| 1: Cancer Res. 2004 Oct 15;64(20):7596-603. |
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RNA interference targeting transforming growth
factor-beta enhances NKG2D-mediated antiglioma immune response, inhibits
glioma cell migration and invasiveness, and abrogates tumorigenicity in
vivo.
Friese MA, Wischhusen J, Wick W, Weiler M, Eisele G, Steinle A, Weller M.
Department of General Neurology, Hertie Institute for Clinical Brain
Research and Institute for Cell Biology, Department of Immunology,
University of Tubingen, Tubingen, Germany.
Transforming growth factor (TGF)-beta is the key molecule implicated in
impaired immune function in human patients with malignant gliomas. Here we
report that patients with glioblastoma, the most common and lethal type of
human glioma, show decreased expression of the activating immunoreceptor
NKG2D in CD8(+) T and natural killer (NK) cells. TGF-beta is responsible for
the down-regulation of NKG2D expression in CD8(+) T and NK cells mediated by
serum and cerebrospinal fluid of glioma patients in vitro. Moreover,
TGF-beta inhibits the transcription of the NKG2D ligand MICA. Interference
with the synthesis of TGF-beta1 and TGF-beta2 by small interfering RNA
technology prevents the down-regulation of NKG2D on immune cells mediated by
LNT-229 glioma cell supernatant and strongly enhances MICA expression in the
glioma cells and promotes their recognition and lysis by CD8(+) T and NK
cells. Furthermore, TGF-beta silencing results in a less migratory and
invasive glioma cell phenotype in vitro. LNT-229 glioma cells deficient in
TGF-beta exhibit a loss of subcutaneous and orthotopic tumorigenicity in
nude mice, and NK cells isolated from these mice show an activated
phenotype. RNA interference targeting TGF-beta1,2 results in a glioma cell
phenotype that is more sensitive to immune cell lysis and less motile in
vitro and nontumorigenic in nude mice, strongly confirming TGF-beta
antagonism as a major therapeutic strategy for the future treatment of
malignant gliomas.
PMID: 15492287 [PubMed - in process]
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| 2: Int J Cancer. 2004 Oct 21 [Epub ahead of print] |
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Impact of the coxsackie and adenovirus receptor (CAR) on
glioma cell growth and invasion: Requirement for the C-terminal domain.
Huang KC, Altinoz M, Wosik K, Larochelle N, Koty Z, Zhu L, Holland PC,
Nalbantoglu J.
Department of Neurology and Neurosurgery, McGill University and the Montreal
Neurological Institute, Montreal, Quebec, Canada.
Expression of the coxsackie and adenovirus receptor (CAR) is downregulated
in malignant glioma cell lines and is barely detectable in high-grade
primary astrocytoma (glioblastoma multiforme). We determined the effect of
forced CAR expression on the invasion and growth of the human glioma cell
line U87-MG, which does not express any CAR. Although retrovirally mediated
expression of full-length CAR in U87-MG cells did not affect monolayer
growth in vitro, it did reduce glioma cell invasion in a 3-dimensional
spheroid model. Furthermore, in xenograft experiments, intracerebral
implantation of glioma cells expressing full-length CAR resulted in tumors
with a significantly reduced volume compared to tumors generated by control
vector-transduced U87-MG cells. In contrast, U87-MG cells expressing
transmembrane CAR with a deletion of the entire cytoplasmic domain (except
for the first 2 intracellular juxtamembrane cysteine amino acids) had rates
of invasion and tumor growth that were similar to those of the control
cells. This difference in behavior between the 2 forms of CAR was not due to
improper cell surface localization of the cytoplasmically deleted CAR as
determined by comparable immunostaining of unpermeabilized cells, equivalent
adenoviral transduction of the cells and similar extent of fractionation
into lipid-rich domains. Taken together, these results suggest that the
decrease or loss of CAR expression in malignant glioma may confer a
selective advantage in growth and invasion to these tumors. (c) 2004
Wiley-Liss, Inc.
PMID: 15499626 [PubMed - as supplied by publisher]
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| 3: Int J Cancer. 2004 Oct 21 [Epub ahead of print] |
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Investigation of human brain tumors for the presence of
polyomavirus genome sequences by two independent laboratories.
Rollison DE, Utaipat U, Ryschkewitsch C, Hou J, Goldthwaite P, Daniel R,
Helzlsouer KJ, Burger PC, Shah KV, Major EO.
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health,
Baltimore, MD, USA.
JC virus (JCV), BK virus (BKV) and simian virus 40 (SV40) may be associated
with human brain tumors. These polyomaviruses have been shown to induce
brain tumors in experimentally infected animals. Several studies have found
polyomavirus genomic sequences in human brain tumor tissues by using
polymerase chain reaction (PCR), while others have not. Inconsistencies in
previous findings may be due in part to small sample sizes and differences
in underlying patient populations, laboratory techniques and quality control
measures. To assess the role of polyomaviruses in human brain tumors and
address inconsistencies of previous reports, we investigated the prevalence
of viral sequences in a series of 225 brain tumor tissue specimens in 2
independent laboratories. PCR followed by Southern hybridization was
performed at the National Institute of Neurological Disorders and Stroke
(NINDS). Real-time quantitative PCR was performed on the same tissues at
Johns Hopkins University (JHU). Only those tumors with amplifiable DNA were
tested further for polyomavirus sequences. Positive and negative control
tissues were included, and all specimens were masked. Amplifiable DNA was
detected in 225/225 (100%) tumors at NINDS, 9 (4%) of which contained
polyomavirus sequences (3 JCV-positive, 3 BKV-positive and 3 SV40-positive).
The JHU laboratory amplified DNA from 165/225 (73%) tumors, of which 1 tumor
tested positive (for SV40). No tumors tested positive in both laboratories.
Results for masked quality control tissues were concordant between
laboratories. Nucleotide sequences for JCV, BKV and SV40 are rarely present
in a large series of adult and pediatric brain tumors. (c) 2004 Wiley-Liss,
Inc.
PMID: 15499616 [PubMed - as supplied by publisher]
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| 4: Int J Cancer. 2004 Oct 21 [Epub ahead of print] |
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Tyrosine phosphorylation of PYK2 mediates
heregulin-induced glioma invasion: Novel heregulin/HER3-stimulated signaling
pathway in glioma.
van der Horst EH, Weber I, Ullrich A.
Cell Dynamics Group, Max Planck Institute for Biochemistry, Munich, Germany.
Receptor tyrosine kinases of the EGFR family transmit extracellular signals
that control diverse cellular functions such as proliferation,
differentiation and survival. Signaling function of a member of this family,
HER3, is believed to be impaired due to deviations in its kinase consensus
motifs. Here we address the functional role and signaling mechanisms of
HER3. HER3 preferentially forms heterodimers with HER2 inducing the most
potent mitogenic signal among EGFR family members. Our data show that in a
glioma-derived cell line the cytoplasmic tyrosine kinase PYK2 is
constitutively associated with HER3 and that stimulation with Heregulin
results in PYK2 tyrosine phosphorylation. HER3, but not HER2, mediates the
phosphorylation of the C-terminal region of PYK2 to promote a mitogenic
response through activation of the MAPK pathway. A central role of PYK2 in
signaling downstream of HER3 is substantiated by the demonstration that
expression of a dominant-negative PYK2-KM construct abrogates the
Heregulin-induced MAPK activity and inhibits the invasive potential of
glioma cells. These results suggest a novel Heregulin/HER3-stimulated
signaling pathway in glioblastoma-derived cell lines that involves
phosphorylation of PYK2 and mediates invasiveness of glioma cells. (c) 2004
Wiley-Liss, Inc.
PMID: 15499613 [PubMed - as supplied by publisher]
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| 5: J Clin Oncol. 2004 Oct 1;22(19):3916-21. |
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Phase I trial of intrathecal liposomal cytarabine in
children with neoplastic meningitis.
Bomgaars L, Geyer JR, Franklin J, Dahl G, Park J, Winick NJ, Klenke R,
Berg SL, Blaney SM.
Texas Children's Cancer Center/Baylor College of Medicine, 6621 Fannin, MC
3-3320, Houston, TX 77030, USA. lbomgaars@txccc.org
PURPOSE: We performed a phase I trial of intrathecal (IT) liposomal
cytarabine (DepoCyt; Enzon Pharmaceuticals, Piscataway, NJ and SkyePharma
Inc, San Diego, CA) to determine the maximum-tolerated dose, the
dose-limiting toxicities, and the plasma and CSF pharmacokinetics of IT
lipsomal cytarabine in children >/= 3 years of age with advanced
meningeal malignancies. PATIENTS AND METHODS: Eighteen assessable patients
received IT liposomal cytarabine through either an indwelling ventricular
access device or via lumbar puncture. Liposomal cytarabine was given once
every 2 weeks during induction, once every 4 weeks during consolidation, and
once every 8 weeks during the maintenance phase of treatment. The initial
dose was 25 mg, with subsequent escalations to 35 and 50 mg. CSF
pharmacokinetic samples were obtained in a subset of patients. RESULTS:
Arachnoiditis, characterized by fever, headache, nausea, vomiting, and back
pain was noted in the first two patients at the 25 mg dose level. Therefore,
subsequent patients were treated with dexamethasone, beginning the day of
liposomal cytarabine administration and continuing for 5 days. Headache
(grade 3) was dose limiting in two of eight patients enrolled at the 50 mg
dose level. Eight of the 14 patients assessable for response demonstrated
evidence of benefit manifest as prolonged disease stabilization or response.
CONCLUSION: The maximum-tolerated dose and recommended phase II dose of
liposomal cytarabine in patients between the ages of 3 and 21 years is 35
mg, administered with dexamethasone (0.15 mg/kg/dose, twice a day for 5
days). A phase II trial of IT liposomal cytarabine in children with CNS
leukemia in second or higher relapse is in development.
Publication Types:
- Clinical Trial
- Clinical Trial, Phase I
PMID: 15459213 [PubMed - indexed for MEDLINE]
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| 6: J Neurol Neurosurg Psychiatry. 2004 Oct;75(10):1489-91. |
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Massive reduction of tumour load and normalisation of
hyperprolactinaemia after high dose cabergoline in metastasised prolactinoma
causing thoracic syringomyelia.
van Uum SH, van Alfen N, Wesseling P, van Lindert E, Pieters GF, Nooijen
P, Hermus AR.
Department of Endocrinology, University Medical Center Nijmegen, The
Netherlands. Stan.VanUum@sjhc.london.on.ca
In 1970 a 20 year old woman presented with a pituitary chromophobe adenoma
for which she underwent transfrontal pituitary surgery. In 1978 she had to
be reoperated on because of local tumour recurrence, resulting in
hypopituitarism. Bromocriptine (5 mg/day) was given for 15 years, but the
plasma prolactin levels remained elevated. In 2000 the patient presented
with signs and symptoms suggestive of a spinal cord lesion at the
mid-thoracic level. A magnetic resonance imaging (MRI) scan showed an
extensive leptomeningeal mass extending from the brainstem to L5, with a
thoracic syringomyelia at the T7-T8 level. The plasma prolactin level was
very high (5114 microg/l). A biopsy showed the presence of a metastasised
prolactinoma.On administration of high dose cabergoline, 0.5 mg twice a day
orally, the plasma prolactin levels decreased within one month and then
normalised within 26 months. Tumour load reduced considerably but
unfortunately, her signs and symptoms did not improve. This case illustrates
that a high dose dopamine agonist might be an important therapeutic option
in patients with a metastasised prolactinoma.
Publication Types:
PMID: 15377706 [PubMed - indexed for MEDLINE]
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| 7: J Neuropathol Exp Neurol. 2004 Sep;63(9):978-89. |
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Role of Ang1 and its interaction with VEGF-A in
astrocytomas.
Zadeh G, Koushan K, Pillo L, Shannon P, Guha A.
From Arthur and Sonia Labatts Brain Tumor Center, Hospital for Sick
Children, University of Toronto, Toronto, Canada.
Angiopoietins (Ang1 and Ang2) modulate the activity of the endothelial cell
(EC)-specific receptor tyrosine kinase Tie2, which together with vascular
endothelial growth factor (VEGF-A) and its EC-specific receptors, VEGFR1 and
VEGFR2, regulate normal physiological vessel development. The functional
role of angiopoietins in tumor angiogenesis, in particular astrocytoma
angiogenesis, remains unclear. In this study, we focus on the specific
contribution of Ang1 to the vascular growth of glioblastoma multiforme (GBM)
and its interactive role with VEGF-A. Subcutaneous and intracranial GBM
xenografts were generated using 3 established astrocytoma cell lines (U87,
U373, and U343) that were transfected to stably over-express Ang1. GBM
xenografts were also generated to express low levels of VEGF-A and high
Angl. We found that Ang1 increases the vascular growth of both subcutaneous
and intracranial xenografts of GBM by approximately 3-fold. However, the
increased vascular growth was only seen in xenografts with concurrent VEGF-A
elevation, since decreasing VEGF-A expression resulted in a loss of the
pro-angiogenic growth advantage seen with Ang1. Collectively, our data
suggest that Ang1 regulates GBM vascularity in a VEGF-A dependent manner,
synergizing the initial pro-angiogenic response that is triggered by VEGF-A
and promoting the vascular growth of GBM.
PMID: 15453096 [PubMed - indexed for MEDLINE]
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| 8: Neurol Res. 2004 Oct;26(7):785-91. |
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IkappaB(alpha)M suppresses angiogenesis and tumorigenesis
promoted by a constitutively active mutant EGFR in human glioma cells.
Wu JL, Abe T, Inoue R, Fujiki M, Kobayashi H.
Department of Neurosurgery, Oita University, School of Medicine, 1-1,
Idaigaoka, Hasama-machi, Oita, Japan.
Human glioma cell lines (G36DeltaEGFR and IN500DeltaEGFR) have been shown to
display an enhanced tumorigenic phenotype, when transfected with a
constitutively active form of the epidermal growth factor receptor
(DeltaEGFR). These cells were transfected with a mutant IkappaB(alpha)
(IkappaB(alpha)M) that is resistant to phosphorylation and degradation, and
hence blocks NF-kappaB activity. Recently, EGFR has been shown to increase
the activity of NF-kappaB and to induce angiogenesis. In this report, we
asked if IkappaB(alpha)M gene transfer into human glioma cell lines would
inhibit tumorigenicity and angiogenesis in glioma. IkappaBalphaM inhibited
in vitro and in vivo expression of vascular endothelial growth factor (VEGF)
and interleukin 8 (IL-8). Human glioma xenografts treated with IkappaBalphaM
gene transfer exhibited significantly decreased angiogenesis both in an
orthotopic and in an ectopic model. The decreased expression of VEGF and
IL-8 directly correlated with decreased tumorigenicity, and tumor
vascularization. Taken in combination, these results provide strong evidence
of IkappaB(alpha)M's role in regulating glioma angiogenesis even in the
presence of constitutive EGFR activation.
PMID: 15494123 [PubMed - in process]
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| 9: Neurol Res. 2004 Oct;26(7):760-2. |
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Intra-vital ultrasonographic monitoring of intra-cerebral
tumor growth in a rat glioma model: technical note.
Nestler U, Luecke M, Joedicke A, Winking M.
Department of Neurosurgery, Justus Liebig University, Giessen, Germany.
The assessment of therapeutic effects in rodent glioma models by comparison
of post mortem tumor sizes has to deal with differing individual growth
kinetics and the possibility of spontaneous tumor regression. This technical
note describes the intravital ultrasonographical monitoring of cerebral
tumor growth in individual animals. In the experiments C6 lacZ glioma cells
were injected intracerebrally into female Wistar rats. Extended craniectomy
allowed for transcutaneous sonographic examination of the tumor growth. Four
animals were followed ultrasonographically, the volumes of the tumors were
calculated and plotted graphically, and on day 21 histological evaluation
was performed. Our results show that ultrasonography is an easy and reliable
imaging modality for frequent assessment of tumor growth kinetics in the
intra-cerebral rat glioma model. It allows for the intravital monitoring of
treatment with new therapeutic strategies and increases the reliability of
the model by visualization of the tumor size before initiation of treatment.
PMID: 15494118 [PubMed - in process]
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| 10: Neuroradiology. 2004 Jan;46(1):65-71. Epub 2003 Nov 27. |
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MRI and intraoperative findings in cavernous haemangiomas
of the spinal cord.
Weinzierl MR, Krings T, Korinth MC, Reinges MH, Gilsbach JM.
Department of Neurosurgery, RWTH Aachen, Pauwelsstrasse 30, 52057, Germany.
Martin.Weinzierl2@post.rwth-aachen.de
More sensitive imaging techniques, such as MRI, have led to an increase in
the number of reported cases of spinal cord cavernous haemangioma (SCCH).
Complete surgical resection has been performed with good outcomes. However,
operative findings do not always confirm preoperative MRI as to the size and
site (superficial or deep) of the lesion. We evaluated whether MRI can be
used to predict whether or not SCCH reach the surface of the spinal cord,
since this has an impact on surgical strategy. We reviewed the preoperative
MRI, case-notes and video recordings of 12 patients who underwent surgery,
at which five superficial and seven deep-seated lesions were identified.
T1-weighted images correctly indicated the site of the lesion in ten,
T2-weighted images in only eight. One deep lesion was thought to be
superficial on both T1- and T2-weighted images. Intravenous contrast medium
was not helpful in diagnosis or localisation. In no case was a surgically
proven superficial lesion interpreted as deep in the spinal cord.
PMID: 14648007 [PubMed - indexed for MEDLINE]
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| 11: Oncogene. 2004 Oct 18 [Epub ahead of print] |
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PKC-eta mediates glioblastoma cell proliferation through
the Akt and mTOR signaling pathways.
Aeder SE, Martin PM, Soh JW, Hussaini IM.
1Department of Pathology and Neurology, University of Virginia,
Charlottesville, VA 22908, USA.
We previously demonstrated that protein kinase C-eta (PKC-eta) mediates a
phorbol 12-myristate-13-acetate (PMA)-induced proliferative response in
human glioblastoma (GBM) cells. In this report, we show that PMA-stimulated
activation of PKC-eta in U-251 GBM cells resulted in activation of both Akt
and the mammalian target of rapamycin (mTOR) signaling pathways and an
increase in cell proliferation. Expression of a kinase dead PKC-eta
(PKC-etaKR) construct reduced the basal and PMA-evoked proliferation of
PKC-eta-expressing U-251 GBM cells, as well as abrogated the PMA-induced
activation of Akt, mTOR, and the mTOR targets 4E-BP1 and STAT-3. Treatment
of cells with the PI-3 kinase inhibitor LY294002 (10 μM) or the mTOR
inhibitor rapamycin (10 nM) also reduced PMA-induced proliferation and
cell-cycle progression. Expression of a constitutively active PKC-eta
(PKC-etaDeltaNPS) construct in a GBM cell line with no endogenous PKC-eta
(U-1242) also provided evidence that PKC-eta targets the Akt and mTOR
signaling pathways. Moreover, activation of 4E-BP1 and STAT-3 in both
PMA-treated U-251 and PKC-etaDeltaNPS-expressing U-1242 GBM cells was
inhibited by rapamycin. However, activation of Akt, but not mTOR was
inhibited by the PI-3 kinase inhibitor LY294002. This study identifies Akt
and mTOR as downstream targets of PKC-eta that are involved in GBM cell
proliferation.Oncogene advance online publication, 18 October 2004;
doi:10.1038/sj.onc.1208093.
PMID: 15489897 [PubMed - as supplied by publisher]
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| 12: Oncogene. 2004 Sep 20;23(43):7274-82. |
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Self-renewal and solid tumor stem cells.
Al-Hajj M, Clarke MF.
University of Michigan Medical School, CCGC Room 4410, 1500 E Medical Center
Drive, Ann Arbor 48109-0936, USA.
Solid tumors arise in organs that contain stem cell populations. The tumors
in these tissues consist of heterogeneous populations of cancer cells that
differ markedly in their ability to proliferate and form new tumors. In both
breast cancers and central nervous system tumors, cancer cells differ in
their ability to form tumors. While the majority of the cancer cells have a
limited ability to divide, a population of cancer stem cells that has the
exclusive ability to extensively proliferate and form new tumors can be
identified based on marker expression. Growing evidence suggests that
pathways that regulate the self-renewal of normal stem cells are deregulated
in cancer stem cells resulting in the continuous expansion of self-renewing
cancer cells and tumor formation. This suggests that agents that target the
defective self-renewal pathways in cancer cells might lead to improved
outcomes in the treatment of these diseases.
Publication Types:
PMID: 15378087 [PubMed - indexed for MEDLINE]
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| 13: Oncogene. 2004 Sep 20;23(43):7267-73. |
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Cancer stem cells in nervous system tumors.
Singh SK, Clarke ID, Hide T, Dirks PB.
The Arthur and Sonia Labatt Brain Tumor Research Centre, The Hospital for
Sick Children, Toronto, Canada.
Most current research on human brain tumors is focused on the molecular and
cellular analysis of the bulk tumor mass. However, evidence in leukemia and
more recently in solid tumors such as breast cancer suggests that the tumor
cell population is heterogeneous with respect to proliferation and
differentiation. Recently, several groups have described the existence of a
cancer stem cell population in human brain tumors of different phenotypes
from both children and adults. The finding of brain tumor stem cells (BTSCs)
has been made by applying the principles for cell culture and analysis of
normal neural stem cells (NSCs) to brain tumor cell populations and by
identification of cell surface markers that allow for isolation of distinct
tumor cell populations that can then be studied in vitro and in vivo. A
population of brain tumor cells can be enriched for BTSCs by cell sorting of
dissociated suspensions of tumor cells for the NSC marker CD133. These
CD133+ cells, which also expressed the NSC marker nestin, but not
differentiated neural lineage markers, represent a minority fraction of the
entire brain tumor cell population, and exclusively generate clonal tumor
spheres in suspension culture and exhibit increased self-renewal capacity.
BTSCs can be induced to differentiate in vitro into tumor cells that
phenotypically resembled the tumor from the patient. Here, we discuss the
evidence for and implications of the discovery of a cancer stem cell in
human brain tumors. The identification of a BTSC provides a powerful tool to
investigate the tumorigenic process in the central nervous system and to
develop therapies targeted to the BTSC. Specific genetic and molecular
analyses of the BTSC will further our understanding of the mechanisms of
brain tumor growth, reinforcing parallels between normal neurogenesis and
brain tumorigenesis.
Publication Types:
PMID: 15378086 [PubMed - indexed for MEDLINE]
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| 14: Pediatr Hematol Oncol. 2004 Apr-May;21(3):279-89. |
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The prognosis and survival of childhood acute
lymphoblastic leukemia with central nervous system relapse.
Unal S, Yetgin S, Cetin M, Gumruk F, Arslan D, Ozyurek E, Tuncer M, Topcu
M.
Hacettepe University, Faculty of Medicine, Department of Pediatrics,
Pediatric Hematology and Neurology Unit, 06100 Ankara, Turkey.
Central nervous system (CNS) relapse in childhood acute lymphoblastic
leukemia (ALL) has been overcome by sensitive therapeutic approachs. This
study was planned to present the development of CNS relapse and survival in
newly diagnosed 190 ALL patients whose cases were followed in the authors'
unit between March 1991 and May 2002. St. Jude Study XI protocol was given
to the patients who applied between March 1991 and March 1997 (group A) (n =
122), and St. Jude Study XIII protocol was given to the patients who applied
between March 1997 and May 2002 (group B) (n = 68). The patients having
isolated CNS relapse in group A received craniospinal irradiation (CSI)
median 3.5 months after CNS relapse (range 2-6 months), a short time after
reinduction, and 2 cures of consolidation. In group B, patients having
isolated CNS relapse received IT once a month and a high-dose methotrexate
treatment once every 8 weeks and 3 or 4, cures later therapy CSI median 7
months after CNS relapse (range 6-8 months) was given. When the overall
survival rates of the 2 groups are compared, a statistically significant
higher survival rate at 5 years was determined in group B than in group A
(respectively, 82.3%, 58.4%) (p < .05). When subgroups of the patients
(that is, those with no relapse, isolated CNS or BM relapse, or CNS + BM
relapse) were compared in both groups, it was found that survival was much
higher for the ones with no relapse and with isolated CNS relapse
(respectively, 87.9%, 72.7%) compared to isolated BM or CNS + BM relapse
groups (respectively, 10%, 13.3%) (p < .05). In a conclusion, for
children with acute lymphoblastic leukemia and an isolated CNS relapse, with
delayed definitive craniospinal irradiation allowing more intensive systemic
and intrathecal chemotherapy results in better overall survival than has
been previously reported.
Publication Types:
PMID: 15202168 [PubMed - indexed for MEDLINE]
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| 15: J Neurooncol. 2004 Jul;68(3):243-4. |
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Neurolymphomatosis.
Baehring J, Cooper D.
Department of Neurology, Neurosurgery, and Internal Medicine, Yale
University School of Medicine, USA.
Publication Types:
PMID: 15332327 [PubMed - indexed for MEDLINE]
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Volume 3, Supplement 9 - 26 October 2004