Table of Contents
1
UI - 11910145
AU - Gunes T; Akcakus M
TI -
Congenital neuroblastoma with cutaneous metastases.
SO - Indian Pediatr 2002 Mar;39(3):308
AD - University of Erciyes, Faculty of Medicine, Department of Pediatrics,
Division of Neonatalogy, 38039, Kayseri, Turkey. trgunes@erciyes.edu.tr
2
UI - 11912515
AU - Fakhari M; Pullirsch D; Paya K; Abraham D; Hofbauer R; Aharinejad S
TI -
Upregulation of vascular endothelial growth factor receptors is
associated with advanced neuroblastoma.
SO - J Pediatr Surg 2002 Apr;37(4):582-7
AD - Laboratory for Cardiovascular Research, Departments of Anatomy,
Pediatric Surgery, and Molecular Biology, University of Vienna, Vienna,
Austria.
BACKGROUND: Angiogenesis is essential for tumor growth and relies on the
production of angiogenic factors. Vascular endothelial growth factor
(VEGF) is a major regulator of angiogenesis that binds to tyrosine
kinase receptors Flt-1 and KDR. The interaction of VEGF and its
receptors at gene and protein levels in neuroblastoma remains widely
unknown. METHODS: Tumor biopsy specimens and serum were obtained from 37
neuroblastoma patients; adrenal biopsy sections and sera of 7 normal
children served as controls. Biopsy specimens were examined by real-time
reverse transcription polymerase chain reaction (RT-PCR) and Western
blotting; serum was analyzed by enzyme-linked immunosorbent assay
(ELISA). VEGF-A(165), B, C, Flt-1, and KDR were analyzed. RESULTS: VEGF
isoforms and its receptors' mRNA were expressed in neuroblastoma and
control tissues. Whereas the ligands were increased in stages III and
IV, the receptors were upregulated in stage III only. At protein level,
VEGF-B and C, Flt-1, and KDR were not detectable in tissue lysates,
whereas VEGF-A was increased in stages III and IV. Serum VEGF protein
levels were upregulated in stage III. CONCLUSIONS: VEGF-A(165) is one of
the major angiogenesis regulators among the ligands' family of VEGF,
whereas its receptors KDR, and most probably Flt-1, may contribute to a
poor prognosis (angiogenic) phenotype, as indicated by their upregulated
MRNA levels in stage III neuroblastoma. VEGF-A(165) mainly contributes
to increased serum VEGF levels and may serve as a diagnostic tool in
advanced-stage neuroblastoma. Copyright 2002, Elsevier Science (USA).
All rights reserved.
3
UI - 11960374
AU - Kim SS; Chae HS; Bach JH; Lee MW; Kim KY; Lee WB; Jung YM; Bonventre JV;
TI -
Suh YH
P53 mediates ceramide-induced apoptosis in SKN-SH cells.
SO - Oncogene 2002 Mar 27;21(13):2020-8
AD - Department of Anatomy, College of Medicine, BioGrand Inc., MRC,
Chung-Ang University, Seoul, Korea 156-756.
Ceramide induces apoptotic cell death in a dose- and time-dependent
manner in neuroblastoma SKN-SH cells. Pretreatment with caspase
inhibitors blocks cell death, suggesting that a set of caspase
activities including caspase 1, as well as caspase 3, are involved in
ceramide-induced apoptosis in SKN-SH cells. Treatment with a caspase
inhibitor 3 h after ceramide addition did not inhibit cell death,
although caspase activity was substantially reduced. Ceramide-induced
apoptosis is accompanied by accumulation of p53 followed by an increase
of Bax and decrease of Bcl-2 levels. Inhibition of p53 expression with
p53 antisense oligonucleotides inhibits apoptosis and prevents the
increase in Bax and decrease in Bcl-2. Furthermore, pretreatment with
p53 antisense oligonucleotides markedly inhibits the induction of
caspase activity. These results suggest that p53 regulates the ratio
Bcl-2/Bax and the expression/activation of caspases during
ceramide-induced apoptosis in SKN-SH cells. Caspase inhibition did not
alter the expression of p53, Bcl-2 and Bax. Thus ceramide-induced
reduction in the Bcl-2/Bax ratio, increase in caspase activity, and
apoptosis is dependent upon increases in cellular p53 levels which play
a critical role in the regulation of apoptotic cell death.
4
UI - 11960382
AU - Godfried MB; Veenstra M; v Sluis P; Boon K; v Asperen R; Hermus MC; v
TI -
Schaik BD; Voute TP; Schwab M; Versteeg R; Caron HN
The N-myc and c-myc downstream pathways include the chromosome 17q genes
nm23-H1 and nm23-H2.
SO - Oncogene 2002 Mar 27;21(13):2097-101
AD - Department of Human Genetics, Academic Medical Center, University of
Amsterdam, PO box 22700, 1100 DE Amsterdam, The Netherlands.
Gain of chromosome 17q material is the most frequent genetic abnormality
in neuroblastomas. The common region of gain is at least 375 cR large,
which has precluded the identification of genes with a role in
neuroblastoma pathogenesis. Neuroblastoma also frequently show
amplification of the N-myc oncogene, which correlates closely with 17q
gain. Both events are strong predictors of unfavorable prognosis. To
identify genes that are part of the N-myc downstream pathway, we
constructed SAGE libraries of an N-myc transfected and a control cell
line. This identified the chromosome 17q genes nm23-H1 and nm23-H2 as
being 6-10 times induced in the N-myc expressing cells. Northern and
Western blot analysis confirmed this up-regulation. Time-course
experiment shows that both genes are induced within 4 h after N-myc is
switched on. Furthermore, we demonstrate also that c-myc can up-regulate
nm23-H1 and nm23-H2 expression. Neuroblastoma tumor and cell line panels
reveal a striking correlation between N-myc amplification and mRNA and
protein expression of both nm23 genes. We show that the nm23 genes are
located at the edge of the common region of chromosome 17q gain
previously described in neuroblastoma cell lines. Our findings suggest
that nm23-H1 and nm23-H2 expression is increased by 17q gain in
neuroblastoma and can be further up-regulated by myc overexpression.
These observations suggest a major role for nm23-H1 and nm23-H2 in
tumorigenesis of unfavorable neuroblastomas.
5
UI - 10999699
AU - Vegunta RK; Morotti RA; Shiels WE 2nd; Rauck A; Besner GE
TI -
Collision tumors in children: a review of the literature and
presentation of a rare case of mesoblastic nephroma and neuroblastoma in
an infant.
SO - J Pediatr Surg 2000 Sep;35(9):1359-61
AD - Department of Surgery, Children's Hospital, Columbus, OH 43205, USA.
A mass made up of 2 distinct synchronous primary malignant tumors is a
rare event in adults, and exceedingly so in children. Such lesions have
been called collision tumors. Reported here is an infant who was found
to have a collision tumor comprised of a neuroblastoma and a congenital
mesoblastic nephroma, in contiguity, in the right kidney. This is the
first report of a collision tumor in an infant. This also is the first
report of a synchronous occurrence of a neuroblastoma and a congenital
mesoblastic nephroma. The authors present this case and discuss the
available literature.
6
UI - 11919591
AU - Abbott A
TI -
Babies' cancer screens 'not needed'.
SO - Nature 2002 Mar 28;416(6879):356
7
UI - 11849745
AU - Iehara T; Hamazaki M; Sawada T
TI -
Cytogenetic analysis of infantile neuroblastomas by comparative genomic
hybridization.
SO - Cancer Lett 2002 Apr 8;178(1):83-9
AD - Department of Pediatrics, Kyoto Prefectural University of Medicine, 465
Kajiicho, Kawaramachi-Hirokoji, Kamigyoku, Kyoto 602, Japan.
iehara@koto.kpu-m.ac.jp
Neuroblastomas are heterogeneous tumors. Their clinical behavior varies
from spontaneous regression to malignant progression. To investigate the
cytogenetic heterogeneity of infantile neuroblastomas, we employed
comparative genomic hybridization (CGH). To characterize chromosomal
imbalances in 35 infantile neuroblastomas, we performed CGH and compared
our results with those of other clinical and biological studies. The
most frequent genetic imbalances were found in chromosome 17 (43%),
including whole chromosome 17 gains in eight patients (23%) and 17q
gains in seven patients (20%). A 1p loss and a 2p gain were detected in
six patients each (17%). Losses of 11q and 14q were detected in two
patients (6%) and one (3%) patient, respectively. The number of gains of
17q were significantly higher in DNA diploid tumors than in aneuploid
tumors (P=0.006). Conversely, whole chromosome 17 gains were not found
in DNA diploid tumors and/or MYCN amplification. Interestingly, nine of
17 tumors that were histologically evaluated showed a spontaneous
regression and did not demonstrate any partial chromosomal abnormalities
(i.e. 17q gain, 1p loss, 2p gain, 11q loss and 14q loss). These results
suggest that a gene on chromosome 17q is associated with neuroblastoma
progression. Finally, our observations indicate that the chromosomal
imbalances observed in infantile neuroblastomas are different from those
observed in older patients.
8
UI - 11925110
AU - Gangopadhyay S; Jalali F; Reda D; Peacock J; Bristow RG; Benchimol S
TI -
Expression of different mutant p53 transgenes in neuroblastoma cells
leads to different cellular responses to genotoxic agents.
SO - Exp Cell Res 2002 Apr 15;275(1):122-31
AD - Ontario Cancer Institute, Department of Medical Biophysics, University
of Toronto, 610 University Avenue, Toronto, Ontario, M5G 2M9, Canada.
The involvement of p53 as a determinant of chemosensitivity or
radiosensitivity is not well understood and is complicated by numerous
contradictory reports. Here we have addressed this issue using a series
of isogenic clones derived from two neuroblastoma cell lines that
express wild-type p53 genes, Nub7 and IMR32. Two different mutant p53
transgenes were used in an attempt to disrupt p53 function in the
clones. Our findings indicate that the cellular response is dependent on
the genotoxic agent used as well as on the specific p53 transgene used.
Cellular radiosensitivity showed no association with apoptosis or with
the ability of the cells to arrest in G1 after irradiation. An
association was observed, however, between gamma-radiation sensitivity
and DNA double-strand break rejoining activity. Copyright 2002 Elsevier
Science (USA).
9
UI - 11966589
AU - White BD; Pozza CH; Davies R; Hanieh A
TI -
A case of primary cerebral neuroblastoma in adolescence.
SO - Australas Radiol 2002 Mar;46(1):60-4
AD - Department of Medical Imaging, North Western Adelaide Health Service,
The Queen Elizabeth Hospital Campus, Woodville, South Australia,
Australia.
Primary cerebral neuroblastoma is one of a group of highly malignant
undifferentiated primitive neuroectodermal tumours arising from germinal
matrix cells of the embryonic neural tube. They occur primarily in young
children and are extremely rare in adults. They may be multicentric and
have often spread throughout the central nervous system at the time of
diagnosis. A case of a 16-year-old man is described, and the recent
literature is reviewed.
10
UI - 11970941
AU - Gupta S; Tasker RC
TI -
Does giving albumin infusion in hypoalbuminaeimic children with
oncological disease affect colloid osmotic pressure and outcome?
SO - Arch Dis Child 2002 May;86(5):380-1
AD - Research Registrar, Paediatric Intensive Care Unit, Addenbrooke's
Hospital, Cambridge.
11
UI - 11765218
AU - Bostel S; Rouzaire-Dubois B; Dubois JM
TI -
Background osmolyte current involved in cell volume regulation of
neuroblastoma x glioma hybrid NG108-15 cells.
SO - Gen Physiol Biophys 2001 Sep;20(3):281-91
AD - Laboratoire de Neurobiologie Cellulaire et Moleculaire, CNRS,
Gif-sur-Yvette, France.
Recently, we showed that at constant extracellular osmolarity, the
volume of NG108-15 cells was dependent on the external NaCl
concentration and we assumed that the responsible mechanism was mediated
by background channels (Rouzaire-Dubois et al. 1999). In order to
confirm this view, the mean cell volume and the background current of
NG108-15 cells were measured under different experimental conditions,
after blockade of specific volume regulating mechanisms and ion
channels. When the external NaCl concentration was decreased, the
reversal potential of the background current was shifted toward negative
values and the membrane conductance decreased. Opposite effects were
observed when the NaCl concentration was increased. Substitution of
external Na+ with various monovalent cations altered the mean cell
volume by: Rb+, +17%; Cs+, +15%; K+, +10%; Li+, -6%; choline, -9%;
N-methylglucamine, -25% . The reversal potential of the background
current and the membrane conductance were altered by these Na+
substitutes in such a way that the cell volume increased linearly with
the background current at -60 mV. Substitution of external Cl- with
various monovalent anions altered the mean cell volume by: I-, +4%; Br-,
0%; NO-, -3%; F-, -5%; isethionate, -30%; gluconate, -50%. Cl-
substitutes did not significantly alter the background current at -60
mV, except F- which increased it by 39%. These results suggest that 1.
the cell volume is dependent on ion fluxes through background channels;
2. electrogenic cation fluxes are larger than anionic ones and the
background current is proportional to the difference between these
fluxes; 3. whereas external cations do not interfere with anion fluxes,
external anions alter cation fluxes.
12
UI - 11980999
AU - Kletzel M; Katzenstein HM; Haut PR; Yu AL; Morgan E; Reynolds M;
TI -
Geissler G; Marymount MH; Liu D; Kalapurakal JA; Shore RM; Bardo DM;
Schmoldt J; Rademaker AW; Cohn SL
Treatment of high-risk neuroblastoma with triple-tandem high-dose
therapy and stem-cell rescue: results of the Chicago Pilot II Study.
SO - J Clin Oncol 2002 May 1;20(9):2284-92
AD - Department of Pediatrics, Northwestern University, Feinberg School of
Medicine, Chicago, IL, USA. mkletzel@northwestern.edu
PURPOSE: To investigate whether intensive induction therapy followed by
triple-tandem cycles of high-dose therapy with peripheral-blood
stem-cell rescue and local irradiation will improve event-free survival
for patients with high-risk neuroblastoma. PATIENTS AND METHODS: From
neuroblastoma patients and one child with recurrent MYCN-amplified
disease were enrolled onto the Chicago Pilot II Protocol. After
induction therapy and surgery, peripheral-blood stem cells were
mobilized with three cycles of high-dose cyclophosphamide and
granulocyte colony-stimulating factor. Patients then underwent
triple-tandem cycles of high-dose therapy with peripheral-blood
stem-cell rescue followed by radiation to the primary site. RESULTS:
Twenty-two of the 26 patients successfully completed induction therapy
and were eligible for the triple-tandem consolidation high-dose therapy.
Sufficient numbers of peripheral-blood stem cells were collected in all
but one patient. Seventeen patients were able to complete all three
cycles of high-dose therapy and peripheral-blood stem-cell rescue, two
patients completed two cycles, and three patients completed one cycle.
There was one toxic death, and one patient died from complications of
treatment for graft failure. With a median follow-up of 38 months, the
3-year event-free survival and survival rates are 57% +/- 11% and 79%
+/- 10%, respectively. CONCLUSION: The results of this pilot study
demonstrate that it is feasible to intensify consolidation with
triple-tandem high-dose chemotherapy and peripheral-blood stem-cell
rescue and local irradiation, and suggest that this treatment strategy
may lead to improved survival for patients with high-risk neuroblastoma.
13
UI - 10918246
AU - Biasotti S; Garaventa A; Villavecchia GP; Cabria M; Nantron M; De
TI -
Bernardi B
False-negative metaiodobenzylguanidine scintigraphy at diagnosis of
neuroblastoma.
SO - Med Pediatr Oncol 2000 Aug;35(2):153-5
AD - Department of Pediatric Hematology-Oncology, Giannina Gaslini Institute,
Genova, Italy.
14
UI - 11813196
AU - Pritchard J
TI -
Re: Commentary by G.J. D'Angio to the article by S. Biasotti et al.
SO - Med Pediatr Oncol 2002 Feb;38(2):152
15
UI - 11878578
AU - Reuland P; Geiger L; Thelen MH; Handgretinger R; Haase B;
TI -
Muller-Schauenburg W; Niethammer D; Bares R
Follow-up in neuroblastoma: comparison of metaiodobenzylguanidine and a
chimeric anti-GD2 antibody for detection of tumor relapse and therapy
response.
SO - J Pediatr Hematol Oncol 2001 Oct;23(7):437-42
AD - Department of Nuclear Medicine, University of Tubingen, FRG, Germany.
Early and correct diagnosis of local tumor recurrence, occurrence of
metastases, and therapy response are essential in patients with
neuroblastoma stage IV. The aim of the study was to evaluate the
diagnostic value of metaiodobenzylguanidine (mIBG) and a chimeric GD2
antibody in the follow-up of patients with neuroblastoma. In a
prospective study, mIBG (N = 31 scans) and immunoscintigraphy were
compared with a chimeric antiganglioside antibody, ch14.18 (MAb) (N = 31
scans), labeled with technetium Tc 99m in the follow-up of 18 patients
with stage IV neuroblastoma. The findings were compared with histologic
findings, other imaging examinations, and clinical changes over the
course of 4 to 6 years. For the diagnosis of local tumor recurrences,
sensitivity was 80% for MAb and 70% for mIBG. Specificity was 93% for
MAb and 72% for mIBG. The MAb was superior for the detection of skeletal
metastases, with a sensitivity of 82% compared with 72% for mIBG.
Specificity was 100% for both techniques. Also, for soft tissue/lymph
node metastases, sensitivity for MAb was higher (50%) than for mIBG
(31%). Specificity was 100% for each technique. In sequential studies,
metastases were detected earlier with MAb (mean: 2.3 m for skeletal
metastases, 3.6 m for soft tissue metastases) than with mIBG. After
therapy, tumor uptake was visualized longer with mIBG (mean 6.3 m) than
with MAb. The chimeric antibody ch14.18 is likely to be valuable for
follow-up examinations and for assessment of therapy response because of
earlier detection of new metastases.
16
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.
17
UI - 11981207
AU - Kim S; Hu W; Kelly DR; Hellmich MR; Evers BM; Chung DH
TI -
Gastrin-releasing peptide is a growth factor for human neuroblastomas.
SO - Ann Surg 2002 May;235(5):621-9; discussion 629-30
AD - Department of Surgery, The University of Texas Medical Branch,
Galveston, Texas 77555-0353, USA.
OBJECTIVE: To evaluate whether gastrin-releasing peptide (GRP) and GRP
receptor (GRP-R) expression correlate with tumor behavior and to examine
the mitogenic actions of GRP on neuroblastomas. SUMMARY BACKGROUND DATA:
Neuroblastoma is the most common solid tumor of infants and children.
Despite recent advances in multimodality treatment regimens, the
survival for advanced-stage tumors remains dismal. Neuroblastomas are
known to produce GRP; however, the proliferative effects of GRP on
neuroblastomas have not been elucidated. METHODS: Sections of
paraffin-embedded neuroblastomas from 33 patients were analyzed for GRP
and GRP-R protein expression by immunohistochemistry. Functional binding
of GRP-R to the Ca2+ signaling pathway was examined. In addition, the
proliferative effect of GRP on neuroblastoma cells (SK-N-SH, IMR-32,
SH-SY5Y, LAN-1) was determined. RESULTS: Immunohistochemical analysis
showed GRP and GRP-R protein expression in neuroblastomas; an increased
expression of GRP-R was noted in a higher percentage of undifferentiated
tumors compared with tumors that were benign. GRP-R mRNA was confirmed
in neuroblastoma cell lines. GRP treatment resulted in intracellular
calcium [Ca2+]i mobilization in two cell lines (SK-N-SH, LAN-1). GRP
treatment stimulated growth of all four neuroblastoma cell lines; this
effect was inhibited in SK-N-SH cells by pretreatment with GRP antibody.
CONCLUSIONS: These findings show increased GRP-R expression in the more
aggressive and undifferentiated neuroblastomas. The synchronous
expression of GRP and its receptor, GRP-R, suggests a role for these
proteins in tumor growth. Moreover, these findings show enhanced
proliferation of neuroblastoma cells in vitro after GRP treatment,
suggesting that GRP may act as an autocrine and/or paracrine growth
factor for neuroblastomas. Treatment with specific GRP-R antagonists may
provide novel adjuvant therapy for neuroblastomas in children.
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