wiley & Sons, Ltd.
5
UI - 12219840
AU - Nowicki M; Miskowiak B
TI -
Comparison of the cell immunophenotype of metastatic and primary foci in
stage IV-S neuroblastoma.
SO - Folia Histochem Cytobiol 2002;40(3):297-303
AD - Department of Paediatric Haematology and Oncology, Institute of
Paediatrics, University of Medical Sciences, Poznan, Poland.
mapar@eucalyptus.usoms.poznan.pl
Neuroblastoma represents one of the most frequently developing malignant
solid tumours in children. At the time of diagnosis, in more than half
of the cases, metastatic cells are also present in the bone marrow. The
present study was aimed at immunocytochemical analysis of selected
neuropeptide manifestation in metastatic cells of neuroblastoma in bone
marrow and at comparing the obtained results with the immunophenotype of
parental neuroblastoma cells. The studies were performed on bone marrow
material obtained from children treated at the Department of Paediatric
Haematology and Oncology, University of Medical Sciences, Poznan,
Poland, in 1998-2000. Immunocytochemical analysis of nervous tissue
markers (employing the immunomax technique) involved 36 bone marrow
preparations obtained from 27 children. The analysis included expression
of neuron-specific enolase (NSE), PGP 9.5 protein, substance P (SP),
chromogranin A (ChA), bombesin (B), galanin (G), neuropeptide Y (NPY)
and vasoactive intestinal peptide (VIP). Close to 90% metastatic cells
in bone marrow were found to exhibit NSE+SP+B+ phenotype and over a half
of the cells manifested additionally expression of PGP 9.5+ChA+NPY+.
Comparison of the obtained results with the immunophenotype of
neuroblastoma cells obtained directly from the primary tumour
demonstrated high correlation of NSE, SP and PGP 9.5 expression. Due to
the relative ease of obtaining the bone marrow material and absence of
neuromarkers in bone marrow metastatic cells in solid tumours other than
neuroblastoma, determination of immunophenotype of the cells may
represent a valuable supplementation in preliminary diagnosis of this
tumour in children.
6
UI - 12234979
AU - Lovat PE; Oliverio S; Ranalli M; Corazzari M; Rodolfo C; Bernassola F;
TI -
Aughton K; Maccarrone M; Hewson QD; Pearson AD; Melino G; Piacentini M;
Redfern CP
GADD153 and 12-lipoxygenase mediate fenretinide-induced apoptosis of
neuroblastoma.
SO - Cancer Res 2002 Sep 15;62(18):5158-67
AD - Department of Child Health, University of Newcastle upon Tyne, Newcastle
upon Tyne, NE2 4HH, United Kingdom.
The synthetic retinoid fenretinide induces apoptosis of neuroblastoma
cells and in vitro acts synergistically with chemotherapeutic drugs used
to treat neuroblastoma. The mechanisms of fenretinide-induced cell death
of neuroblastoma cells are complex, involving cellular signaling
pathways as yet incompletely defined but, in part, involving the
generation of reactive oxygen species (ROS). In an attempt to
characterize the mechanism of action of fenretinide, cDNA array filters
were screened to identify apoptotic genes regulated in response to
treatment of SH-SY5Y cells with fenretinide. Expression of the
stress-induced transcription factor, GADD153, was up-regulated at both
the protein and mRNA levels in response to fenretinide. Overexpression
of GADD153 increased apoptosis in the presence and absence of
fenretinide, whereas reduced expression of GADD153 by expression of
antisense DNA abrogated the response to fenretinide. Although
fenretinide is a partial retinoic acid receptor (RAR)-beta/gamma
agonist, RARbeta/gamma antagonists did not block the induction of
GADD153 by fenretinide; conversely, the induction of GADD153 was blocked
by antioxidants. Enzyme inhibitors were used to identify pathways
mediating the ROS-dependent effects of fenretinide: inhibitors of
phospholipase A(2) and lypoxygenases (LOX), and specific inhibitors of
12-LOX, but not 5-LOX or 15-LOX, inhibited the induction of ROS,
apoptosis, and GADD153 in response to fenretinide. The inhibition of ROS
and apoptosis was reversed by the addition of the 12-LOX products, 12
(S)-hydroperoxyeicosatetraenoic acid (12-HpETE) and 12
(S)-hydroxyeicosatetraenoic acid (12-HETE). Fenretinide did not increase
free arachidonic acid levels, but increased LOX activity without a
detectable increase in 12-LOX protein. These results suggest that
fenretinide induces apoptosis via RAR-dependent and -independent
pathways in which the RAR-independent pathway is characterized by a
fenretinide-dependent increase in 12-LOX activity, leading to the
induction of GADD153. The targeting of 12-LOX and/or GADD153 in
neuroblastoma cells may thus present a novel pathway for the development
of drugs inducing apoptosis of neuroblastoma with improved tumor
specificity.
7
UI - 12045713
AU - Pagani A; Macri L; Faulkner LB; Tintori V; Paoli A; Garaventa A;
TI -
Bussolati G
Detection procedures for neuroblastoma cells metastatic to blood and
bone marrow: blinded comparison of chromogranin A heminested reverse
transcription polymerase chain reaction to tyrosine hydroxylase nested
reverse transcription polymerase chain reaction and to anti-GD2
immunocytology.
SO - Diagn Mol Pathol 2002 Jun;11(2):98-106
AD - Department of Biomedical Sciences and Human Oncology, University of
Torino, Italy/ASL10, Pathology Service, Pinerolo, Italy.
Specific and sensitive tumor cell detection is becoming increasingly
important for diagnosing and staging as well as for the therapeutic
management of neuroblastoma patients. We propose a chromogranin A
heminested reverse transcription polymerase chain reaction (CgA hn
RT-PCR) procedure for the detection of neuroblastoma minimal residual
disease in peripheral blood and bone marrow samples. The results were
checked in comparison with the presently available procedures (i.e.,
with the tyrosine hydroxylase nested RT-PCR [TH n RT-PCR] and with the
immunocytochemical approach using anti-GD2 antibodies). Controls from
healthy patients or from people with unrelated disease (12 samples of
bone marrow and 23 samples of peripheral blood) and serial dilution
experiments using neuroblastoma cell lines (SKNLP, SKNFI, STA6, STA8)
showed CgA hn RT-PCR full specificity and sensitivity ranging from 10(3)
to 10(6) (depending on the cell line). The results compared favorably
with those obtained using TH n RT-PCR. Preliminary data obtained
analyzing bone marrow and peripheral blood specimens from stage IV
neuroblastomas showed substantially overlapping results between CgA and
TH n RT-PCR procedures. Our data support the potential usefulness of CgA
heminested RT-PCR as a specific and sensitive procedure for minimal
disease detection in neuroblastoma. A prospective evaluation of this
tool in clinical studies might be warranted.
8
UI - 11968012
AU - Saeki M; Maeda S; Kamisaki Y
TI -
Vanadate protects human neuroblastoma SH-SY5Y cells against
peroxynitrite-induced cell death.
SO - J Cell Biochem 2002;85(4):721-7
AD - Department of Pharmacology, Graduate School of Dentistry, Osaka
University, Osaka, Japan. msaeki@dent.osaka-u.ac.jp
We investigated the effect of vanadate, a tyrosine phosphatase
inhibitor, on cell death induced by peroxynitrite in human neuroblastoma
SH-SY5Y cells. Vanadate prevented cell death induced by
3-morpholinosydnonimine (SIN-1), a peroxynitrite donor; whereas
SIN-1-induced cell death was not prevented by neither okadaic acid, an
inhibitor of serine/threonine phosphatases 1 and 2A, nor cyclosporin A,
an inhibitor of serine/threonine phosphatase 2B. Vanadate did not
prevent cell death induced by
N-ethyl-2-(1-ethyl-hydroxy-2-nitrosohydrazino)-ethanamine, a nitric
oxide donor. Wortmannin, an inhibitor of phosphatidylinositol 3-kinase
(PI3-kinase), did not block the protective effect of vanadate,
suggesting that the protective effect of vanadate is independent on
PI3-kinase. Vanadate increased tyrosine phosphorylation of several
proteins including the focal adhesion protein p130 Crk-associated
substrate (p130(cas)). By the treatment with SIN-1, the endogenous
association of p130(cas) and Crk was disrupted, and the association was
restored by vanadate treatment. These results suggest that disruption of
tyrosine phosphorylation signaling may be critical for
peroxynitrite-induced cell death, and that vanadate prevents cell death
at least in part through the enhancement in tyrosine phosphorylation of
the proteins including p130(cas). Copyright 2002 Wiley-Liss, Inc.
9
UI - 10823586
AU - Tindberg N; Porsmyr-Palmertz M; Simi A
TI -
Contribution of MAP kinase pathways to the activation of ATF-2 in human
neuroblastoma cells.
SO - Neurochem Res 2000 Apr;25(4):527-31
AD - Institute of Environmental Medicine, Division of Molecular Toxicology,
Karolinska Institutet, Stockholm, Sweden. nictin@ki.se
Activated Transcription Factor-2 (ATF-2) is important during development
of and during injury to the brain. Both Jun N-terminal Kinases (JNKs)
and p38 Mitogen-Activated Protein Kinases (p38MAPKs) may phosphorylate
ATF-2, but the contribution of these two pathways in cells has never
been investigated. We have assayed endogenous p38MAPK activity in
SK-N-MC and SH-SY5Y human neuroblastoma cells for activation of a
GAL4/ATF-2 fusionprotein, by means of titrations of transfected
expression plasmids and by using the p38MAPK inhibitor SB203580. It was
found that basal activation of ATF-2 was independent of p38MAPK and that
whereas MAPK kinase-3 (MKK3) was a weak inducer of ATF-2 activation, it
was a potent activator of the stress activated transcription factor
CHOP. In contrast, ATF-2 was very potently activated by the JNK pathway
activator MAPK kinase kinase-1 (MEKK1). Thus, kinases downstream of
MEKK1 appear relevant, but it is unlikely that p38MAPKs contribute
quantitatively to activation of ATF-2 in these cells.
10
UI - 11836564
AU - Woo IS; Kohno T; Inoue K; Ishii S; Yokota J
TI -
Infrequent mutations of the activating transcription factor-2 gene in
human lung cancer, neuroblastoma and breast cancer.
SO - Int J Oncol 2002 Mar;20(3):527-31
AD - Biology Division, National Cancer Center Research Institute, Tokyo
104-0045, Japan.
The activating transcription factor 2 (ATF-2) gene, which encodes a
transcription factor involved in multiple intracellular signal
transduction pathways, is located on human chromosome 2q32, which is a
common region of LOH in human lung cancer. In neuroblastoma and breast
cancer, a high incidence of LOH was detected on chromosome 2q. Recently
we found that breast cancer is frequently developed in heterozygous
mutant mice for the ATF-2 gene. Therefore, the ATF-2 gene was considered
as a candidate tumor suppressor gene on 2q. To assess the role of the
ATF-2 gene as a tumor suppressor in human carcinogenesis, we examined
genetic alterations of the ATF-2 gene in 9 breast cancer cell lines, 10
neuroblastoma cell lines and 46 lung cancer cell lines. For this
purpose, we first determined the exon-intron structure of the ATF-2 gene
in the human genome. The ATF-2 gene was composed of 14 exons and 13
introns, and the ATG start codon and the TGA stop codon were present in
exons 3 and 14, respectively. Genetic variants of the ATF-2 gene were
detected in 5 of the 46 (10.6%) lung cancers, but not in neuroblastomas
and breast cancers. Three of the five variants detected in lung cancers
were genetic polymorphisms, while the remaining two, consisting of
non-synonymous and synonymous substitutions, were possibly somatic
mutations. The present result indicates that the ATF-2 gene is not a
major tumor suppressor gene on chromosome 2q, however, it is possible
that ATF-2 alterations may be involved in the development of a small
subset of lung cancers.
11
UI - 11936917
AU - Rinaldo A; Ferlito A; Shaha AR; Wei WI; Lund VJ
TI -
Esthesioneuroblastoma and cervical lymph node metastases: clinical and
therapeutic implications.
SO - Acta Otolaryngol 2002 Mar;122(2):215-21
AD - Department of Otolaryngology-Head and Neck Surgery, University of Udine,
Policlinico Universitario, Italy.
12
UI - 11956663
AU - Sardi I; Tintori V; Marchi C; Veltroni M; Lippi A; Tucci F; Tamburini A;
TI -
Bernini G; Faulkner L
Molecular profiling of high-risk neuroblastoma by cDNA array.
SO - Int J Mol Med 2002 May;9(5):541-5
AD - Unita di Oncoematologia, Ospedale Pediatrico A. Meyer, via L. Giordano
13, 50132 Florence, Italy. iacoposardi@hotmail.com
The aim of this study was to investigate gene expression changes in
disseminated neuroblastoma by cDNA array technique. Three stage IV
neuroblastomas and one neuroblastoma cell line (SK-N-FI) were analyzed.
Expression profiles were confirmed by semiquantitative RT-PCR and in
some instances by Northern blotting. Comparison of expression profiles
identified several genes which were highly expressed as well as some
which were down-regulated in tumor samples relatively to SK-N-FI cells.
The tumors studied lacked N-myc overexpression, while showing
up-regulation of basic transcription factors, growth factors and
receptors such as NSEP, c-myc binding protein MM1, thymosin beta10
(TMSB10), TNF-R superfamily member 10A (TNFRSF10A) and FZ9. These
results suggest that cDNA array technology is a powerful tool to
identify a set of genes involved in neuroblastoma genesis and
progression. Thus, the sensitive cDNA array may provide new insight into
many aspects of pediatric tumors and play crucial role in the
administration of adjuvant therapy of patients with neuroblastoma.
13
UI - 11989968
AU - Oravecz K; Kalka D; Jeney F; Cantz M; Zs-Nagy I
TI -
Hydroxyl free radicals induce cell differentiation in SK-N-MC
neuroblastoma cells.
SO - Tissue Cell 2002 Feb;34(1):33-8
AD - Department of Gerontology, University of Debrecen, Medical and Health
Science Center, Faculty of Medicine, Hungary.
The SK-N-MC cell line is frequently used as a model of neuronal
differentiation induced by 5-bromodeoxyuridine (BrdU). In this study,
the differentiation properties of this cell line were investigated under
hydroxyl free radical generation, and compared to BrdU treatment.
Hydroxyl free radicals were generated in the cultures by the Fenton
reaction, i.e. by simultaneous addition of ADP-Fe2+ complex and H2O2.
Microscopic morphological signs, as well as the acetylcholinesterase and
ganglioside sialidase activities were considered as markers of neuronal
differentiation of this cholinergic neuroblastoma cell line. Apart from
the altered morphological appearance, the marker enzymes displayed
significant increases after both types of intervention. We suggest that
hydroxyl free radicals can induce in vitro cell differentiation. They
apparently play a more complex role in cell physiology than simply
causing oxidative damage.
14
UI - 12175987
AU - Beierle EA; Dai W; Langham MR Jr; Copeland EM 3rd; Chen MK
TI -
Caspase 3 expression is altered in a coculture model of neuroblastoma.
SO - J Surg Res 2002 Aug;106(2):323-7
AD - Department of Surgery, University of Florida, Gainesville 32610, USA.
BACKGROUND: Previously, we demonstrated that neuroblastoma cells
cocultured with hepatocytes are protected from apoptosis, while
apoptosis is upregulated in the hepatocytes. The mechanisms responsible
for these findings are unknown. We hypothesize that caspase 3, a
cysteine protease central to the apoptotic pathway, will be altered in
this coculture model that simulates metastatic neuroblastoma. METHODS:
Control human neuroblastoma cells and liver cells are plated in standard
media. For the study group, a noncontact, coculture system is used.
Hepatocytes are plated on cell culture inserts, placed above a growing
layer of neuroblastoma cells, and incubated. Activated caspase 3 is
measured after 1, 2, 3, or 4 days. RESULTS: Activated caspase 3 levels
are significantly decreased in the cocultured neuroblastoma cells on
days 2, 3, and 4. Conversely, cocultured hepatocytes have a significant
increase in caspase 3 activation at all time periods, with the largest
difference seen after 1 day in coculture. CONCLUSIONS: The capacity for
neuroblastoma to differentially alter caspase 3 activation may provide a
significant survival advantage for the neuroblastoma cells in metastatic
environments. Understanding the mechanisms for this altered regulation
may lead to improved and better targeted therapy for this malignancy.
15
UI - 12352451
AU - Granata C; Rizzo A; Carlini C; Gambini C; Magnano G; Conte M
TI -
Primary paratesticular neuroblastoma.
SO - J Urol 2002 Oct;168(4 Pt 1):1530-1
AD - Department of Surgery, Giannini Gaslini Children's Hospital, Genoa,
Italy.
16
UI - 12358785
AU - Xiao H; Hirata Y; Isobe K; Kiuchi K
TI -
Glial cell line-derived neurotrophic factor up-regulates the expression
of tyrosine hydroxylase gene in human neuroblastoma cell lines.
SO - J Neurochem 2002 Aug;82(4):801-8
AD - Laboratory for Genes of Motor Systems, Bio-Mimetic Control Research
Center, RIKEN, Nagoya, Japan.
The role of glial cell line-derived neurotrophic factor (GDNF) in the
survival of dopaminergic neurons has been well documented, but its
effect on dopamine biosynthesis remains to be elucidated. In this study,
the effect of GDNF on the gene expression of tyrosine hydroxylase (TH),
the rate-limiting enzyme of dopamine biosynthesis, was investigated. We
found that GDNF elevated the expression of the TH gene at both mRNA and
protein levels in TGW cells, a human neuroblastoma cell line. GDNF
significantly enhances the transcription rate of the TH gene as
actinomycin D prevented the induction of TH mRNA and GDNF increased the
activity of the TH promoter. In addition, GDNF exerts a relatively weak
but significant effect on the stability of TH mRNA, because GDNF delayed
the degradation of TH mRNA and strengthened a special TH mRNA/protein
interaction known to be relevant with TH mRNA stability. By comparing
several human neurogenic cell lines, we found that GDNF-induced TH
expression was only observed in the cells possessing Ret protein and
coincided with the expression levels. Taken together, these results
indicate that GDNF up-regulates the expression of the TH gene by
promoting the transcription of the TH gene and the stability of TH mRNA
with the Ret receptor dependency in some neuroblastoma cell lines. Thus,
GDNF exerts its neurotrophic role not only in promoting cells survival,
but also in affecting dopamine biosynthesis.
17
UI - 11054669
AU - Grynfeld A; Pahlman S; Axelson H
TI -
Induced neuroblastoma cell differentiation, associated with transient
HES-1 activity and reduced HASH-1 expression, is inhibited by Notch1.
SO - Int J Cancer 2000 Nov 1;88(3):401-10
AD - Department of Laboratory Medicine, Molecular Medicine, University
Hospital MAS, Lund University, Malmo, Sweden.
Neuroblastoma is a childhood tumor that originates from the sympathetic
nervous system. The tumor cells have embryonic features, presumably as a
consequence of an impaired capacity to respond to signals and
transcriptional control mechanisms operating during normal
differentiation. Two basic helix-loop-helix transcription factors, human
achaete-scute homologue-1 (HASH-1) and hairy/enhancer of split
homologue-1 (HES-1), are crucial for proper development of some neuronal
cells. Here, their potential roles during sympathetic differentiation of
human neuroblastoma cells have been investigated. In all tested
protocols for induction of differentiation of SH-SY5Y and SK-N-BE(2)
neuroblastoma cells, HASH-1 expression was rapidly decreased with a
concomitant, often transient, increase in HES-1 expression. In gel
mobility shift assays, using extracts from neuroblastoma cells, HES-1
bound to an oligonucleotide corresponding to a sequence in the HASH-1
promoter including the so-called N-box, suggesting that the transiently
increased HES-1 activity in differentiating neuroblastoma cells is
involved in down-regulation of HASH-1. Constitutive expression of the
intracellular domain of Notch1, which activates the HES-1 promoter in
SH-SY5Y cells, inhibited spontaneous and induced morphological
differentiation of these neuroblastoma cells. Our data show that
functional sympathetic neuronal differentiation of neuroblastoma cells
is associated with transient activation of HES-1 and down-regulation of
HASH-1 expression.
18
UI - 12236041
AU - Lima M; Domini M; Ruggeri G; Bertozzi M; Lauro V; Libri M; Gentili A;
TI -
Pelusi G; Messina P
Retroperitoneoscopic adrenalectomy in a residual of neuroblastoma.
SO - Pediatr Med Chir 2002 May-Jun;24(3):234-6
AD - Istituto di Clinica Chirurgica Pediatrica, Universita Policlinico S.
Orsola, Bologna, Italia.
The authors report a case of retroperitoneoscopic adrenalectomy in a
child with neuroblastoma previously treated by chemotherapy. Usually the
presence of malignant tumours is a contraindication to
retroperitoneoscopic surgery. A restaging of the tumor was done by
retroperitoneoscopy. The residual adrenal gland was excised by
mini-invasive surgery of the retroperitoneal space. The histopathologic
examination confirmed the presence of a residual neuroblastoma in the
adrenal gland. This case report shows a possible of a new indication for
the retroperitoneoscopy.
19
UI - 12354292
AU - Maccarrone M; Navarra M; Catani V; Corasaniti MT; Bagetta G;
TI -
Finazzi-Agro A
Cholesterol-dependent modulation of the toxicity of HIV-1 coat protein
gp120 in human neuroblastoma cells.
SO - J Neurochem 2002 Sep;82(6):1444-52
AD - Department of Experimental Medicine and Biochemical Sciences, University
of Rome Tor Vergata, Rome, Italy. Macarrone@med.uniroma2.it
The human immunodeficiency virus type 1 (HIV-1) coat glycoprotein gp120
binds to its (co)receptors and orchestrates cell entry by the direct
fusion of viral and target cell membranes. Here, we modulated membrane
fluidity of human neuroblastoma CHP100 cells by modulating their
cholesterol content, and investigated the ability of gp120 to induce
cell death in comparison with the untreated cells. We show that in
normal CHP100 cells gp120 induces necrosis by: (i) increased
cyclooxygenase and 5-lipoxygenase activity, and metabolites generated
thereof (prostaglandin E2 and leukotriene B4, respectively); (ii)
increased membrane lipoperoxidation; and (iii) increased mitochondrial
uncoupling. These events were triggered by a rapid increase in
intracellular calcium, and in cholesterol-depleted cells engaged CXCR4
chemokine receptors. The intracellular calcium chelator EGTA-AM
protected CHP100 cells almost completely against the toxic effects of
gp120. However, gp120-induced necrosis and related biochemical changes
were negligible in cholesterol-enriched, and significantly enhanced in
cholesterol-depleted, CHP100 cells exposed to the viral glycoprotein
under the same experimental conditions. Taken together, these results
suggest that membrane fluidity may control the neurotoxic effects of
HIV-1 glycoprotein gp120.
20
UI - 12127685
AU - Westermann F; Schwab M
TI -
Genetic parameters of neuroblastomas.
SO - Cancer Lett 2002 Oct 28;184(2):127-47
AD - Department of Cytogenetics (H0400), German Cancer Research Center, Im
Neuenheimer Feld 280, 69120 Heidelberg, Germany. f.westermann@dkfz.de
Neuroblastoma is a malignant childhood tumor of migrating
neuroectodermal cells derived from the neural crest and destined for the
adrenal medulla and the sympathetic nervous system. The biological
behavior of neuroblastomas is extremely variable and in some respects
unique. Neuroblastomas tend to regress spontaneously in a portion of
infants or to differentiate into a benign ganglioneuroma in some older
patients. Unfortunately, in the majority of patients neuroblastoma is
metastatic at the time of diagnosis, and it usually undergoes rapid
progression with a fatal outcome. The mechanisms leading to this diverse
clinical behavior of neuroblastomas are largely unclear. From the
analysis of tumors at the cytogenetic and molecular level non-random
genetic changes have been identified, including ploidy changes,
amplification of the oncogene MYCN, deletions of chromosome 1p, gains of
chromosome arm 17q, and deletions of 11q as well as of other genomic
regions that allow tumors to be classified into subsets with distinct
biological features and clinical behavior. MYCN status is widely
accepted for therapy stratification. Additional genetic parameters are
currently under investigation to refine risk assessment, but so far the
molecular monitoring tools for prediction of therapy response and
disease outcome are still incomplete. This should lead to more
risk-adapted therapies according to the clinical-genetic parameters by
which individual tumors are characterized. This review aims at
discussing the role of genomic changes in neuroblastomas of diverse
biological and clinical types.
21
UI - 12218704
AU - Plant LD; Boyle JP; Thomas NM; Hipkins NJ; Benedikz E; Hooper NM;
TI -
Henderson Z; Vaughan PF; Peers C; Cowburn RF; Pearson HA
Presenilin-1 mutations alter K+ currents in the human neuroblastoma cell
line, SH-SY5Y.
SO - Neuroreport 2002 Aug 27;13(12):1553-6
AD - School of Biomedical Sciences, University of Leeds, Leeds, UK.
Mutations in presenilin 1 (PS1) are the major cause of autosomal
dominant Alzheimer's disease. We have measured the voltage-gated K+
current in the human neuroblastoma cell line SH-SY5Y using whole-cell
patch-clamp. When cells were stably transfected to over-express PS1, no
change in K+ current was observed. However, over-expression of a
deletion mutation (deltaE9) in PS1 led to a decreased K+ current. These
changes were channel specific since no change in the Na+ current could
be observed in the same cells. Confocal microscopy revealed that the
K(V)3.1 K+ channel subunit had a diminished plasma membrane distribution
when the deltaE9 over-expressing cells were compared to control cells.
Intracellular retention of Kv3.1 is consistent with the notion that PS1
can modulate the activity and trafficking of ion channels in central
neurones and implicates a compromise in electrical signalling as an
underlying factor in the pathogenesis of familial Alzheimer's disease.
Copyright 2002 Lippincott Williams & Wilkins.
22
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.
23
UI - 12358735
AU - Murillo-Carretero M; Ruano MJ; Matarredona ER; Villalobo A; Estrada C
TI -
Antiproliferative effect of nitric oxide on epidermal growth
factor-responsive human neuroblastoma cells.
SO - J Neurochem 2002 Oct;83(1):119-31
AD - Area de Fisiologia, Facultad de Medicina, Universidad de Cadiz, Plaza
Fragela 9, 11003 Cadiz, Spain.
Addition of nitric oxide (NO) donors to NB69 neuroblastoma cells
produced a cGMP-independent decrease in cell proliferation, without
affecting cell viability or apoptosis. The potency of short half-life NO
donors was higher when cell proliferation was stimulated by epidermal
growth factor (EGF), as compared with cultures exposed to fetal calf
serum (FCS). Immunoprecipitation and western blot analysis of the EGF
receptor (EGFR) revealed a significant reduction of its EGF-induced
tyrosine phosphorylation in cells treated with the NO donor
2-(N,N-diethylamino)-diazenolate-2-oxide (DEA-NO). When total cell
lysates were subjected to western blotting, we observed that DEA-NO also
reduced tyrosine phosphorylation in EGF-activated phosphoproteins, but
not in those proteins whose tyrosine phosphorylation was evident in the
absence of EGF. The effect of NO on EGFR transphosphorylation was
concentration-dependent and transient, with a total recovery observed
between 1.5 and 3 h after addition of DEA-NO to the cells. When cells
were incubated for 15 min with DEA-NO and then washed, the EGFR
transphosphorylation returned to control levels immediately, indicating
that the interaction of NO with the receptor molecule was fully
reversible. NB69 cells expressed both the neuronal and the inducible
isoforms of NO synthase (NOS) when cultured in the presence of FCS;
under this condition, the NOS inhibitor, N(omega)-nitro-L-arginine
methyl ester, produced a small but significant increase in cell
proliferation. The results suggest that NO is an endogenous antimitotic
agent and that its interaction with EGFR contributes to cytostasis in
NB69 cells.
24
UI - 11891459
AU - Hosalkar HS; Pill SG; Sun PP; Drummond DS
TI -
Progressive spinal lordosis after laminoplasty in a child with thoracic
neuroblastoma.
SO - J Spinal Disord Tech 2002 Feb;15(1):79-83
AD - Division of Orthopaedic Surgery The Children's Hospital of Philadelphia,
Philadelphia, Pennsylvania 19104, USA.
Laminoplasty has been advocated increasingly after spinal tumor excision
in children. Results have shown that it offers the required
decompression, while maintaining spinal stability and the integrity of
the posterior vertebral elements. To the authors' knowledge, there has
been no description of a progressive lordotic deformity of the thoracic
spine after this procedure. A case of an 8-year-old boy with thoracic
neuroblastoma developing progressive thoracic lordosis after
laminoplasty is reviewed, and a possible cause is suggested. Discussing
this potential complication with parents and the patient, and following
up with regular clinical and radiographic assessments is advised.
25
UI - 1292857
AU - Loret C; Leneuve P; Bozzola M; Lhiaubet AM; Schimpff RM; Rostene W
TI -
[Effect of interleukins and somatomedins on the production of
neurotensin by cell line SH-SY5Y derived from human neuroblastoma]
SO - C R Acad Sci III 1992;315(11):415-20
AD - I.N.S.E.R.M. U.142, Hopital Saint-Antoine, Paris.
The goal of this study was to investigate the regulation by insulin-like
growth factors 1 and 2, and interleukins on the production of
neurotensin in the SH-SY5Y cell line derived from a human neuroblastoma.
Cultures were performed in RPMI1640 culture medium with heated foetal
calf serum 12%. After 24 hrs. of fasting without serum, interleukins-1
alpha, IL-2, IL-4 and insulin-like growth factors 1 and 2 were added.
Results showed: 1) A mitogenic effect of ILs (p < 0.001) and of IGFs (p
< 0.001). 2) The presence of neurotensin in HCl0.1N cellular extracts
(0.06 fmol/micrograms protein). 3) The increase of cellular neurotensin
content in the presence of IL-4 (560%), IL-2 (480%), IGF-1 (610%) and
IGF-2 (200%). Our results indicate that the human neuroblastoma cell
line SH-SY5Y produces neurotensin and that ILs and IGFs act in vitro to
modulate this production.
26
UI - 7693312
AU - Sautiere PE; Caillet-Boudin ML; Wattez A; Buee-Scherrer V; Delacourte A
TI -
[Detection of Alzheimer type pathological epitopes on Tau proteins of
neuroblastoma cells after treatment with okadaic acid]
SO - C R Acad Sci III 1993;316(5):533-5
AD - INSERM U156, Laboratoire de Neurosciences, Lille, France.
In Alzheimer's disease, Tau proteins are abnormally phosphorylated. In
this paper, we describe a cellular model producing such pathological Tau
proteins. After differentiation by NGF and treatment with okadaic acid
(an inhibitor of phosphatases 1 and 2 A), neuroblastoma SKNSH-SY 5Y
cells produced Tau proteins with an increased apparent molecular weight
and a more acidic isoelectric point when compared to Tau proteins from
control cells. These modified tau proteins bore Alzheimer-type epitopes
detectable by antibodies specific to phosphorylated Alzheimer epitopes.
This model is the first step toward a pharmacological approach of
neuroprotection.
27
UI - 12223953
AU - Kriet M; Laktaoui A; Zrara S; Harmouchi N; Souhail H; Chana H; Terhzaz A
TI -
[Olfactory esthesioneuroblastoma with an ophtalmological presentation: a
case report]
SO - J Fr Ophtalmol 2002 Jun;25(6):632-5
AD - Service d'Ophtalmologie, Rabat, France.
Esthesioneuroblastoma (ENB) is a rare malignant tumor, which develops
from the olfactory neuroepithelium and is one of the rarest tumors of
the nasal cavity. Revelation by ocular signs is unusual. We report the
original observation of a case of ENB of the olfactive placodes in a
28-year-old adult discovered during exophthalmia. The authors studied
the clinical, radiological, pathological, and therapeutic aspects. ENB
should not be forgotten in case of unilateral tumorous exophthalmia
associating rhinological signs.
28
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
UI - 12243826
AU - Gruber G; Laedrach K; Baumert B; Caversaccio M; Raveh J; Greiner R
TI -
Esthesioneuroblastoma: irradiation alone and surgery alone are not
enough.
SO - Int J Radiat Oncol Biol Phys 2002 Oct 1;54(2):486-91
AD - Department of Radiation-Oncology, University of Berne, Inselspital,
Bern, Switzerland. guenther.gruber@insel.ch
PURPOSE: To evaluate the long-term outcome of patients with
esthesioneuroblastoma treated with neoadjuvant or definitive
radiotherapy (RT). METHODS AND MATERIALS: Between 1980 and 2001, 28
patients with histologically confirmed esthesioneuroblastoma underwent
RT, with a median dose of 60 Gy (range 38-73). The median age was 58
years (range 16-85). According to the Kadish classification, 4 patients
had Stage A, 8 Stage B, and 16 Stage C tumors. Radical resection was
performed in 13 cases, in 9 before RT and in 4 after RT because of
stable or progressive disease. The outcome analyses included the median
age (58 years), Kadish stage, skull base penetration, intraorbital
extension, resection status, and total dose (
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