MIBG is available in UK (for a diferent tumor.)
http://www.cancerhelp.org.uk/help/default.asp?page=7193

St. Bart's, in London, is doing experimental treatments.
< http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20080321/cancer_project_0803
21/20080321?hub=TopStories >
Ask to have her transferred there.
Best wishes
J

On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:neuroplastoma <<

NeuroBlastoma ..

The treatment has been known for quite some time ..

Deferoxamine has been shown to reverse this.

It is an iron chelator ..

CANCERLIT®
AUTHOR: Fan L, Iyer J, Zhu S, Frick KK, Wada RK, Eskenazi
AE, Berg PE,   Ikegaki N, Kennett RH, Frantz CN
TITLE:
Inhibition of N-myc expression and induction of apoptosis by   iron
chelation in human neuroblastoma cells.
SOURCE:
Cancer Res; 61(3):1073-9 2001   UI: 21115842
ABSTRACT:
Neuroblastoma is the second most common solid malignancy of
childhood.
Enhanced expression of the amplified N-myc gene in the   tumor cells
may be associated with poor patient prognosis and may   contribute to
tumor
development and progression.
The use of   deferoxamine mesylate (DFO), an iron chelator, to treat
neuroblastoma   is being investigated in national clinical studies.
We show here by   TUNEL assay and DNA laddering that DFO induces
apoptosis in cultured   human neuroblastoma cells, which is preceded
by a
decrease in the   expression of N-myc and the altered expression of
some other
oncogenes   (up-regulating c-fos and down-regulating c-myb) but not
housekeeping   genes.
The decrease in N-myc expression is iron-specific but does not
result from inhibition of ribonucleotide reductase, because specific
inhibition of this iron-containing enzyme by hydroxyurea does not
affect N-myc protein levels.
Nuclear run-on and transient reporter gene expression experiments show
that the decrease in N-myc expression   occurs at the level of
initiation of transcription and by inhibiting   N-myc promoter
activity.
Comparison across neuroblastoma cell lines of   the amount of residual
cellular
N-myc protein with the extent of   apoptosis measured as pan-caspase
activity
after 48 h of iron   chelation reveals no correlation, suggesting that
the
decrease in   N-myc expression is unlikely to mediate apoptosis.
In conclusion,  chelation of cellular iron by DFO may alter the
expression of multiple   genes affecting the malignant phenotype by
multiple pathways.
Given   the clinical importance of N-myc overexpression in
neuroblastoma   malignancy, decreasing N-myc expression by DFO might
be useful as an
adjunct to current
MESH TERMS: Aphidicolin/Pharmacology   Apoptosis/*Drug Effects
Deferoxamine/*Pharmacology   Gene Expression/Drug Effects   Gene
Expression
Regulation, Neoplastic/Drug Effects   Genes, Reporter/Drug Effects
Genes,
myc/*Drug Effects/Genetics   Human   Hydroxyurea/Pharmacology
Inhibitory
Concentration 50   Iron/Metabolism   Iron Chelating Agents/
*Pharmacology
Neuroblastoma/Genetics/*Metabolism/*Pathology   Promoter Regions
(Genetics)/Drug Effects   Proto-Oncogene Proteins c-myc/Antagonists
and
Inhib/*Biosynthesis   Proto-Oncogenes/Drug Effects   RNA,
Messenger/Biosynthesis/Genetics   Substrate Specificity   Support, Non-
U.S.
Gov't   Support, U.S. Gov't, P.H.S.   Transcription, Genetic/Drug
Effects
Tumor Cells, Cultured   LANGUAGE: ENG   PUBLICATION TYPE: JOURNAL
ARTICLE
TITLE ABBREVIATION: Cancer Res   YEAR: 2001   ADDRESS: Department of
Pediatrics
and the Greenebaum Cancer Center,   University of Maryland School of
Medicine,
Baltimore 21201, USA.   ENTRY MONTH: 200104   CAS NO.: 0 (Iron
Chelating
Agents)   0 (Proto-Oncogene Proteins c-myc)   0 (RNA, Messenger)
127-07-1
(Hydroxyurea)   38966-21-1 (Aphidicolin)   70-51-9 (Deferoxamine)
7439-89-6
(Iron)   ID: NS34432\NS\NINDS

------------------------------

Biochim Biophys Acta 2002 Oct 2;1603(1):31 Related Articles,  Links

The role of iron in cell cycle progression and the proliferation of
neoplastic
cells.

Le N, Richardson D.

The Iron Metabolism and Chelation Group, The Heart Research Institute,
145
Missenden Rd, Camperdown, New South Wales, 2050, Sydney, Australia

Iron (Fe) is an obligate requirement for life and it is well known
that Fe
depletion leads to G(1)/S arrest and apoptosis.
These facts, together with
studies showing that Fe chelators can inhibit the growth of aggressive
tumours
such as neuroblastoma, suggest that Fe-deprivation may be an
important
therapeutic strategy.
To optimise the anti-proliferative effects of Fe chelators, the role
of Fe in cell cycle control requires intense investigation.
For many years, Fe chelators were known to prevent the activity of the
R2
subunit of ribonucleotide reductase (RR) that catalyzes the conversion
of
ribonucleotides into deoxyribonucleotides (dNTPs) for DNA synthesis.
In addition, Fe depletion may also inhibit the newly identified p53-
inducible form
of this molecule called p53R2.
This protein has the same Fe-binding sites as found in R2, and its
activity is thought to supply dNTPs for the critical process of DNA
repair.
Iron chelation also causes hypophosphorylation of the retinoblastoma
protein (pRb) and decreases the expression of cyclins A, B and D,
which are vital for cell cycle progression.
Other regulatory molecules whose expression is affected by Fe
depletion include p53 and hypoxia inducible factor-1alpha
(HIF-1alpha).
The levels of p53 increase following Fe chelation via the ability of
HIF-1alpha to bind and stabilize p53.
The activity of HIF-1alpha is controlled by an Fe-dependent enzyme
known as HIF-alpha prolyl hydroxylase (PH).
Chelation of Fe from this enzyme inhibits its activity, leading to
stabilization of HIF-1alpha and the subsequent effects on downstream
targets critical for angiogenesis and tumour growth.
The levels of p53 may also increase after Fe chelation by
phosphorylation of this protein at serine-15 and -37.
This prevents the interaction of p53 with murine double minute-2
(mdm-2)
and its degradation. Iron chelation also markedly increases the mRNA
levels of
the p53-inducible cyclin-dependent kinase (cdk) inhibitor, p21(WAF1/
CIP1).
Surprisingly, the increase in p21(WAF1/CIP1) mRNA was not reciprocated
at the
protein level, and this may result in cell cycle dysregulation.
This review will focus on the molecular mechanisms induced following
Fe chelation and the role of Fe in cell cycle progression.

PMID: 12242109 [PubMed - in process]
--------------------------------------------------------------------------

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:Neuroblastoma <<

"Deferoxamine has antitumor activity"

http://tinyurl.com/5y2q42

[Cancer Research 50, 4929-4930, August 15, 1990]
© 1990 American Association for Cancer Research

Effects of a Single Course of Deferoxamine in Neuroblastoma Patients1
Alberto Donfrancesco2, Giovanni Deb, Carlo Dominici, Domenico Pileggi,
Manuel A. Castello and Lawrence Helson
Pediatric Oncology Service, Ospedale Bambino Gesu' [A. D., G. D., D.
P.] and Department of Pediatrics, University "La Sapienza" [C. D., M.
A. C.], Rome, Italy, and Department of Pediatrics, New York Medical
College, New York, New York [L. H.]

A phase II trial of a single 5-day course of deferoxamine in 9
patients with neuroblastomas was completed. Within 2 days of
completion of treatment responses were observed in 7 of 9 patients and
there was no drug toxicity. These responses were a decrease in bone
marrow infiltration and, in one patient, a measurable reduction in her
tumor mass. We conclude that deferoxamine given as an 8-h i.v.
infusion daily for 5 days at 150 mg/kg/day has antitumor activity.

1 This work was supported by the Neuroblastoma Foundation of New
York.

2 To whom requests for reprints should be addressed, at Servizio di
Oncologia, Ospedale Bambino Gesu', Piazza S. Onofrio, 4, 00165 Rome,
Italy.

Received 9/11/89. Revised 4/16/90.

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:neuroblastoma <<

Role of deferoxamine in tumor therapy
DONFRANCESCO A. (1) ; DEB G. (1) ; DE SIO L. (1) ; COZZA R. (1) ;
CASTELLANO A. (1) ;
(1) Department of Oncology, Bambino Gesù Hospital, Rome, ITALIE

Abstract
Several studies are consistent with the hypothesis that available iron
may have some role in promoting tumor cell growth with different
biological mechanisms.
For this reason, several studies have been carried out to demonstrate
the antitumor activity of deferoxamine (DFO), an iron chelator with a
high affinity for ferritin-bound iron. In particular, the effects of
DFO have been studied in patients with neuroblastoma, where ferritin
is in part tumor derived and high concentrations correlate with poor
outcome.
To date, in vitro and in vivo studies demonstrating the antitumor
effects of DFO are very promising, but further investigations are
required to establish an exact role for DFO in the treatment of
cancer.
Revue / Journal Title
Acta haematologica   ISSN 0001-5792   CODEN ACHAAH
Source / Source
1996, vol. 95, no 1 (93 p.)  (16 ref.), pp. 66-69
Langue / Language
Anglais

Editeur / Publisher
Karger, Basel, SUISSE (1948) (Revue)

Mots-clés anglais / English Keywords
Neuroblastoma ; Chemical bond ; Iron ; Ferritin ; Chemotherapy ;
Antidote ; Chelating agent ; Generalization ; Treatment efficiency ;
Human ; Nervous system diseases ; Autonomic neuropathy ; Malignant
tumor ;
Mots-clés français / French Keywords
Neuroblastome ; Liaison chimique ; Fer ; Ferritine ; Chimiothérapie ;
Antidote ; Chélateur ; Déféroxamine ; Généralisation ; Efficacité
traitement ; Homme ; Système nerveux pathologie ; Système nerveux
sympathique pathologie ; Tumeur maligne ;
Mots-clés espagnols / Spanish Keywords
Neuroblastoma ; Enlace químico ; Hierro ; Ferritina ; Quimioterapia ;
Antídoto ; Quelante ; Generalización ; Eficacia tratamiento ; Hombre ;
Sistema nervioso patología ; Sistema nervioso simpático patología ;
Tumor maligno ;
Localisation / Location
INIST-CNRS, Cote INIST : 5518, 35400005293239.0070

Copyright 2007 INIST-CNRS. All rights reserved

Toute reproduction ou diffusion même partielle, par quelque procédé ou
sur tout support que ce soit, ne pourra être faite sans l'accord
préalable écrit de l'INIST-CNRS.
No part of these records may be reproduced of distributed, in any form
or by any means, without the prior written permission of INIST-CNRS.

Nº notice refdoc (ud4) : 3035643

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:neuroblastoma <<

"Desferrioxamine is already in clinical trial for neuroblastoma"

http://www.nature.com/bjp/journal/v135/n6/full/0704507a.html

Paper
British Journal of Pharmacology (2002) 135, 1393–1402; doi:10.1038/
sj.bjp.0704507

Desferrithiocin is a more potent antineoplastic agent than
desferrioxamine
Anthony Kicic1, Anita C G Chua1 and Erica Baker1

1Department of Physiology, University of Western Australia, Nedlands
6907, Western Australia, Australia

Correspondence: Erica Baker, Department of Physiology, University of
Western Australia, Nedlands 6907, Western Australia, Australia. E-
mail: baker@cyllene.uwa.edu.au

Received 24 October 2001; Accepted 15 November 2001.

Top of pageAbstract
Desferrithiocin (DFT) is an orally effective Fe chelator, with a
similar high affinity and selectivity for Fe to desferrioxamine (DFO),
which has been shown clinically to possess antineoplastic activity. In
this study, DFT was assessed for antineoplastic potential in
hepatocellular carcinoma cell lines (HCC). This was done as there are
few treatments for this aggressive neoplasm. The effects of DFT on
cell proliferation, cell cycle progression, Fe uptake and toxicity
were examined. To establish whether DFT was selective for cancer cells
a comparison was made with normal (non-proliferating) hepatocytes and
non-tumorigenic (proliferating) fibroblasts (SWISS-3T3). DFT was a
potent inhibitor of HCC proliferation (IC5040 M). DFO also inhibited
HCC proliferation under the same conditions, but was much less active
(IC50=110 – 210 M). When saturated with Fe, the activity of DFT, like
DFO, was greatly diminished, suggesting it may act by depriving the
cells of Fe or inactivating essential Fe pool(s). Indeed DFT rapidly
decreased Fe uptake from Tf-59Fe by hepatoma cells and also by normal
hepatocytes. However, DFT (and DFO) had much less effect on cell
survival in hepatocytes and fibroblasts than in hepatoma cells. DFT
may, like DFO, inhibit the cell cycle in the S phase of DNA synthesis.
Both chelators showed low toxicity. These results indicate that DFT
has potent antineoplastic activity in HCC. Further investigation into
the DFT class of Fe chelators seems warranted, particularly in view of
its high activity in relation to DFO, a chelator which is already in
clinical trial for neuroblastoma.

Keywords: Desferrithiocin, desferrioxamine, Fe chelators, Fe uptake,
hepatocellular carcinoma

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:neuroblastoma <<

"Cytotoxicity of deferoxamine for neuroblastoma cell lines"

Molecular Cancer Therapeutics 6, 886-897, March 1, 2007. doi:
10.1158/1535-7163.MCT-04-0331
© 2007 American Association for Cancer Research

Research Articles: Therapeutics, Targets, and Development

A fluorescence microplate cytotoxicity assay with a 4-log dynamic
range that identifies synergistic drug combinations
Tomas Frgala, Ondrej Kalous, Robert T. Proffitt and C. Patrick
Reynolds
Developmental Therapeutics Program, USC-CHLA Institute for Pediatric
Clinical Research, Childrens Hospital of Los Angeles and Division
Hematology-Oncology, Department of Pediatrics, The University of
Southern California Keck School of Medicine, Los Angeles, California

Requests for reprints: C. Patrick Reynolds, Developmental Therapeutics
Program, USC-CHLA Institute for Pediatric Clinical Research, Childrens
Hospital Los Angeles, MS#57, 4650 Sunset Boulevard, Los Angeles, CA
90027. Phone: 323-669-5646; Fax: 323-664-9226. E-mail:
preynolds@chla.usc.edu

Abstract

Purpose: Cytotoxicity assays in 96-well tissue culture plates allow
rapid sample handling for multicondition experiments but have a
limited dynamic range. Using DIMSCAN, a fluorescence digital image
system for quantifying relative cell numbers in tissue culture plates,
we have developed a 96-well cytotoxicity assay with a >4-log dynamic
range. Methods: To overcome background fluorescence that limits
detection of viable cells with fluorescein diacetate, we used 2'4'5'6'-
tetrabromofluorescein (eosin Y) to quench background fluorescence in
the medium and in nonviable cells to enhance the reduction of
background fluorescence achieved with digital image thresholding. The
sensitivity and linearity of the new assay were tested with serial
dilutions of neuroblastoma and leukemia cell lines. DIMSCAN was
compared with other in vitro cytotoxicity assays: 3-(4,5-
dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony
formation, and trypan blue dye exclusion. Results: Without background
fluorescence reduction, scans produced a nearly flat curve across
various cell concentrations from 100 to 106 cells per well. Either
digital image thresholding or eosin Y dramatically reduced background
fluorescence, and combining them achieved a linear correlation (r >
0.9) of relative fluorescence to viable cell number over >4 logs of
dynamic range, even in the presence of 4 x 104 nonviable cells per
well. Cytotoxicity of deferoxamine for neuroblastoma cell lines
measured by the DIMSCAN assay achieved dose-response curves similar to
data obtained by manual trypan blue counts or colony formation in soft
agar but with a wider dynamic range. Long-term cultures documented the
clonogenic ability of viable cells detected by DIMSCAN over the entire
dynamic range. The cytotoxicity of two drug combinations (buthionine
sulfoximine + melphalan or fenretinide + safingol) was tested using
both DIMSCAN and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
bromide (MTT) assays, and the wider dynamic range of DIMSCAN
facilitated detection of synergistic interactions. Conclusion: DIMSCAN
offers the ability to rapidly and efficiently conduct cytotoxicity
assays in 96-well plates with a dynamic range of >4 logs. This assay
enables rapid testing of anticancer drug combinations in microplates.
[Mol Cancer Ther 2007;6(3):886–97]

--------------------------------------------------------------------------------
Footnotes
Grant support: National Cancer Institute grants CA82830 and CA81403,
Ashley Barrasso Foundation, and Childrens Hospital of Los Angeles
Research Institute Career Development Award (T. Frgala).

The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
advertisement in accordance with 18 U.S.C. Section 1734 solely to
indicate this fact.

Note: Certain intellectual property rights pertaining to the contents
of this article are retained by Childrens Hospital Los Angeles as
described in U.S. patents 6,459,805 and 6,665,430.

Received 12/10/04; revised 12/ 9/06; accepted 2/ 1/07.

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:Neuroblastoma <<

"Neuroblastoma is extremely sensitive to inhibition by deferrioxamine"

Cancer Res. 1993 Sep 1;53 (17):3968-75 8358725 (P,S,E,B)
Neuroblastoma sensitivity to growth inhibition by deferrioxamine:
evidence for a block in G1 phase of the cell cycle.

[My paper] C Brodie, G Siriwardana, J Lucas, R Schleicher, N Terada, A
Szepesi, E Gelfand, P Seligman
Department of Medicine, University of Colorado Health Sciences Center,
Denver 80262.
Iron (Fe) is known to be necessary for cellular proliferation.
Previous studies have suggested that neuroblastoma cells appear to be
relatively sensitive to growth inhibition by a specific Fe chelator,
deferrioxamine (DFO), in vitro.
Also, DFO has been recently used for the treatment of neuroblastoma
patients.
In this paper we demonstrate that neuroblastoma cell proliferation in
vitro is extremely sensitive to inhibition by DFO as compared to
another cell line with almost identical growth kinetics.
Neuroblastoma cells treated with DFO adapt appropriately to Fe
chelation as measured by marked upregulation of transferrin receptor
mRNA, increased functional transferrin receptor, and decreased
cellular ferritin concentration.
Further studies that quantitated cellular incorporation of 59Fe from
added transferrin-59Fe in the presence of DFO indicated that
neuroblastoma cells were more sensitive to inhibition of Fe
incorporation by the chelator as compared to the other cell line.
Neuroblastoma cells treated with DFO showed a consistent arrest in the
G1 phase of the cell cycle.
For cells taken from the "resting" state this block occurred before
the vast majority of cells had entered S or G2-M phases of the cell
cycle.
Further evidence that neuroblastoma cells were arrested before the G1-
S interface was provided when cells inhibited by DFO and released into
aphidicolin exhibit arrest at the G1-S interface, whereas release from
aphidicolin into DFO resulted in entry into S phase.
Also, DFO-treated cells exhibited a decrease in both p34cdc2
immunoreactive protein as well as kinase activity.
The results of these latter studies strongly indicate evidence for a
Fe requirement for malignant cell proliferation before the onset of
DNA synthesis.
Our results also provide a basis for further studies that will better
define a therapeutic approach to patients with neuroblastoma utilizing
DFO treatment.
Mesh-terms: Aphidicolin :: pharmacology; Cell Count :: drug effects;
Cell Division :: drug effects; Deferoxamine :: administration &
dosage; Deferoxamine :: pharmacology; Drug Screening Assays,
Antitumor; Ferritin :: metabolism; G1 Phase :: drug effects; Glioma ::
drug therapy; Glioma :: metabolism; Glioma :: pathology; Human;
Iron :: metabolism; Neuroblastoma :: drug therapy; Neuroblastoma ::
metabolism; Neuroblastoma :: pathology; Receptors, Transferrin ::
metabolism; S Phase :: drug effects; Support, Non-U.S. Gov't; Support,
U.S. Gov't, P.H.S.; Transferrin :: metabolism; Tumor Cells, Cultured;

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On May 9, 1:03 pm, help_save_ser...@yahoo.co.uk wrote:neuroblastoma <<

"Effective antiproliferative agents"

Title: The iron metabolism of the human neuroblastoma cell: lack of
relationship between the efficacy of iron chelation and the inhibition
of DNA synthesis.
Author: Richardson, D R : Ponka, P
Citation: J-Lab-Clin-Med. 1994 Nov; 124(5): 660-71
Abstract: The mechanisms of iron uptake from transferrin and the
effects of iron chelators on these processes were investigated in
human neuroblastoma cells. This study was performed because numerous
reports have indicated that neuroblastoma cells contain iron-rich
ferritin and are also especially sensitive to iron chelation by
deferoxamine. The mechanisms of iron and transferrin uptake were
examined in the human neuroblastoma cell line SK-N-MC by using human
transferrin labeled with iodine 125 and iron 59. Internalized and
membrane-bound 59Fe and 125I-transferrin were separated with the
protease pronase. Total internalized and membrane 125I-transferrin
uptake was biphasic with time, whereas total and internalized 59Fe
uptake was linear. Iron uptake from transferrin was prevented by
incubation at 4 degrees C and also by lysosomotrophic agents. In
addition, 59Fe uptake occurred by two processes. The first process was
consistent with receptor-mediated endocytosis involving
internalization of transferrin bound to specific binding sites. Iron
uptake also occurred by a second process, which was not saturable up
to a transferrin concentration of 0.06 mg/ml. In terms of quantitative
iron uptake, however, the second process was far less important than
receptor-mediated endocytosis. Deferoxamine (0.25 mmol/L) only
slightly increased 59Fe release from prelabeled cells; the orally
effective iron chelator pyridoxal isonicotinoyl hydrazone (0.25 mmol/
L) was six times more effective. Moreover, when pyridoxal
isonicotinoyl hydrazone (0.2 mmol/L) was added together with labeled
transferrin over a 2-hour incubation, 59Fe uptake from transferrin
decreased to 18% of the control value, whereas deferoxamine (0.2 mmol/
L) had no appreciable effect. Even though deferoxamine (0.1 mmol/L)
had little effect on 59Fe uptake or release, it reduced uptake of
tritiated thymidine to 33% of the control value after a 24-hour
incubation. Three analogs of pyridoxal isonicotinoyl hydrazone,
pyridoxal benzoyl hydrazone (#101), pyridoxal p-methoxybenzoyl
hydrazone (#107), and pyridoxal m-fluorobenzoyl hydrazone (#109), had
chelation activities comparable to that of pyridoxal isonicotinoyl
hydrazone and were more effective than either deferoxamine or
pyridoxal isonicotinoyl hydrazone at preventing tritiated thymidine
uptake. These results suggest that the pyridoxal isonicotinoyl
hydrazone analogs have potential as effective antiproliferative agents
and deserve further investigation.
Review References: None
Notes: None
Language: English
Publication Type: Journal-Article
Keywords: DNA antagonists and inhibitors : Iron metabolism :
Neuroblastoma metabolism
URL: http://www.mosby.com/lab

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