Table of Contents
1
UI - 21288352
AU - Rubie H
TI -
[New prognostic factors of neuroblastoma]
SO - Arch Pediatr 2001 May;8 Suppl 2():366s-368s
AD - Unite d'hemato-oncologie pediatrique, hopital des Enfants, 330, avenue
de Grande-Bretagne, BP 3119, 31026 Toulouse, France.
2
UI - 21364053
AU - Hervas Benito I; Rivas Sanchez A; Bello Arques P; Canete A; Fernandez
TI -
JM; Saura Quiles A; Gonzalez Cabezas P; Ruiz Rodriguez JC; Castell V;
Perez Pastor JL; Monfort JA; Mateo Navarro A
[Value of 123I-MIBG scanning, neuron-specific enolase and serum ferritin
in the diagnosis and follow-up of patients with neuroblastoma]
SO - Rev Esp Med Nucl 2001 Aug;20(5):369-76
AD - Servicio de Medicina Nuclear del Hospital Universitario La Fe, Valencia.
ihervas@inicia.es
INTRODUCTION: The neuroblastoma (NB) is one of the most common pediatric
malignant neoplasms. The most commonly used tumor markers in the
diagnosis and follow-up of this tumor are the serum neuron-specific
enolase (NSE), ferritin and lactic dehydrogenase and urinary
vanillymandelic and homovanillic acid. The common imaging modalities are
CT, MRI and 123I or 131I-meta-iodobenzylguanidine scintigraphy. AIM: The
aim of this study is to assess the value of
123I-meta-iodobenzylguanidine (MIBG) scintigraphy and serum
determinations of NSE and ferritin in the diagnosis and evolution of NB
patients. MATERIAL AND METHODS: 20 patients (8 female, 12 male) whose
ages ranged from 2 months to 9 years with a mean age of 2.64 years
diagnosed of NB. 47 123I-MIBG scans, 47 NSE determinations and 47
ferritin ones were selected. RESULTS: At the time of diagnosis, 100% of
the 123I-MIBG scans were positive. 65% of NSE determinations presented
clearly pathological levels and 15% were very near to the cut-off point.
Only 45% of the ferritin levels were increased. The differences between
the lesions visible by 123I-MIBG scanning before and 3 months after
treatment as well as NSE and ferritin levels were studied. When the
Student's T test was applied, we found statistically significant pre and
post-treatment differences in 123I-MIBG scanning and NSE. In the case of
ferritin, there was no statistical significance in spite of the decrease
in the values. The direct correlation and Spearman correlation between
laboratory data and 123I-MIBG scanning as well as correlation between
NSE and ferritin were also studied. There was a good correlation between
123I-MIBG and NSE and between NSE and ferritin. We have also studied the
data in 7 relapses. CONCLUSIONS: 123I-MIBG scintigraphy and serum
determination of NSE are two successful diagnostic tools for the
diagnosis and evolution of NB patients.
3
UI - 21396154
AU - Chao KS; Kaplan C; Simpson JR; Haughey B; Spector GJ; Sessions DG;
TI -
Arquette M
Esthesioneuroblastoma: the impact of treatment modality.
SO - Head Neck 2001 Sep;23(9):749-57
AD - Radiation Oncology Center, Mallinckrodt Institute of Radiology,
Washington University Medical Center, WU Box 8224, 4939 Children's
Place, Suite 5500, St. Louis, MO 63110, USA. chao@radonc.wustl.edu
BACKGROUND: We evaluated the impact of treatment modality on
esthesioneuroblastoma. METHODS: Between 1976 and 1996, 25 patients with
esthesioneuroblastoma were treated at Mallinckrodt Institute of
Radiology. There were 11 male and 14 female patients; their ages ranged
from 16 to 73 years (median, 57 years). The tumors were Kadish stage A
in 3, Stage B in 13, C in 8, and modified D in 1 (cervical nodal
metastasis). Seventeen patients were treated with surgery and radiation
therapy, six were treated with irradiation alone, and two were treated
with surgery only. Eight patients received neoadjuvant chemotherapy.
Median follow-up was 8 years (range, 2-24 years). RESULTS: The 5-year
actuarial overall survival, disease-free survival, and local tumor
control rates were 66.3%, 56.3%, and 73.0%, respectively. Kadish stage
was not a significant prognosticator for local control or disease-free
survival. Five-year local control rates were 87.4% for the combination
of surgery and radiation therapy and 51.2% for irradiation alone. Two
patients with Kadish stage A and B disease underwent surgical resection
alone; both failed locally. In contrast, 33.3% of patients (three of
nine) with Kadish stage A or B disease who received adjuvant radiation
therapy had a local recurrence develop. With adjuvant radiation therapy,
the surgical margin status did not influence local tumor control. Among
the eight patients who received neoadjuvant chemotherapy, six patients
showed no response, one had partial response, and one showed a complete
response. CONCLUSIONS: Surgical resection plus adjuvant radiation
therapy yielded the best treatment outcome. More effective chemotherapy
agents with a reproducible effectiveness are needed for patients with
locally advanced esthesioneuroblastoma. Copyright 2001 John Wiley &
Sons, Inc.
4
UI - 21468608
AU - Jones TA; Flomen RH; Senger G; Nizetic D; Sheer D
TI -
The homeobox gene MEIS1 is amplified in IMR-32 and highly expressed in
other neuroblastoma cell lines.
SO - Eur J Cancer 2000 Dec;36(18):2368-74
AD - Human Cytogenetics Laboratory, Imperial Cancer Research Fund, Lincoln's
Inn Fields, London, UK.
Neuroblastoma is a childhood tumour of the sympathetic nervous system
that demonstrates striking clinical heterogeneity. In order to determine
which genes are abnormally expressed in neuroblastoma, we screened
regions of amplification from the short arm of chromosome 2 in the
neuroblastoma cell line IMR-32 and found that the homeobox gene, myeloid
ecotropic integration site 1 (MEIS1), is highly amplified. MEIS1
normally maps to chromosome band 2p14. High expression of MEIS1 without
amplification was also found in other neuroblastoma cell lines, with and
without MYCN amplification, and in medulloblastoma and crythroleukaemia
cell lines. MEIS1 is highly expressed in cerebellum and ubiquitously
expressed in normal immunohaematopoietic tissues and is thought to be
important in cell proliferation and differentiation. While several lines
of evidence point towards a role for homeobox genes in the development
of other malignancies, this is the first report showing the
amplification of a homeobox gene in neuroblastoma.
5
UI - 21160442
AU - Corrias MV; Occhino M; Croce M; De Ambrosis A; Pistillo MP; Bocca P;
TI -
Pistoia V; Ferrini S
Lack of HLA-class I antigens in human neuroblastoma cells: analysis of
its relationship to TAP and tapasin expression.
SO - Tissue Antigens 2001 Feb;57(2):110-7
AD - Laboratorio di Oncologia, Istituto Scientifico G. Gaslini, Genoa, Italy.
We studied the constitutive and the interferon (IFN)-gamma-induced
expression of HLA class I antigen heavy chain, beta2-microglobulin
(beta2m), TAP-1, TAP-2 and tapasin in a panel of eleven neuroblastoma
cell lines. Surface expression of HLA class I antigens was low in eight
out of eight neuroblastoma cell lines bearing MYC-N amplification and/or
1p deletion, while two out of three neuroblastoma cell lines lacking
these genetic alterations showed normal expression. IFN-gamma treatment
restored HLA class I antigen surface expression in all neuroblastoma
cell lines. Eight out of 11 neuroblastoma cell lines did not express
TAP-1 mRNA and three of them also lacked TAP-2 mRNA. beta2 m mRNA was
barely detectable or absent in five neuroblastoma cell lines, while
tapasin mRNA was always expressed. IFN-gamma upregulated the expression
of HLA class I heavy chain, beta2 m, TAP-1, TAP-2 and tapasin, as
detected at mRNA or protein level. Post-transcriptional events were
involved in altered TAP-1 and beta2 m expression in one peculiar
neuroblastoma cell line. These data indicate that multiple mechanisms
play a role in the HLA class I antigen-deficient phenotype of human
neuroblastoma.
6
UI - 21219828
AU - Jang IS; Juhnn YS
TI -
Adaptation of cAMP signaling system in SH-SY5Y neuroblastoma cells
following expression of a constitutively active stimulatory G protein
alpha, Q227L Gsalpha.
SO - Exp Mol Med 2001 Mar 31;33(1):37-45
AD - Department of Biochemistry and Cancer Research Institute, Seoul National
University College of Medicine, Korea.
Heterotrimeric GTP-binding proteins (G protein) are known to participate
in the transduction of signals from ligand activated receptors to
effector molecules to elicit cellular responses. Sustained activation of
cAMP-G protein signaling system by agonist results in desensitization of
the pathway at receptor levels, however it is not clear whether such
receptor responses induce other changes in post-receptor signaling path
that are associated with maintenance of AMP levels, i.e. cAMP-forming
adenylate cyclase (AC), cAMP-degrading cyclic nucleotide
phosphodiesterase (PDE) and cAMP-dependent protein kinase (PKA).
Experiments were performed to determine the expression of AC, PDE, and
PKA isoforms in SH-SY5Y neuroblastoma cells, in which cAMP system was
activated by expressing a constitutively activated mutant of stimulatory
G protein (Q227L Gsalpha). Expression of ACI mRNA was increased, but
levels of ACVIII and ACIX mRNA were decreased. All of the 4 expressed
isoforms of PDE (PDE1C, PDE2, PDE 4A, and PDE4B) were increased in mRNA
expression; the levels of PKA RIalpha, RIbeta, and RIIbeta were
increased moderately, however, those of RIIalpha and Calpha were
increased remarkably. The activities of AC, PDE and PKA were also
increased in the SH-SY5Y cells expressing Q227L Gsalpha. The similar
changes in expression and activity of AC, PDE and PKA were observed in
the SH-SY5Y cells treated with dbcAMP for 6 days. Consequently, it is
concluded that the cAMP system adapts at the post-receptor level to a
sustained activation of the system by differential expression of the
isoforms of AC, PDE, and PKA in SH-SY5Y neuroblastoma. We also showed
that an increase in cellular cAMP concentration might mediate the
observed changes in the cAMP system.
7
UI - 21256790
AU - Antony P; Freysz L; Horrocks LA; Farooqui AA
TI -
Effect of retinoic acid on the Ca2+-independent phospholipase A2 in
nuclei of LA-N-1 neuroblastoma cells.
SO - Neurochem Res 2001 Jan;26(1):83-8
AD - Laboratoire de Neurobiologie Moleculaire des Interactions Cellulaires,
Institut de Chimie Biologique, Faculte de Medecine, Strasbourg, France.
LA-N-1 neuroblastoma cell cultures contain Ca2+-independent
phospholipases A2 hydrolyzing phosphatidylethanolamine and ethanolamine
plasmalogens. These enzymes differ from each other in their molecular
mass, substrate specificity, and kinetic properties. Subcellular
distribution studies have indicated that the activity of these
phospholipases is not only localized in the cytosol but also in
non-nuclear membranes and in nuclei. The treatment of LA-N-1
neuroblastoma cell cultures with retinoic acid results in a marked
stimulation of Ca2+-independent phospholipases A2 hydrolyzing
phosphatidylethanolamine and plasmenylethanolamine. The increase of the
activities of both enzymes was first observed in nuclei followed by
those present in the cytosol. No effect of retinoic acid on either
phospholipase activity could be observed in non-nuclear membranes. The
stimulation of these enzymes may be involved in the generation and
regulation of arachidonic acid and its metabolites during
differentiation.
8
UI - 21409967
AU - Moukheiber AK; Nicollas R; Roman S; Coze C; Triglia JM
TI -
Primary pediatric neuroblastic tumors of the neck.
SO - Int J Pediatr Otorhinolaryngol 2001 Aug 20;60(2):155-61
AD - Department of Pediatric Otorhinolaryngology, Head and Neck Surgery, La
Timone Children's Hospital, Marseille Medical School, Boulevard Jean
Moulin, 13385 Marseille cedex 5, France.
Neuroblastic tumors are the third most common cause of solid tumors in
early childhood. Cervical tumors account for only 5% of cases. In this
report, we describe a series of four pediatric neuroblastic tumors of
the neck. The histological diagnosis was ganglioneuroblastoma in three
cases and neuroblastoma in one case. Presenting signs were solitary
cervical mass in two cases and respiratory distress in association with
Claude-Bernard Horner's syndrome in two cases. Mean age at presentation
was 15 months. Cervical computed tomography scan and/or magnetic
resonance imaging depicted calcifications within the tumor in 50% of
cases and allowed accurate assessment of extension. Increased urine
catecholamine levels were observed only in the patient with
neuroblastoma. Scintigraphy with [131]iodine-methyliodobenzylguanidine
demonstrated selective uptake by the tumor in two cases. Amplification
of N-myc oncogene, a documented unfavorable prognostic sign, was not
found in any case. Surgical treatment was performed in all patients.
Neoadjuvant chemotherapy was performed in one case. All patients
underwent regular surveillance. No evidence of recurrence has been
observed with a mean follow-up period of 7 years.
9
UI - 21449311
AU - Neitzschman H; Ram SK; Beiderman B; Ram PB
TI -
Radiology case of the month. Posterior mediastinal mass.
SO - J La State Med Soc 2001 Aug;153(8):399-400
AD - Tulane University Health Sciences Center, New Orleans, Louisiana, USA.
An 11-year-old white boy presented with gradual onset of persistent
shortness of breath for the previous few weeks. X-ray, CT, and MRI of
the chest were performed.
10
UI - 21443306
AU - Mora J; Cheung NK; Juan G; Illei P; Cheung I; Akram M; Chi S; Ladanyi M;
TI -
Cordon-Cardo C; Gerald WL
Neuroblastic and Schwannian stromal cells of neuroblastoma are derived
from a tumoral progenitor cell.
SO - Cancer Res 2001 Sep 15;61(18):6892-8
AD - Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New
York, New York 10021, USA.
The coexistence of neuroblastic and Schwannian stromal (SS) cells in
differentiating neuroblastoma (NB), and derivation of Schwannian-like
cells from neuroblastic clones in vitro, were accepted previously as
evidence of a common pluripotent tumor stem line. This paradigm was
challenged when SS cells were suggested to be reactive in nature. The
advent of microdissection techniques, PCR-based allelic analysis, and in
situ fluorescent cytometry made possible the analysis of pure cell
populations in fresh surgical specimens, allowing unequivocal
determination of clonal origins of various cell subtypes. To overcome
the complexity and heterogeneity of three-dimensional tissue structure,
we used: (a) Laser-Capture Microdissection to obtain histologically
homogeneous cell subtype populations for allelotype analysis at
chromosomes 1p36, 11q23, 14q32, and 17q and study of MYCN copy number;
(b) multiparametric analysis by Laser-Scanning Cytometry of morphology,
DNA content, and immunophenotype of intact cells from touch imprints;
and (c) bicolor fluorescence in situ hybridization on touch imprints
from manually microdissected neuroblast and stroma-rich areas.
Histologically distinct SS and neuroblastic cells isolated by
Laser-Capture Microdissection had the same genetic composition in 27 of
28 NB analyzed by allelic imbalance and gene copy number. In all 20
cases studied by Laser-Scanning Cytometry, SS cells identified by
morphology and S-100 immunostaining had identical DNA content and
GD2-staining pattern as their neuroblastic counterparts. In 7 cases,
fluorescence in situ hybridization demonstrated the same chromosomal
makeup for SS and neuroblastic cells. These results provide unequivocal
evidence that neuroblastic and SS cells in NB are derived from
genetically identical neoplastic cells and support the classical
paradigm that NB arises from tumoral cells capable of development along
multiple lineages.
11
UI - 21450511
AU - Kawakami M; Koda M; Matsunaga N; Kishimoto Y; Shabana M; Kato H;
TI -
Nishimuki E; Kojo H; Miura K; Kawasaki H
Adult-type neuroblastoma originated in retroperitoneum beginning with
obstructive jaundice.
SO - Clin Imaging 2001 Jul-Aug;25(4):284-7
AD - Second Department of Internal Medicine, Faculty of Medicine, Tottori
University, 36-1 Nishi-machi, Yonago, Tottori 683-0802, Japan.
Abdominal neuroblastoma in adults is a rare neoplasm and only 30
patients have been described in Japan since 1985. The patient was a
43-year-old woman with jaundice. The tumor originated from
retroperitoneum. The enlarged gall bladder and dilatation of
intrahepatic bile ducts were noted by ultrasonography and computed
tomography. We report the first adult-type neuroblastoma with
obstructive jaundice.
12
UI - 20370603
AU - Hornick CA; Anthony CT; Hughey S; Gebhardt BM; Espenan GD; Woltering EA
TI -
Progressive nuclear translocation of somatostatin analogs.
SO - J Nucl Med 2000 Jul;41(7):1256-63
AD - Department of Physiology, The Stanley S. Scott Cancer Center, New
Orleans, Louisiana, USA.
Optimal cancer radiotherapy using Auger electron emitters requires
selective localization of radionuclides in close proximity to tumor DNA.
METHODS: Intracellular trafficking of (125)I-Tyr1-somatostatin-14
somatotropin-release inhibiting factor (SRIF) and 2 of its analogs,
(125)I-WOC 4a and (111)In-pentetreotide, was studied in human
neuroblastoma cells. RESULTS: After 24-h incubation, SRIF was degraded
or recycled, whereas its protease-resistant analogs progressively
accumulated in nuclear fractions. (111)In-pentetreotide binding to DNA
increased over time in somatostatin receptor-positive cells but not in
somatostatin receptor-negative cells. CONCLUSION: These in vitro studies
show that prolonged exposure to radiolabeled SRIF analogs significantly
increases their cellular internalization, nuclear translocation, and DNA
binding. Clinically, infusion of radiolabeled somatostatin analogs may
enhance tumor uptake and retention and provide more effective in situ
radiotherapy.
13
UI - 21282068
AU - Campus R; Conte M; Rizzo A; Granata C; Gambini C; Carlini C; De Bernardi
TI -
B; Di Battista C; Jasonni V
[Intractable diarrhea and neuroblastoma: report of a clinical case]
SO - Pediatr Med Chir 2000;22(1):47-8
AD - Divisione e Cattedra di Chirurgia Pediatrica, Istituto Giannina Gaslini,
Genova, Italia.
One of the typical presentations of neuroblastoma is intractable
diarrhea or wdha (watery diarrhea, hypokalemia, achloridria). The case
admitted to our Pediatric Surgery Department presented watery diarrhea
due to VIP hyperincretion caused by a stage 1 neuroblastoma, whose
ablation allowed a complete resolution of the clinical conditions. This
case report can be useful in the discussion of the differential
diagnosis of the most common clinical pictures.
14
UI - 21341704
AU - Mehes G; Luegmayr A; Ambros IM; Ladenstein R; Ambros PF
TI -
Combined automatic immunological and molecular cytogenetic analysis
allows exact identification and quantification of tumor cells in the
bone marrow.
SO - Clin Cancer Res 2001 Jul;7(7):1969-75
AD - Children's Cancer Research Institute, St. Anna Kinderspital, A-1090
Vienna, Austria.
PURPOSE: To improve the detection of disseminated tumor cells in bone
marrow (BM) and peripheral blood samples of solid tumor patients, a
novel computer-assisted scanning system for automatic search, image
analysis, and repositioning of these cells was developed. This system
allows precise identification and quantification of tumor cells by
sequential immunological and molecular cytogenetic analysis. In this
study, we attempt to demonstrate the practical use of this approach by
analyzing BM samples from neuroblastoma patients. EXPERIMENTAL DESIGN:
The disialo-ganglioside (GD2) molecule was used as the immunological
target. The GD2 molecule was described as being specific for
neuroblastoma cells, although false positive reactions had been
suspected. To verify or disprove the neoplastic nature of the
immunologically positive cells, sequential fluorescence in situ
hybridization was performed on these cells to search for those genetic
aberrations found in the corresponding primary tumors. A total of 115
samples from 40 newly diagnosed patients were evaluated for the presence
of GD2(+) cells in the BM. RESULTS: GD2 positivity was detected in 95.2%
of stage 4 patients, in 100% of stage 4s patients, and in 38.5% of
patients with localized/regional disease. In stage 4 and 4s BM samples,
the GD2(+) cells were unequivocally identified as tumor cells based on
the molecular cytogenetic aberrations found by fluorescence in situ
hybridization. However, in BM samples from patients with
localized/regional disease, all GD2(+) cells were concluded to represent
false positivity due to the absence of genetic aberrations. CONCLUSIONS:
Automatic search and sequential molecular cytogenetic analysis of the
immunologically positive cells provide precise information on both the
number and cytogenetic profile of disseminated tumor cells.
15
UI - 21383064
AU - de Boer J
TI -
Chips help diagnosis of childhood cancers.
SO - Trends Cell Biol 2001 Aug;11(8):323
16
UI - 21403127
AU - Teitz T; Lahti JM; Kidd VJ
TI -
Aggressive childhood neuroblastomas do not express caspase-8: an
important component of programmed cell death.
SO - J Mol Med 2001 Aug;79(8):428-36
AD - Department of Tumor Cell Biology, St. Jude Children's Research Hospital,
332 N. Lauderdale, Memphis, TN 38105, USA. tal.teitz@stjude.org
Neuroblastomas that overexpress N-Myc due to amplification of the MYCN
oncogene are aggressive tumors that become very resistant to treatment
by chemotherapy and irradiation. to identify tumor suppressor genes in
this group of neuroblastomas we analyzed the expression and function of
both apoptosis-related cell cycle regulatory genes in cell lines and
patient tumor samples. We found that in a high percentage of
neuroblastoma cell lines and patient samples with amplified MYCN,
caspase-8 mRNA is not expressed. The caspase-8 gene, CASP8, was deleted
or silenced by methylation in the neuroblastoma cell lines while
methylation of its promoter region was the predominant mechanism for its
inactivation in the patient tumor samples. Reintroduction of caspase-8
into the neuroblastoma cell lines resensitized these cells to
drug-induced and survival factor dependent apoptosis. Subsequently
others have also shown that caspase-8 is silenced by methylation in
neuroblastoma and peripheral neural ectodermal tumors, and that the
caspase-9 regulator Apaf-1 is silenced by methylation in melanoma cell
lines and patient samples. We conclude that caspase-8 acts as a tumor
suppressor gene in neuroblastomas, that its silencing provides a
permissive environment for MYCN gene amplification once the tumors are
treated with chemotherapeutic drugs/irradiation, and that expression of
this gene in these tumor cells may be of clinical benefit. We also
discuss the possible significance of the neural crest cell progenitor
cell origin and the silencing of important apoptotic regulators via
methylation in both neuroblastoma and melanoma tumors.
17
UI - 21443723
AU - Kopitz J; von Reitzenstein C; Andre S; Kaltner H; Uhl J; Ehemann V;
TI -
Cantz M; Gabius HJ
Negative regulation of neuroblastoma cell growth by
carbohydrate-dependent surface binding of galectin-1 and functional
divergence from galectin-3.
SO - J Biol Chem 2001 Sep 21;276(38):35917-23
AD - Institut fur Pathochemie und Neurochemie and the Pathologisches
Institut, Klinikum der Ruprecht-Karls-Universitat, Im Neuenheimer Feld
220, D-69120 Heidelberg, Germany.
The cell density-dependent growth inhibition of human SK-N-MC
neuroblastoma cells is initiated by increased ganglioside sialidase
activity leading to elevated cell surface presentation of ganglioside
GM1, a ligand of galectin-1. We herein show that the extent of the cell
surface expression of the galectin coincides with marked increases of
the sialidase activity. Reverse transcriptase-polymerase chain reaction
analysis excludes a regulation at the transcriptional level. Exposure of
cells to purified galectin-1 reveals its carbohydrate-dependent activity
to reduce cell proliferation. Assays to detect DNA fragmentation
biochemically and cytometrically and to block caspases render it
unlikely that galectin-1 acts as a classical proapoptotic factor on
these cells. Because the chimeric galectin-3 shares binding sites and
binding parameters with galectin-1 for these cells, we tested whether
this galectin will elicit the same response as the homodimeric
cross-linking galectin-1. Evidently, galectin-3 fails to affect cell
growth by itself but interferes with galectin-1 upon coincubation. Its
proteolytically truncated variant, the C-terminal lectin domain with
impaired capacity to form aggregates when surface bound, has only weak
binding properties. Thus, the way in which the galectin-1 interacts
topologically with an apparently common set of ligands relative to
galectin-3 is crucial for eliciting post-binding events. We conclude
that galectin-1 is a probable effector in the sialidase-dependent growth
control in this system. Moreover, the experiments with galectin-3 reveal
functional divergence, most probably based on different topologies of
presentation of homologous carbohydrate-binding sites.
18
UI - 21372266
AU - Gohil A; Croffie JM; Fitzgerald JF; Gupta SK; Del Rosario MA
TI -
Reversible intestinal pseudoobstruction associated with neural crest
tumors.
SO - J Pediatr Gastroenterol Nutr 2001 Jul;33(1):86-8
AD - James Whitcomb Riley Hospital for Children, Indiana University School of
Medicine, 702 Barnhill Drive, Indianapolis, IN 46202, U.S.A.
19
UI - 21523829
AU - Guzhova I; Hultquist A; Cetinkaya C; Nilsson K; Pahlman S; Larsson LG
TI -
Interferon-gamma cooperates with retinoic acid and phorbol ester to
induce differentiation and growth inhibition of human neuroblastoma
cells.
SO - Int J Cancer 2001 Oct 1;94(1):97-108
AD - Department of Genetics and Pathology, University of Uppsala, University
Hospital, Uppsala, Sweden.
The prognosis of patients with advanced stages of neuroblastoma with
N-myc amplification remains poor despite escalated therapy, a situation
that has called for alternative therapeutic approaches. Neuroblastoma
cells, which represent immature peripheral neuronal cells, treated with
certain physiologic and nonphysiologic agents such as retinoic acid
(RA), phorbol esters and interferons (IFN) in vitro undergo cellular
differentiation and stop to divide, a process that mimics normal
neuronal development. Such "differentiation therapy" using RA after
autologous bone marrow transplantation has recently given encouraging
results in neuroblastoma patients with advanced disease. Considering
approaches for improved differentiation therapy, we investigated
possible synergistic effects of combining agents known to influence
neuroblastoma growth and differentiation in vitro. Our results show that
combined treatment with IFN-gamma and RA or the phorbol ester
12-O-tetradecanoyl-phorbol acetate (TPA) had synergistic or enhancing
effects on morphologic differentiation and neurite outgrowth in 5 of 5
neuroblastoma cell lines, 3 of which expressed very high levels of N-myc
mRNA due to N-myc amplification. The combinations RA+IFN-gamma or
TPA+IFN-gamma also enhanced induced growth inhibition in all 5 cell
lines, in several cases resulting in complete growth arrest under
conditions where cells stimulated with either agent alone continued to
grow. The phenotypic effects of the combined RA+IFN-gamma or
TPA+IFN-gamma treatments were in most, but not all, investigated cases
accompanied by moderate reductions in N-myc expression, suggesting that
the cooperative signals may counteract N-Myc activity at several levels.
The cooperativity between IFN-gamma and other differentiation signals
may be relevant for approaches to improve the therapy for high-risk
neuroblastoma with N-myc-amplification. Copyright 2001 Wiley-Liss, Inc.
20
UI - 21523848
AU - Rossig C; Bollard CM; Nuchtern JG; Merchant DA; Brenner MK
TI -
Targeting of G(D2)-positive tumor cells by human T lymphocytes
engineered to express chimeric T-cell receptor genes.
SO - Int J Cancer 2001 Oct 15;94(2):228-36
AD - Center for Cell and Gene Therapy, Baylor College of Medicine, Houston,
TX 77030, USA.
Genetic engineering of human T lymphocytes to express tumor
antigen-specific chimeric immune receptors is an attractive means for
providing large numbers of effector cells for adoptive immunotherapy
while bypassing major mechanisms of tumor escape from immune
recognition. We have applied this strategy to the targeting of a
G(D2)-positive tumor, neuroblastoma, which is the commonest extracranial
solid tumor of childhood. Chimeric immune receptors were generated by
joining an extracellular antigen-binding domain derived from either of
the 2 ganglioside G(D2)-specific antibodies sc7A4 and sc14.G2a to a
cytoplasmic signaling domain. The variable domains of hybridoma antibody
14.G2a were cloned and selected using a phage display approach. Upon
coincubation with G(D2)-expressing tumor cell targets, human T
lymphocytes transduced with recombinant retroviruses encoding chimeric
receptors based on sc14.G2a, but not sc7A4, secreted significant levels
of cytokines in a pattern comparable to the cytokine response obtained
by engagement of the CD3 receptor. T cells transduced with the
sc14.G2a-based chimeric T-cell receptors also displayed specific lysis
of G(D2)-positive neuroblastoma cells, which was blocked in the presence
of monoclonal antibody 14.G2a. In the absence of nonspecific stimulation
of transduced cells, their functionality declined over time and
antigenic stimulation of the chimeric receptor alone did not induce
commitment to proliferation. These results support the feasibility of
redirecting human T lymphocytes to a tumor-associated ganglioside
epitope but emphasize that successful chimeric receptor-mediated
adoptive immunotherapy will require additional strategies that overcome
functional inactivation of gene-modified primary T lymphocytes.
Copyright 2001 Wiley-Liss, Inc.
21
UI - 21475583
AU - Rana B; Pearson AD; Redfern CP
TI -
RXR beta isoforms in neuroblastoma cells and evidence for a novel 3'-end
transcript.
SO - FEBS Lett 2001 Sep 28;506(1):39-44
AD - Department of Endocrinology, Medical Molecualr Biology Group, Medical
School, University of Newcastle upon Tyne, UK.
RXR beta is predominantly involved in retinoid responses in
neuroblastoma cells, in particular the N-type SH SY 5Y cells and the
S-type SH S EP cells, both derivatives of a mixed phenotype
neuroblastoma cell line. The aim of this study was to identify RXR beta
isoforms expressed in neuroblastoma cells and to characterise a putative
novel RXR beta transcript. RXR beta 1 and RXR beta 2 were expressed in
these neuroblastoma cells. An isoform with an insertion into the ligand
binding domain, RXR beta(SLSR) (referred to in previous studies as RXR
beta 3), was expressed at a similar level to RXR beta. A novel RXR beta
transcript was identified by RNase protection assays and was at least as
abundant as the expected RXR beta transcript and expressed in other cell
types. Evidence suggests that this novel transcript was transcribed from
an internal promoter between exons 5 and 6, contained a retained intron
(intron 6) and was alternatively spliced with and without the SLSR
insertion. These data show that the pattern of RXR beta expression is
complex. The relative abundance of the novel RXR beta transcript
suggests that it may be an important aspect of RXR beta function or
regulation in a range of cell types.
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