| 1: Br
J Cancer. 2006 Sep 5; [Epub ahead of print] |
|
-
Phase II trial of radiotherapy after hyperbaric
oxygenation with chemotherapy for high-grade gliomas.
Ogawa K, Yoshii Y, Inoue O, Toita T, Saito A,
Kakinohana Y, Adachi G, Iraha S, Tamaki W, Sugimoto
K, Hyodo A, Murayama S.
1Department of Radiology, University of the Ryukyus School of Medicine, 207
Uehara, Nishihara-cho, Okinawa 903-0215, Japan.
We conducted a phase II trial to evaluate the efficacy and toxicity of
radiotherapy immediately after hyperbaric oxygenation (HBO) with
chemotherapy in adults with high-grade gliomas. Patients with histologically
confirmed high-grade gliomas were administered radiotherapy in daily 2 Gy
fractions for 5 consecutive days per week up to a total dose of 60 Gy. Each
fraction was administered immediately after HBO with the period of time from
completion of decompression to irradiation being less than 15 min.
Chemotherapy consisted of procarbazine, nimustine (ACNU) and vincristine and
was administered during and after radiotherapy. A total of 41 patients (31
patients with glioblastoma and 10 patients with grade 3 gliomas) were
enrolled. All 41 patients were able to complete a total radiotherapy dose of
60 Gy immediately after HBO with one course of concurrent chemotherapy. Of
30 assessable patients, 17 (57%) had an objective response including four CR
and 13 PR. The median time to progression and the median survival time in
glioblastoma patients were 12.3 months and 17.3 months, respectively. On
univariate analysis, histologic grade (P=0.0001) and Karnofsky performance
status (P=0.036) had a significant impact on survival, and on multivariate
analysis, histologic grade alone was a significant prognostic factor for
survival (P=0.001). Although grade 4 leukopenia and grade 4 thrombocytopenia
occurred in 10 and 7% of all patients, respectively, these were transient
with no patients developing neutropenic fever or intracranial haemorrhage.
No serious nonhaematological or late toxicities were seen. These results
indicated that radiotherapy delivered immediately after HBO with
chemotherapy was safe with virtually no late toxicity in patients with
high-grade gliomas. Further studies are required to strictly evaluate the
effectiveness of radiotherapy after HBO for these tumours.British Journal of
Cancer advance online publication, 5 September 2006;
doi:10.1038/sj.bjc.6603342 www.bjcancer.com.
PMID: 16953239 [PubMed - as supplied by publisher]2
-
| 2: Br
J Neurosurg. 2006 Aug;20(4):250-3. |
|
-
A rare case of recurrent secretory meningioma with
malignant transformation.
Shivane
AG, Chakrabarty
A, Baborie
A, Thiryayi
W, Donaldson
MH, Ross
S.
Departments of Histopathology.
A 72-year-old woman previously operated for a sphenoid-ridge meningioma, now
presented with double vision. Histology showed a secretory meningioma with
an epithelial-appearing, malignant component. Malignant transformation in a
secretory meningioma is not known. This is the first report of such an
occurrence.
PMID: 16954080 [PubMed - in process]2
-
| 3: Br
J Neurosurg. 2006 Aug;20(4):246-9. |
|
-
Aggressive and invasive growth of tectal glioma after
surgical intervention and chemoradiotherapy.
Matsuno
A, Nagashima
H, Ishii
H, Iwamuro
H, Nagashima
T.
Department of Neurosurgery, Teikyo University Ichihara Hospital, Anesaki,
Ichihara City, Chiba.
A tectal glioma presenting with late-onset aqueduct stenosis and obstructive
hydrocephalus is usually categorized as a benign glioma. Apparent clinical
or radiological progression justifies biopsy of the tumour. In this case, an
unusual tumour shows aggressive and invasive growth after surgical
intervention and chemoradiotherapy.
PMID: 16954079 [PubMed - in process]2
-
| 4: Br
J Neurosurg. 2006 Aug;20(4):239-41. |
|
-
Disseminated intravascular coagulation complicating
resection of a malignant meningioma.
Brecknell
JE, McLean
CA, Hirano
H, Malham
GM.
Departments of Neurosurgery.
A 70-year-old woman developed disseminated intravascular coagulation (DIC)
during a craniotomy for a parasagittal anaplastic/malignant meningioma. This
was successfully treated with rapid resection of the tumour and
haematological replacement, but a poor neurological outcome resulted. The
tumour was demonstrated to express tissue factor, an important causative
factor in other tumour associated DIC and previously shown to be expressed
by malignant meningiomas. A link between the two is suggested.
PMID: 16954076 [PubMed - in process]2
-
| 5: Br
J Neurosurg. 2006 Aug;20(4):233-5. |
|
-
De novo meningioma arising at a previous burr hole site.
Rodrigues
D, Scoones
D, Bradey
N, Aziz
F, Kane
P.
Departments of Neurosurgery.
A case of meningioma that developed at a site of a previously performed burr
hole is reported. To the best of our knowledge, this is the first reported
case of a meningioma arising at a previous burr hole site. The possible
reasons for its causation are discussed.
PMID: 16954074 [PubMed - in process]2
-
| 6: Cancer.
2006 Sep 5; [Epub ahead of print] |
|
-
Gliomatosis cerebri: 20 Years of experience at the
Children's Hospital of Philadelphia.
Armstrong
GT, Phillips
PC, Rorke-Adams
LB, Judkins
AR, Localio
AR, Fisher
MJ.
Division of Oncology, The Children's Hospital of Philadelphia, University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
BACKGROUND.: Gliomatosis cerebri (GC) is a rare and typically fatal glial
neoplasm of the central nervous system. In this report, the authors describe
the largest cohort of children to date with GC and explore relations between
potential prognostic factors, treatment, and survival. METHODS.: Imaging,
pathologic, and outcome data were reviewed from 13 patients who were
diagnosed with GC and were treated at the Children's Hospital of
Philadelphia (CHOP) between 1982 and 2005. All patients had GC confirmed by
biopsy. Twelve patients received cranial irradiation, and 8 of those
patients received adjuvant chemotherapy. A single patient age 1 year
received chemotherapy alone. A review of the literature identified 51
pediatric patients with GC. RESULTS.: The progression-free survival rate in
this study was 13% (range, 1.5-43 months), and the overall survival (OS)
rate was 64% (range, 6.5-67 months) at 2 years. OS was significantly shorter
for patients who presented in the first decade of life (P = .04). The time
to progression was prolonged significantly for patients who had no evidence
of tumor enhancement on imaging studies (P = .03). When survival data from
patients reported in the literature were combined with the CHOP cohort,
treatment prolonged OS significantly (P = .003). CONCLUSIONS.: The outcome
of pediatric patients with GC was extremely poor; however, the current
results indicated that treatment may prolong OS. Age < 10 years and
contrast enhancement on magnetic resonance imaging studies at diagnosis may
be risk factors for shorter survival in pediatric patients with GC. Cancer
2006. (c) 2006 American Cancer Society.
PMID: 16955507 [PubMed - as supplied by publisher]2
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| 7: Cancer
Res. 2006 Sep 1;66(17):8912-7. |
|
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The extent and severity of vascular leakage as evidence
of tumor aggressiveness in high-grade gliomas.
Cao
Y, Nagesh
V, Hamstra
D, Tsien
CI, Ross
BD, Chenevert
TL, Junck
L, Lawrence
TS.
Departments of Radiation Oncology, Radiology, and Neurology, University of
Michigan, Ann Arbor, Michigan.
Magnetic resonance imaging reveals heterogeneous regions within high-grade
gliomas, such as a contrast-enhanced rim, a necrotic core, and
non-contrast-enhanced abnormalities. It is unclear which of these regions
best describes tumor aggressiveness. We hypothesized that the vascular
leakage volume, reflecting disorganized angiogenesis typical of glioblastoma,
would be a strong predictor of clinical outcome. The FLAIR tumor volume,
post-gadolinium T1 tumor volume, tumor vascular leakage volume determined by
dynamic contrast-enhanced imaging, and volume of the contrast-enhanced rim
seen on post-gadolinium T1-weighted images were defined for 20 patients
about to undergo treatment for newly diagnosed high-grade gliomas. The
potential for imaging characteristics to improve prediction of survival and
time to progression over clinical variables was tested by using Cox
regression analysis. Single-variable Cox regression analysis of each of the
four tumor subvolumes revealed that the vascular leakage volume was the only
significant predictor of survival. When the joint effect of clinical
variables and the vascular leakage volume were tested for prediction of
survival, only the age and the vascular leakage volume were selected as
significant predictors. However, when time to progression was tested as a
dependent variable, both the vascular leakage volume and the vascular
permeability were selected as copredictors, along with surgical status. Our
findings suggest that for patients with high-grade glioma, time to
progression after radiation therapy is influenced by both underlying
biological aggressiveness (vascularity) and volume of aggressive tumor. In
contrast, survival depends chiefly on the volume of aggressive tumor at the
time of presentation. (Cancer Res 2006; 66(17): 8912-7).
PMID: 16951209 [PubMed - in process]3
-
| 8: Cancer
Res. 2006 Sep 1;66(17):8722-30. |
|
-
AAL881, a Novel Small Molecule Inhibitor of RAF and
Vascular Endothelial Growth Factor Receptor Activities, Blocks the Growth of
Malignant Glioma.
Sathornsumetee
S, Hjelmeland
AB, Keir
ST, McLendon
RE, Batt
D, Ramsey
T, Yusuff
N, Rasheed
BK, Kieran
MW, Laforme
A, Bigner
DD, Friedman
HS, Rich
JN.
Departments of Surgery, Pathology, Pediatrics, Medicine, and Neurobiology,
Duke University Medical Center, Durham, North Carolina.
Malignant gliomas are highly proliferative and angiogenic cancers resistant
to conventional therapies. Although RAS and RAF mutations are uncommon in
gliomas, RAS activity is increased in gliomas. Additionally, vascular
endothelial growth factor and its cognate receptors are highly expressed in
gliomas. We now report that AAL881, a novel low-molecular weight inhibitor
of the kinase activities associated with B-RAF, C-RAF (RAF-1), and VEGF
receptor-2 (VEGFR2), showed activity against glioma cell lines and
xenografts. In culture, AAL881 inhibited the downstream effectors of RAF in
a concentration-dependent manner, with inhibition of proliferation
associated with a G(1) cell cycle arrest, induction of apoptosis, and
decreased colony formation. AAL881 decreased the proliferation of bovine
aortic endothelial cells as well as the tumor cell secretion of vascular
endothelial growth factor and inhibited the invasion of glioma cells through
an artificial extracellular matrix. Orally administered AAL881 was well
tolerated with minimal weight loss in non-tumor-bearing mice. Established
s.c. human malignant glioma xenografts grown in immunocompromised mice
treated with a 10-day course of oral AAL881 exhibited growth delays relative
to control tumors, frequently resulting in long-term complete regressions.
AAL881 treatment extended the survival of immunocompromised mice bearing
orthotopic glioma xenografts compared with placebo controls. The
intraparenchymal portions of orthotopic AAL881-treated tumors underwent
widespread necrosis consistent with vascular disruption compared with the
subarachnoid elements. These effects are distinct from our prior experience
with VEGFR2 inhibitors, suggesting that targeting RAF itself or in
combination with VEGFR2 induces profound tumor responses in gliomas and may
serve as a novel therapeutic approach in patients with malignant gliomas.
(Cancer Res 2006; 66(17): 8722-30).
PMID: 16951188 [PubMed - in process]2
-
| 9: Cancer
Res. 2006 Sep 1;66(17):8662-71. |
|
-
Calreticulin, a Molecular Chaperone in the Endoplasmic
Reticulum, Modulates Radiosensitivity of Human Glioblastoma U251MG Cells.
Okunaga
T, Urata
Y, Goto
S, Matsuo
T, Mizota
S, Tsutsumi
K, Nagata
I, Kondo
T, Ihara
Y.
Department of Biochemistry and Molecular Biology in Disease, Atomic Bomb
Disease Institute.
Radiotherapy is the primary and most important adjuvant therapy for
malignant gliomas. Although the mechanism of radiation resistance in gliomas
has been studied for decades, it is still not clear how the resistance is
related with functions of molecular chaperones in the endoplasmic reticulum.
Calreticulin (CRT) is a Ca(2+)-binding molecular chaperone in the
endoplasmic reticulum. Recently, it was reported that changes in
intracellular Ca(2+) homeostasis play a role in the modulation of apoptosis.
In the present study, we found that the level of CRT was higher in
neuroglioma H4 cells than in glioblastoma cells (U251MG and T98G), and was
well correlated with the sensitivity to gamma-irradiation. To examine the
role of CRT in the radiosensitivity of malignant gliomas, the CRT gene was
introduced into U251MG cells, which express low levels of CRT, and the
effect of overexpression of CRT on the radiosensitivity was examined. The
cells transfected with the CRT gene exhibited enhanced radiation-induced
apoptosis compared with untransfected control cells. In CRT-overexpressing
cells, cell survival signaling via Akt was markedly suppressed. Furthermore,
the gene expression of protein phosphatase 2Acalpha (PP2Acalpha), which is
responsible for the dephosphorylation and inactivation of Akt, was
up-regulated in CRT-overexpressing cells, and the regulation was dependent
on Ca(2+). Thus, overexpression of CRT modulates radiation-induced apoptosis
by suppressing Akt signaling through the up-regulation of PP2Acalpha
expression via altered Ca(2+) homeostasis. These results show the novel
mechanism by which CRT is involved in the regulation of radiosensitivity and
radiation-induced apoptosis in malignant glioma cells. (Cancer Res 2006;
66(17): 8662-71).
PMID: 16951181 [PubMed - in process]1
-
| 10: Cancer
Res. 2006 Sep 1;66(17):8550-7. |
|
-
A1 adenosine receptors in microglia control glioblastoma-host
interaction.
Synowitz
M, Glass
R, Farber
K, Markovic
D, Kronenberg
G, Herrmann
K, Schnermann
J, Nolte
C, van
Rooijen N, Kiwit
J, Kettenmann
H.
Cellular Neuroscience Group, Max Delbruck Center for Molecular Medicine.
We report that experimental glioblastoma grow more vigorously in A(1)
adenosine receptor (A(1)AR)-deficient mice associated with a strong
accumulation of microglial cells at and around the tumors. A(1)ARs were
prominently expressed in microglia associated with tumor cells as revealed
with immunocytochemistry but low in microglia in the unaffected brain
tissue. The A(1)AR could also be detected on microglia from human
glioblastoma resections. To study functional interactions between tumor and
host cells, we studied glioblastoma growth in organotypical brain slice
cultures. A(1)AR agonists suppressed tumor growth. When, however, microglial
cells were depleted from the slices, the agonists even stimulated tumor
growth. Thus, adenosine attenuates glioblastoma growth acting via A(1)AR in
microglia. (Cancer Res 2006; 66(17): 8550-7).
PMID: 16951167 [PubMed - in process]1
-
| 11: Cancer
Res. 2006 Sep 1;66(17):8511-8519. |
|
-
Ionizing Radiation Enhances Matrix Metalloproteinase-2
Secretion and Invasion of Glioma Cells through Src/Epidermal Growth Factor
Receptor-Mediated p38/Akt and Phosphatidylinositol 3-Kinase/Akt Signaling
Pathways.
Park
CM, Park
MJ, Kwak
HJ, Lee
HC, Kim
MS, Lee
SH, Park
IC, Rhee
CH, Hong
SI.
Laboratory of Functional Genomics, Department of Neurosurgery, and
Laboratory Medicine and Clinical Pathology, Korea Institute of Radiological
and Medical Sciences, Seoul, Korea and Research Institute and Hospital,
National Cancer Center, Goyang, Gyeonggi, Korea.
Glioblastoma is a severe type of primary brain tumor, and its highly
invasive character is considered to be a major therapeutic obstacle. Several
recent studies have reported that ionizing radiation (IR) enhances the
invasion of tumor cells, but the mechanisms for this effect are not well
understood. In this study, we investigated the possible signaling mechanisms
involved in IR-induced invasion of glioma cells. IR increased the matrix
metalloproteinase (MMP)-2 promoter activity, mRNA transcription, and protein
secretion along with the invasiveness of glioma cells lacking functional
PTEN (U87, U251, U373, and C6) but not those harboring wild-type (WT)-PTEN
(LN18 and LN428). IR activated phosphatidylinositol 3-kinase (PI3K), Akt,
and mammalian target of rapamycin, and blockade of these kinases by specific
inhibitors (LY294002, Akt inhibitor IV, and rapamycin, respectively) and
transfection of dominant-negative (DN) mutants (DN-p85 and DN-Akt) or WT-PTEN
suppressed the IR-induced MMP-2 secretion in U251 and U373 cells. In
addition, inhibitors of epidermal growth factor receptor (EGFR; AG490 and
AG1478), Src (PP2), and p38 (SB203580), EGFR neutralizing antibody, and
transfection of DN-Src and DN-p38 significantly blocked IR-induced Akt
phosphorylation and MMP-2 secretion. IR-induced activation of EGFR was
suppressed by PP2, whereas LY294002 and SB203580 did not affect the
activations of p38 and PI3K, respectively. Finally, these kinase inhibitors
significantly reduced the IR-induced invasiveness of these cells on Matrigel.
Taken together, our findings suggest that IR induces Src-dependent EGFR
activation, which triggers the p38/Akt and PI3K/Akt signaling pathways,
leading to increased MMP-2 expression and heightened invasiveness of PTEN
mutant glioma cells. (Cancer Res 2006; 66(17): 8511-9).
PMID: 16951163 [PubMed - as supplied by publisher]1
-
| 12: Cancer
Res. 2006 Sep 1;66(17):8492-500. |
|
-
Ephrin-B3 Ligand Promotes Glioma Invasion through
Activation of Rac1.
Nakada
M, Drake
KL, Nakada
S, Niska
JA, Berens
ME.
The Translational Genomics Research Institute, Phoenix, Arizona.
Eph receptor tyrosine kinases are involved in nervous system development.
Eph ligands, termed ephrins, are transmembrane proteins that bind to Eph
receptors, the mutual activation of which causes repulsive effects in
reciprocally contacting cells. Previously, we showed that overexpression of
EphB2 in glioma cells increases cell invasion. Here, expression profiles of
ephrin-B family members were determined in four glioma cell lines and in
invading glioblastoma cells collected by laser capture microdissection.
Ephrin-B3 mRNA was up-regulated in migrating cells of four of four glioma
cell lines (1.3- to 1.7-fold) and in invading tumor cells of eight of eight
biopsy specimens (1.2- to 10.0-fold). Forced expression of ephrin-B3 in low
expressor cell lines (U87, T98G) stimulated cell migration and invasion in
vitro and ex vivo, concomitant with tyrosine phosphorylation of ephrin-B3.
In high expressor cell lines (U251, SNB19), ephrin-B3 colocalized with Rac1
to lamellipodia of motile wild-type cells. Cells transfected with ephrin-B3
small interfering RNA (siRNA) showed significant morphologic change and
decreased invasion in vitro and ex vivo. Depletion of endogenous ephrin-B3
expression abrogated the increase of migration and invasion induced by
EphB2/Fc, indicating increased invasion is dependent on ephrin-B3
activation. Furthermore, using a Rac1-GTP pull-down assay, we showed that
ephrin-B3 is associated with Rac1 activation. Reduction of Rac1 by siRNA
negated the increased invasion by addition of EphB2/Fc. In human glioma
specimens, ephrin-B3 expression and phosphorylation correlated with
increasing tumor grade. Immunohistochemistry revealed robust staining for
phosphorylated ephrin-B and ephrin-B3 in invading glioblastoma cells. These
data show that ephrin-B3 expression and signaling through Rac1 are
critically important to glioma invasion. (Cancer Res 2006; 66(17):
8492-500).
PMID: 16951161 [PubMed - in process]1
-
| 13: Cancer
Res. 2006 Sep 1;66(17):8469-76. |
|
-
Genome-wide Hypomethylation in Human Glioblastomas
Associated with Specific Copy Number Alteration, Methylenetetrahydrofolate
Reductase Allele Status, and Increased Proliferation.
Cadieux
B, Ching
TT, Vandenberg
SR, Costello
JF.
The Brain Tumor Research Center, Departments of Neurological Surgery and
Pathology, University of California, San Francisco, California.
Genome-wide reduction in 5-methylcytosine is an epigenetic hallmark of human
tumorigenesis. Experimentally induced hypomethylation in mice promotes
genomic instability and is sufficient to initiate tumorigenesis. Here, we
report that global hypomethylation is common in primary human glioblastomas
[glioblastoma multiforme (GBM)] and can affect up to an estimated 10 million
CpG dinucleotides per haploid tumor genome. Demethylation involves satellite
2 (Sat2) pericentromeric DNA at chromosomes 1 and 16, the subtelomeric
repeat sequence D4Z4 at chromosomes 4q and 10q, and interspersed Alu
elements. Severe hypomethylation of Sat2 sequences is associated with copy
number alterations of the adjacent euchromatin, suggesting that
hypomethylation may be one factor predisposing to specific genetic
alterations commonly occurring in GBMs. An additional apparent consequence
of global hypomethylation is reactivation of the cancer-testis antigen
MAGEA1 via promoter demethylation, but only in GBMs and GBM cell lines
exhibiting a 5-methylcytosine content below a threshold of approximately
50%. Primary GBMs with significant hypomethylation tended to be heterozygous
or homozygous for the low-functioning Val allele of the rate-limiting methyl
group metabolism gene methylenetetrahydrofolate reductase (MTHFR), or had a
deletion encompassing this gene at 1p36. Tumors with severe genomic
hypomethylation also had an elevated proliferation index and deletion of the
MTHFR gene. These data suggest a model whereby either excessive cell
proliferation in the context of inadequate methyl donor production from
MTHFR deficiency promotes genomic hypomethylation and further genomic
instability, or that MTHFR deficiency-associated demethylation leads to
increased proliferative activity in GBM. (Cancer Res 2006; 66(17): 8469-76).
PMID: 16951158 [PubMed - in process]1
-
| 14: Childs
Nerv Syst. 2006 Sep 2; [Epub ahead of print] |
|
-
Thalamic gliomas in children: an extensive clinical,
neuroradiological and pathological study of 14 cases.
Fernandez
C, Maues
de Paula A, Colin
C, Quilichini
B, Bouvier-Labit
C, Girard
N, Scavarda
D, Lena
G, Figarella-Branger
D.
Department of Pathology and Neuropathology, Hopital de la Timone, 264 rue
Saint-Pierre, 13385, Marseille Cedex 05, France.
OBJECT: Thalamic tumors represent only 1 to 5% of brain neoplasms but
frequently affect children. However, pediatric series are rare and go back
to several years in spite of recent advances in the neuroradiological,
pathological, and molecular fields. METHODS: We report a series of 14
pediatric thalamic gliomas with clinical, neuroradiological, and
pathological studies including p53 immunostaining in 11 cases and 1p19q
status in three cases. RESULTS: Our series included five pilocytic
astrocytomas, seven oligodendrogliomas, and two glioblastomas. Pilocytic
astrocytomas were characterized by strong contrast enhancement, lack of p53
expression, and excellent prognosis. Oligodendrogliomas frequently
demonstrated an aspect of unilateral thalamic enlargement lacking or with
slight contrast enhancement. Some of them expressed p53 or demonstrated 1p
loss. Anaplastic oligodendrogliomas and glioblastomas displayed a poor
outcome, with a mean survival of 8 months after surgery. CONCLUSION: Our
series of pediatric thalamic gliomas clearly distinguishes pilocytic
astrocytomas from anaplastic oligodendrogliomas regarding neuroimaging,
pathology, and prognosis.
PMID: 16951965 [PubMed - as supplied by publisher]2
-
| 15: Childs
Nerv Syst. 2006 Sep 2; [Epub ahead of print] |
|
-
Current concepts in the molecular genetics of pediatric
brain tumors: implications for emerging therapies.
Tamber
MS, Bansal
K, Liang
ML, Mainprize
TG, Salhia
B, Northcott
P, Taylor
M, Rutka
JT.
Division of Neurosurgery, The Hospital for Sick Children, The University of
Toronto, Toronto, Ontario, Canada.
BACKGROUND: The revolution in molecular biology that has taken place over
the past 2 decades has provided researchers with new and powerful tools for
detailed study of the molecular mechanisms giving rise to the spectrum of
pediatric brain tumors. Application of these tools has greatly advanced our
understanding of the molecular pathogenesis of these lesions. REVIEW: After
familiarizing readers with some promising new techniques in the field of
oncogenomics, this review will present the current state of knowledge as it
pertains to the molecular biology of pediatric brain neoplasms. Along the
way, we hope to highlight specific instances where the detailed mechanistic
knowledge acquired thus far may be exploited for therapeutic advantage.
PMID: 16951964 [PubMed - as supplied by publisher]2
-
| 16: Clin Neuropathol. 2006 Jul-Aug;25(4):204. |
|
Comment on:
- Clin
Neuropathol. 2005 Nov-Dec;24(6):257-61.
History and nature of pseudopsammoma bodies.
Matyja
E, Naganska
E.
Publication Types:
PMID: 16866303 [PubMed - indexed for MEDLINE]
-
| 17: Clin Neuropathol. 2006 Jul-Aug;25(4):200-3. |
|
Gliosarcoma with liposarcomatous component, bone
infiltration and extracranial growth.
Borota
OC, Scheie
D, Bjerkhagen
B, Jacobsen
EA, Skullerud
K.
Department of Pathology, The University Hospital
Rikshospitalet-Radiumhospitalet, Sognsvannsveien 20, 0027 Oslo, Norway.
olivera.borota@rikshospitalet.no
Gliosarcoma is a highly malignant brain tumor consisting of both a
glioblastoma and a mesenchymal component. The latter typically resembles
fibrosarcoma, but differentiation patterns resembling osteosarcoma,
chondrosarcoma, angiosarcoma and rhabdomyosarcoma have also been described.
Molecular-genetic studies have shown that both glioblastoma and the
mesenchymal component share identical cytogenetic abnormalities or
mutations, suggesting a monoclonal origin from glial cells. We report an
unusual case of gliosarcoma that presented as a large intracerebral tumor
with infiltration of the temporal bone and the soft tissues in the
infratemporal fossa. Microscopically, the tumor consisted of alternating
areas of glioblastoma and fibrosarcoma. Focally, areas ofosteosarcomatous
and liposarcomatous differentiation were found. Although gliosarcoma with
transcranial penetration is very rare, it should be suspected in case of
intracranial tumor with glioblastoma-imaging features, infiltration of bone
and extracranial growth. Our case of liposarcomatous differentiation in
gliosarcoma--together with another very recently reported similar
case--expands the morphologic heterogeneity of this peculiar brain tumor.
Publication Types:
PMID: 16866302 [PubMed - indexed for MEDLINE]3
-
| 18: Clin Neuropathol. 2006 Jul-Aug;25(4):185-92. |
|
Papillary tumor of the pineal region--a new pathological
entity.
Kern
M, Robbins
P, Lee
G, Watson
P.
Neurosurgical Service of Western Australia, Sir Charles Gairdner Hospital,
Perth, Australia. michael_kern@gmx.de
Papillary tumor of the pineal region has recently been proposed as a new,
distinct clinicopathological entity. On the basis of the immunophenotypic
and ultrastructural properties of these lesions, origin from specialized
ependymocytes of the subcommissural organ was postulated. We present the
third publication on a papillary pineal tumor and describe the
morphological, immunohistochemical and ultrastructural features of this
neoplasm. The patient was a young woman who presented with signs of raised
intracranial pressure and Parinaud syndrome. Magnetic resonance imaging
revealed a neoplastic lesion in the pineal region. She underwent surgical
resection of the tumor through a midline infratentorial-supracerebellar
approach. Papillary tumor of the pineal region represents a new, distinct
clinicopathological entity. The differential diagnosis, possible
histogenesis and management of these lesions are discussed.
Publication Types:
PMID: 16866300 [PubMed - indexed for MEDLINE]2
-
| 19: Eur
J Cancer. 2006 Sep 4; [Epub ahead of print] |
|
-
Treatment of high risk medulloblastomas in children above
the age of 3 years: A SFOP study.
Verlooy
J, Mosseri
V, Bracard
S, Tubiana
AL, Kalifa
C, Pichon
F, Frappaz
D, Chastagner
P, Pagnier
A, Bertozzi
AI, Gentet
JC, Sariban
E, Rialland
X, Edan
C, Bours
D, Zerah
M, Le
Gales C, Alapetite
C, Doz
F.
Department of Paediatric Oncology, Institut Curie, Service d'Oncologie
Pediatrique, 26 rue d'Ulm, 75231 Paris Cedex 05, France.
AIM: Improvement of EFS of children older than 3 years with high risk
medulloblastoma. METHODS: Between 1993 and 1999, 115 patients (3-18 years,
mean 8 years) with high risk medulloblastoma were included. After surgery
treatment consisted of chemotherapy ('8in1' and etoposide/carboplatin)
before and after craniospinal radiotherapy. RESULTS: Patients were staged
using Chang-criteria (PF residue only, M1 and M2/M3) by local investigator
as well as by central review panel (82.4% concordance). Chemotherapy was
well tolerated without major delays in radiotherapy. With a mean follow up
of 81 months (9-119), 5-year EFS was 49.8% and OS 60.1%. In detail according
to subgroups EFS was 68.8% for PF residue only, 58.8% for M1 disease and
43.1% for M2/M3. CONCLUSION: M1 patients are legitimate high risk patients.
Survival rates are still very low for high risk medulloblastoma patients and
future trials should therefore focus on more intensive
(chemotherapy/radiotherapy) treatment.
PMID: 16956759 [PubMed - as supplied by publisher]2
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| 20: J Neurooncol. 2006 Sep 6; [Epub ahead of print] |
|
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Clear cell Meningioma, an uncommon variant of meningioma:
a clinicopathologic study of nine cases.
Jain
D, Sharma
MC, Sarkar
C, Suri
V, Garg
A, Singh
M, Sharma
BS, Mahapatra
AK.
Department of Pathology, All India Institute of Medical Sciences, New Delhi,
110029, India, sharmamehar@yahoo.co.in.
AIMS: Clear cell meningioma (CCM) is an uncommon variant of meningioma,
which affect younger patients, occur more often in spinal or cerebello
pontine locations and shows a higher recurrence rate. Only few case reports
have been described in the literature. The study has been undertaken to
document the clinicopathological features of nine cases of CCM, operated at
All India Institute of Medical Sciences during 1998 to December 2005.
METHODS: Clinical information was retrieved from the records of our
Neurosurgery Department. The cases were stained with H&E, periodic Acid
Schiff (PAS) with and without diastase. Immunohistochemistry for
pancytokeratin, epithelial membrane antigen, vimentin, glial fibrillary
acidic protein, and MIB-1 was done in all cases. RESULTS: During a period of
8 years, nine cases of CCM were diagnosed. Age ranged from 10 to 65 years
(median age 26.0 years) with female predominance. Most common location was
posterior fossa (CP angle). Clinically most of the patients presented with
history of headache and features of cranial nerve palsies. The duration of
symptoms varied from 3 to 60 months (mean 16.7 and median of 4 months).
Radiologically lesions showed homogenous enhancement and were isointense to
brain parenchyma. Histopathologic examination revealed tumor cells to be
arranged in sheets with clear cytoplasm and monomorphic nuclei. MIB-1
labeling index (LI) ranged from 2 to 12% with a mean of 9%. Follow up varied
from 3 to 84 months (median 36 months) and recurrence was noted in two
patients after 2 and 3 years of surgery, respectively, despite their low
MIB-1 labeling indices. CONCLUSIONS: CCM is a rare variant of meningioma
with poor outcome. Less than 50 cases have been described in the literature.
Low rate of recurrence and recurrence despite their low MIB-1 LI are some of
the features, which needs to be documented. Hence, larger number of cases
with adequate follow-up data need to be studied further to establish the
clinical significance of this variant.
PMID: 16955223 [PubMed - as supplied by publisher]2
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| 21: J Neurooncol. 2006 Sep 6; [Epub ahead of print] |
|
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Human glioblastoma biopsy spheroids xenografted into the
nude rat brain show growth inhibition after stereotactic radiosurgery.
Thorsen
F, Enger
PO, Wang
J, Bjerkvig
R, Pedersen
PH.
Department of Oncology and Medical Physics, Haukeland University Hospital,
Jonas Lies vei 65, 5021, Bergen, Norway.
BACKGROUND: The Gamma Knife is currently used to boost treatment of
malignant gliomas. However, few experimental studies have focused on its
radiobiological effects. In this work, the growth and invasiveness of human
glioblastoma spheroids xenografted into nude rat brains were assessed after
radiosurgery. Temporary in vitro as well as long-term in vivo radiation
effects were studied. METHODS: Glioblastoma biopsy spheroids were irradiated
with 12 or 24 Gy. Short-term in vitro spheroid viability and tumour cell
migration was determined by microscopic techniques. Pre-irradiated
glioblastoma spheroids were implanted into brains of immunosuppressed rats.
Long-term tumour development was assessed by magnetic resonance (MR)
imaging, and animal survival was recorded. An immunohistochemical analysis
was performed on the sectioned rat brains. RESULTS: Both un-irradiated and
irradiated spheroids remained viable during 2 months in culture, but a
dose-dependent inhibition of tumour growth and migration was seen. MR
imaging 4 weeks after implantation also showed a dose-dependent inhibition
in tumour development. Median animal survival times were 25.5 days (control
group), 43 days (12 Gy group) and 96 days (24 Gy group). The study of in
vivo long-term radiation effects on the remaining viable tumour population
showed no difference in Ki-67 labelling index and microvascular density
before and after radiosurgery. CONCLUSIONS: A dose-dependent inhibition of
tumour growth and invasion, as well as a dose-dependent increase in animal
survival was observed. The model system described is well suited for
assessing the radiobiological effects of Gamma Knife radiosurgery. The
results indicate that radiosurgery of malignant gliomas might be effective
in controlling tumour progression in selected glioblastoma patients.
PMID: 16955221 [PubMed - as supplied by publisher]2
-
| 22: J Neurooncol. 2006 Sep 6; [Epub ahead of print] |
|
-
Growth inhibition and induction of apoptosis and
differentiation of tanshinone IIA in human glioma cells.
Wang
J, Wang
X, Jiang
S, Yuan
S, Lin
P, Zhang
J, Lu
Y, Wang
Q, Xiong
Z, Wu
Y, Ren
J, Yang
H.
Division of Experimental Oncology, State Key Laboratory of Biotherapy, West
China Hospital, Sichuan University, Chengdu, 610041, Sichuan, P.R. China,
xiujiewang@yahoo.com.
Tanshinone IIA is a derivative of phenanthrene-quinone isolated from Danshen,
a widely used Chinese herbal medicine. It has antioxidant properties,
cytotoxic activities against multiple human cancer cells, inducing apoptosis
and differentiation of some human cancer cells. The purpose of this study is
to confirm its anticancer activity on human glioma cells, and to elucidate
mechanism of its activity. Human glioma cells were tested in vitro for
cytotoxicity, colony formation inhibition, BrdU incorporation after
treatment with tanshinone IIA. Its effect of apoptosis induction was
detected through EB/AO staining, cell cycle analysis and the expressions of
ADPRTL1 and CYP1A1 genes, the differentiation induction effect was
investigated through morphology, mRNA and protein expressions of GFAP and
nestin genes by RT-PCR and immunocytochemistry. Tanshinone IIA demonstrated
a dose- and time-dependent inhibitory effect on cell growth, IC(50) was 100
ng/ml, and it significantly inhibited colony formation and BrdU
incorporation of human glioma cells. After treatment with 25-100 ng/ml of
tanshinone IIA, the apoptotic cells increased significantly (P < 0.01),
the cells in G(0)/G(1) phase increased (P < 0.01), and decreased in S
phase, ADPRTL1 and CYP1A1 mRNA expression increased 1-2 folds. The cells
treated with 100 ng/ml tanshinone IIA demonstrated astrocytes or neuron-like
morphology, GFAP mRNA and protein expressions increased, nestin mRNA and
protein expressions decreased significantly. The findings in this study
suggested that tanshinone IIA exhibited strong effects on growth inhibition
and induction of apoptosis and differentiation in human glioma cells. It
might serve as a novel promising differentiation-inducing and/or therapeutic
agent for human gliomas, and need to be investigated further.
PMID: 16955220 [PubMed - as supplied by publisher]2
-
| 23: J Neurooncol. 2006 Sep 6; [Epub ahead of print] |
|
-
Evaluation of molecular genetic alterations associated
with tumor progression in a case of gliomatosis cerebri.
Braeuninger
S, Schneider-Stock
R, Kirches
E, Powers
JM, Korones
DN, Mawrin
C.
Department of Neuropathology, Otto-von-Guericke-University, Leipziger Str.
44, D-39120 , Magdeburg, Germany, christian.mawrin@medizin.uni-magdeburg.de.
Gliomatosis cerebri (GC) is a rare tumor characterized by widespread
infiltration of the brain and spinal cord. Although GC usually demonstrates
histomorphological features of a low-grade tumor, the formation of secondary
highly malignant tumor regions may occur. In order to reveal molecular
genetic changes associated with tumor progression in GC, we analyzed factors
known to be associated with malignant progression in common astocytomas in
an unusual GC case of an 18-year-old patient suffering from this disease for
almost 7 years. We detected allelic losses in the Rb gene and in exon 4 of
the TP53 gene in a tumor region corresponding to a glioblastoma multiforme.
EGFR or MDM2 gene amplifications were absent, and no PTEN mutation or
allelic loss on chromosome 10 could be detected. Moreover, compared to
tumor-free brain tissue of this patient, tumor regions showed increased EGFR
expression. These findings show that malignant progression in GC might be
associated with the acquisition of molecular genetic changes also found in
low-grade astrocytomas with progression to secondary glioblastoma. These
data support the notion that GC can be regarded as a subtype of a common
astrocytoma.
PMID: 16955219 [PubMed - as supplied by publisher]
-
| 24: J Neurooncol. 2006 Jun;78(2):145-51. Epub 2006 May 13. |
|
-
PET Imaging of cerebral astrocytoma with 13N-ammonia.
Xiangsong
Z, Changhong
L, Weian
C, Dong
Z.
Department of Nuclear Medicine, The First Affiliated Hospital, Sun Yat-sen
University, Guangzhou, China. sd_zh@163.net
We performed this study in order to assess the clinical potential of
(13)N-ammonia PET in patients with cerebral astrocytoma. METHODS: Dynamic
13N-ammonia PET was performed in 25 patients with suspected cerebral gliomas
or recurrent cerebral astrocytomas (19 male and 6 female patients; age range
18-64 years) detected by MRI. The histopathological diagnoses were made for
all cases either by biopsy or craniotomy, except for one patient with brain
infarction and one patient with brain radiation necrosis confirmed by
repeated MRI imaging. PET images were visually inspected, and the
tumor-to-white matter count (T/W) ratios and the perfusion index (PI) of the
tumors were determined. RESULTS: Six out of nine cases of low-grade gliomas
were detected with 13N-ammonia PET, and three non-astrocytoma low-grade
gliomas were not detected with 13N-ammonia PET. All 11 high-grade
astrocytomas exhibited markedly increased uptake of 13N-ammonia. The five
non-neoplastic lesions exhibited low uptake, low T/W ratios and low PI. The
significant differences were observed between high-grade and low-grade
gliomas with respect to both the T/W ratios and PI (T/W ratios: 5.92+/-2.27,
n=11 vs. 1.66+/-0.61, n=9, P<0.01; PI: 5.22+/-1.67, n=11 vs. 1.60+/-0.54,
n=9, P<0.01). There were the significant differences between the T/W
ratios and PI in low-grade astrocytomas and that in non-neoplastic lesions
(T/W ratios: 2.00+/-0.42, n=6 vs. 0.97+/-0.11, n=5, P<0.01; PI:
1.89+/-0.37, n=6 vs. 0.99+/-0.03, n=5, P<0.01). CONCLUSIONS: There is a
substantial uptake of 13N-ammonia in cerebral astrocytomas. 13N-ammonia PET
may enable differentiation between low- and high-grade astrocytomas, and has
the potential to enable differentiation between low-grade astrocytomas and
non-neoplastic lesions.
Publication Types:
PMID: 16739028 [PubMed - indexed for MEDLINE]2
-
| 25: J Neurooncol. 2006 Jun;78(2):107-11. Epub 2006 May 13. |
|
-
A dyad symmetry element in the fibroblast growth factor-2
gene promoter with different levels of activity in astrocytoma and
hepatocelluar carcinoma cell lines.
Ueba
T, Mori
H, Takahashi
JA, Nozaki
K, Hashimoto
N.
Department of Neurosurgery, Kishiwada City Hospital, Kishiwada, 596-8501,
Osaka, and Department of Neurosurgery, Kyoto University Graduate School of
Medicine, Japan. tueba@kuhp.kyoto-u.ac.jp
Fibroblast growth factor-2 (FGF-2) gene expression is reported to be
spatially and temporally regulated in the process of development, normal
growth, and wound healing. We postulated that its constitutive expression in
human malignant astrocytoma cells is due to loss of function of the
regulatory mechanism of FGF-2 gene expression. Here, we report the
characterization of a unique element in the FGF-2 gene promoter. We
investigated the transcriptional regulation of the FGF-2 gene in a human
malignant astrocytoma (U87MG) and a human hepatocellular carcinoma (HepG2)
cell line. We found that a dyad symmetry element (DSE) in the FGF-2 gene
promoter exhibited different promoter activities; in HepG2 cells it did,
while in U87MG cells it did not, exhibit repressive activity. Examination of
the relative promoter activities of the DSE in a thymidine kinase promoter
revealed it exerted different activities, just as it did in the 2 cell lines
studied.Gel shift assay demonstrated that 2 proteins bound to the DSE in
nuclear extracts from HepG2 cells and that one protein was missing in
nuclear extracts from U87MG cells. These results suggest that the DSE has a
crucial role as a transcriptional regulatory element of FGF-2 gene
expression.
PMID: 16739027 [PubMed - indexed for MEDLINE]1
-
| 26: J Neurooncol. 2006 Jun;78(2):123-7. Epub 2006 Apr 14. |
|
-
Gemistocytic astrocytomas: histomorphology, proliferative
potential and genetic alterations--a study of 32 cases.
Avninder
S, Sharma
MC, Deb
P, Mehta
VS, Karak
AK, Mahapatra
AK, Sarkar
C.
Department of Pathology, All India Institute of Medical Sciences, Ansari
Nagar, 110029, New Delhi, India.
Gemistocytic astrocytomas (GAs) are a distinct variant of astrocytomas,
generally classified as WHO grade II, and are associated with an aggressive
biological behavior. This study was undertaken to determine the
histomorphological spectrum, and correlate these with their proliferative
potential and genetic alterations, in order to establish a biological basis
for their unfavorable prognosis.A total of 32 GAs diagnosed during an
11-year period (1993-2003) were included in the study. Immunoreactivity for
CD3 (T-cells), CD20 (B-cells) and CD68 (macrophages) were evaluated to
characterize the perivascular inflammatory infiltrates, while p53, epidermal
growth factor receptor (EGFR), cyclin D1 and p27-immunolabeling were studied
to analyze the tumor biology.Overall, the mean gemistocytic index in the
study was 39.6% (range, 12.2-80.8%), with multinucleation in gemistocytes
and mitosis being present in 56.2% and 15.6% respectively. Perivascular
mononuclear cell cuffing was seen in 56.2% cases, which was immunopositive
for CD3 and CD68 in 14 cases each, with 13 cases being immunopositive for
both. Similar type of inflammatory infiltrates was also present within the
tumor parenchyma.Proliferation index depicted by MIB-1 LI was low (mean:
3.7%; range: 0.5-10.5%), with 70% cases having LI of <5%. MIB-1 labeling
was restricted to the small astrocytic cells, similar to p27 and cyclin D1
immunoreactivity, both of which were present in 71.5% cases. In contrast,
p53 protein expression was present in 75% cases, and was strongly positive
in both gemistocytes and small cells, denoting neoplastic population.
However, EGFR protein expression was consistently negative in all
cases.Gemistocytes lack proliferative activity possibly indicating terminal
differentiation, while small cells are the proliferating cells and their
overall percentage may reflect the biological aggressiveness of these tumors
and help to identify GAs of higher grade undergoing malignant progression.
Therefore it appears that GAs should not be uniformly graded as grade II but
should be subdivided into grades II and III neoplasms based on histological
features and MIB-1 LI. The poor prognosis in GAs could be attributed both to
the high frequency of p53 mutations and low p27 LI.
PMID: 16614946 [PubMed - indexed for MEDLINE]3
-
| 27: J Neurooncol. 2006 Jun;78(2):213-5. Epub 2006 Apr 14. |
|
-
Loss of heterozygosity of the APC gene found in a single
case of oligoastrocytoma.
Pecina-Slaus
N, Beros
V, Houra
K, Cupic
H.
Publication Types:
PMID: 16614944 [PubMed - indexed for MEDLINE]
-
| 28: J Neurooncol. 2006 Jun;78(2):209-10. Epub 2006 Apr 6. |
|
-
Multiple intracranial metastases from a malignant
peripheral nerve sheath tumor of the extremities.
Stark
AM, Mehdorn
HM.
Publication Types:
PMID: 16598432 [PubMed - indexed for MEDLINE]
-
| 29: J Neurooncol. 2006 Jun;78(2):187-90. Epub 2006 Apr 6. |
|
-
A case of intra-dural malignant peripheral nerve sheath
tumor in thoracic spine associated with neurofibromatosis type 1.
Albayrak
BS, Gorgulu
A, Kose
T.
Department of Neurosurgery, Suleyman Demirel University, Medical Faculty
Hospital, Isparta, Turkey. serdarbaki@gmail.com
We present a 25-year-old male patient with neurofibromatosis type 1 (NF1).
Thoracic intra-dural extra-medullary tumoral mass was excised gross-totally
and the patient was referred to oncology unit. Histopathological diagnosis
was malignant peripheral nerve sheath tumor (MPNST), a rare sarcoma with a
dismal prognosis. Tumor recurred in its previous site with an adjacent
apical mass in the left lung 7 weeks following initial surgery and repeat
surgery was performed with complete removal of intra-dural tumor. We report
the first patient with intra-dural MPNST localized proximal to conus
medullaris; in upper thoracic spine. It must always be considered the
possibility of a rare but a devastating tumor, MPNST beside schwannomas and
neurofibromas in patients with NF1 when an intra-spinal mass is diagnosed.
Publication Types:
PMID: 16598431 [PubMed - indexed for MEDLINE]2
-
| 30: J Neurooncol. 2006 Jun;78(2):135-43. Epub 2006 Apr 6. |
|
-
Synergy of gene-mediated immunoprophylaxis and microbeam
radiation therapy for advanced intracerebral rat 9L gliosarcomas.
Smilowitz
HM, Blattmann
H, Brauer-Krisch
E, Bravin
A, Di
Michiel M, Gebbers
JO, Hanson
AL, Lyubimova
N, Slatkin
DN, Stepanek
J, Laissue
JA.
Department of Pharmacology, UCHC, Farmington, CT, USA.
PURPOSE: Microbeam radiation therapy (MRT), a novel experimental
radiosurgery that largely spares the developing CNS and other normal
tissues, is tolerated well by developing animals and palliates advanced 9LGS
tumors. This report, to our knowledge, is the first demonstration that
gene-mediated immunotherapy (GMIMPR) enhances the efficacy of MRT for
advanced 9LGS tumors. METHODS: Seventy-six male Fischer 344 rats were
implanted ic with 10(4)9LGS cells on d0. By d14, the cells had generated
approximately approximately 40 mm3 ic 9LGS tumours, experimental models for
therapy of moderately aggressive human malignant astrocytomas. Each of the
14 untreated (control) rats died from a large (>100 mg) ic tumor before
d29 (median, d21). On d14, the remaining 62 rats were given deliberately
suboptimal microbeam radiation therapy (MRT) by a single lateral exposure of
the tumor-bearing zone of the head to a 10.1 mm-wide, approximately
approximately 11 mm-high array of 20-39 microm-wide, nearly parallel beams
of synchrotron wiggler-generated radiation (mainly approximately 50-150 keV
X-rays) that delivered 625 Gy peak skin doses at approximately approximately
211 microm ctc intervals in approximately approximately 300 ms either
without additional treatments (MRT-only, 25 rats), with post-MRT GMIMPR (MRT+GMIMPR,
23 rats: multiple sc injections of irradiated (clonogenically-disabled) GM-CSF
gene-transfected 9LGS cells), or with post-MRT IMPR (MRT+IMPR, 14 rats:
multiple sc injections of irradiated (clonogenically-disabled) 9LGS cells.
RESULTS: The median post-implantation survivals of rats in the MRT-only,
MRT+GMIMPR and MRT+IMPR groups were over twice that of controls; further,
approximately approximately 20% of rats in MRT-only and MRT+IMPR groups
survived >1 yr with no obvious disabilities. Moreover, over 40% of
MRT+GMIMPR rats survived >1 yr with no obvious disabilities, a
significant (P<0.04) increase over the MRT-only and MRT+IMPR groups.
SIGNIFICANCE: These data suggest that the combination of MRT+GMIMPR might be
better than MRT only for unifocal CNS tumors, particularly in infants and
young children.
Publication Types:
PMID: 16598429 [PubMed - indexed for MEDLINE]2
-
| 31: J Neurooncol. 2006 Jun;78(2):153-6. Epub 2006 Mar 31. |
|
-
Somnolence syndrome after focal radiation therapy to the
pineal region: case report and review of the literature.
Kelsey
CR, Marks
LB.
Department of Radiation Oncology, Duke University Medical Center, Durham,
NC, USA. kelse003@mc.duke.edu
Somnolence syndrome classically occurs in children after cranial irradiation
for acute lymphocytic leukemia. Symptoms include somnolence, fever, nausea
and vomiting, and headache. The authors report a 29 year-old female who
developed symptoms compatible with the somnolence syndrome after completing
radiation therapy for a benign meningioma near the pineal region. Five weeks
after completing conformal radiation therapy (54 Gy), she developed profound
fatigue, headaches, and 102-degree fevers. Physical examination and routine
laboratory work were unrevealing. Imaging was not performed. Prednisone was
prescribed and within 1 week her symptoms had largely resolved. This is the
first report of the somnolence syndrome after focal radiation therapy. The
possible etiology of the somnolence syndrome is discussed.
Publication Types:
PMID: 16575537 [PubMed - indexed for MEDLINE]2
-
| 32: J Neurooncol. 2006 Jun;78(2):197. Epub 2006 Mar 31. |
|
-
Two exceptional phenomena in an anaplastic
oligo-astrocytoma.
Hanse
MC, Franssen
JH, Sleeboom
HP, Hoffmann
CF, Taal
W.
Neuro-Oncology Unit, Daniel den Hoed Oncology Center, Erasmus University
Medical Center, Rotterdam, The Netherlands. moniquehanse@planet.nl
Publication Types:
PMID: 16575535 [PubMed - indexed for MEDLINE]
-
| 33: J
Neuropathol Exp Neurol. 2006 Sep;65(9):846-854. |
|
-
Correlation Among Pathology, Genotype, and Patient
Outcomes in Glioblastoma.
Homma
T, Fukushima
T, Vaccarella
S, Yonekawa
Y, Di
Patre PL, Franceschi
S, Ohgaki
H.
From the International Agency for Research on Cancer (TH, TF, SV, SF, HO),
Lyon, France; the Department of Neurosurgery (YY), University of Zurich,
Zurich, Switzerland; and the Department of Pathology and Laboratory Medicine
(PLDP), University of Texas Medical Branch, Galveston, Texas.
Glioblastomas are histologically and genetically heterogeneous. We have
investigated to what extent histologic features reflect the genetic profile
and whether they are predictive of clinical outcome. Key histologic
characteristics, including major cell types (small cell, nonsmall cell),
other components such as oligodendroglial components, gemistocytes,
multinucleated giant cells, as well as necrosis and microvascular
proliferation, of 420 cases of glioblastoma within a population-based study
(1) were reassessed and correlated with patients' clinical outcome and key
genetic alterations. EGFR amplification and p16 homozygous deletion were
significantly more frequent in small cell glioblastomas than in nonsmall
cell glioblastomas (EGFR, 46% vs 26%, p = 0.0002; p16 39% vs 25%, p =
0.0167). Multivariate analyses with adjustment for age and gender showed
that small cell glioblastomas had frequent EGFR amplification and p16
deletion but infrequent PTEN mutations. An oligodendroglial component was
detected in 20% of glioblastomas; these patients were significantly younger
(54.4 +/- 13.6 vs 59.2 +/- 13.8 years; p = 0.0049) and survived longer (10.3
+/- 8.3 vs 8.2 +/- 8.4 months; p = 0.0647). However, multivariate analyses
with adjustment for age and gender did not show the presence of an
oligodendroglial component to be predictive of longer survival. After
adjustment for age and gender, LOH 1p was associated with longer survival
(hazard ratio, 0.7; 95% confidence interval [CI], 0.5-1.0), whereas LOH 10q
was associated with shorter survival (hazard ratio, 1.4; 95% CI, 1.0-1.8) of
patients with glioblastoma. Glioblastomas containing >/=5% multinucleated
giant cells showed more frequent TP53 mutation and infrequent EGFR
amplification than those containing <5% multinucleated giant cells (TP53,
45% vs 24%, p = 0.0001; EGFR, 24% vs 42%, p = 0.0005). Vascular
proliferation was observed in all glioblastomas, whereas large ischemic
and/or pseudopalisading necrosis was observed in 366 of 420 (87%) cases.
Glioblastomas with necrosis were associated with older age (59.2 +/- 13.3 vs
51.6 +/- 15.3 years; p = 0.0001) and shorter survival (7.9 +/- 6.8 vs 12.9
+/- 14.2 months; p = 0.0017). Multivariate analyses with adjustment for age
and gender confirmed this observation (hazard ratio, 1.5; 95% CI, 1.1-2.0).
Multivariate analysis with adjustment for age and gender showed that
necrosis was significantly associated with wild-type TP53 and absence of an
oligodendroglial component. These results suggest that some histologic
features in glioblastomas are associated with specific genetic alterations
and with clinical outcome.
PMID: 16957578 [PubMed - as supplied by publisher]3
-
| 34: J
Nucl Med. 2006 Sep;47(9):1538-45. |
|
-
Early Response of {sigma}-Receptor Ligands and Metabolic
PET Tracers to 3 Forms of Chemotherapy: An In Vitro Study in Glioma Cells.
van
Waarde A, Been
LB, Ishiwata
K, Dierckx
RA, Elsinga
PH.
Department of Nuclear Medicine and Molecular Imaging, University Medical
Center Groningen, University of Groningen, Groningen, The Netherlands; and
2Positron Medical Center, Tokyo Metropolitan Institute of Gerontology,
Tokyo, Japan.
The significant presence of nontumor cell populations within tumors can
complicate the assessment of in vivo tumor metabolism during therapy. To
more clearly define the impact of cytotoxic agents, we compared early
changes in the uptake of 6 PET tracers in cultured glioma cells. Doxorubicin
(1 mumol/L), cisplatin (10 mumol/L), and 5-fluorouracil (10 mmol/L) were
selected to target different aspects of cellular metabolism. METHODS: The
tracers were 2 extracellular sigma-receptor ligands, (18)F-FE-SA5845 (nonsubtype
selective) and (11)C-SA4503 (sigma-1), the nucleoside
3'-deoxy-3'-(18)F-fluorothymidine ((18)F-FLT), (11)C-choline,
(11)C-methionine, and (18)F-FDG. C6 glioma cells were grown as monolayers
and exposed to cytotoxic agents at concentrations at least 1 order of
magnitude higher than the concentration for 50% growth inhibition of this
cell line. Effects on cellular parameters were measured after 0, 1, 2, 3, 4,
and 24 h. RESULTS: All treatments resulted in a decline in cell numbers
within 24 h. The binding of the sigma-ligands (11)C-SA4503 and
(18)F-FE-SA5845 and the uptake of (11)C-choline (normalized for the number
of viable cells) were strongly increased. The uptake of (18)F-FDG showed
little change, and cellular accumulation of (18)F-FLT and (11)C-methionine
was decreased. Uptake of (18)F-FLT and (11)C-methionine was related to the
fraction of cells in S-phase, but not under all conditions: (a) doxorubicin
caused a more rapid decline in (18)F-FLT uptake than in the S-phase fraction
because of depletion of cellular adenosine triphosphate, and (b) cisplatin
inhibited the transport of (11)C-methionine across the tumor cell membrane.
CONCLUSION: Increased binding of sigma-ligands and an increased uptake of
(11)C-choline after chemotherapy may reflect active membrane repair in
damaged cells. (18)F-FLT and (11)C-methionine behaved as proliferation
markers. However, the accumulation of (18)F-FDG reflected not the
proliferation rate but, rather, the number of viable cells per well.
PMID: 16954564 [PubMed - in process]2
-
| 35: Neurosurgery.
2006 Sep;59(3):570-6; discussion 570-6. |
|
-
Visual outcome of tuberculum sellae meningiomas after
extradural optic nerve decompression.
Mathiesen
T, Kihlstrom
L.
Department of Neurosurgery, Karolinska Hospital, Stockholm, Sweden.
Tiit.Mathiesen@karolinska.se
OBJECTIVE: Meningiomas of the tuberculum sellae have a close relationship
with the optic apparatus. Even modern series show a 10 to 20% risk of visual
deterioration after surgery. We have attempted to improve visual outcome by
extradural decompression of the optic canal and anterior clinoid process,
followed by intradural release of the optic nerve; this study provides an
analysis of visual outcomes with this approach. METHODS: Treatment,
histopathology, and follow-up data of 29 consecutive patients undergoing
surgery for tuberculum sellae meningiomas with initial release of the optic
nerve were prospectively collected. RESULTS: Radical tumor removal was
possible in all 23 patients with primary tumors and in three out of six
patients with recurrent tumors. All patients but two of the worst affected
with preoperative visual compromise improved from surgery; there were no
instances of visual deterioration. Five patients with normal preoperative
vision remained intact and visual improvement was 22 (91%) out of 24
patients in the remaining patients. In total, 13 patients (42%) had
completely normal vision at follow-up. Mainly patients younger than 60 years
experienced complete normalization after surgery. Two patients underwent
transsphenoidal surgery for cerebrospinal fluid leaks. Postoperative
endocrinological symptoms were temporary diabetes insipidus in one patient
and permanent diabetes insipidus in another patient undergoing elective
sectioning of the pituitary stalk because of a recurrent tumor with invasive
growth into the stalk. CONCLUSION: Adding early optic nerve decompression by
extradural clinoidectomy and optic canal unroofing to a frontopterional
approach seemed to improve visual outcomes because there were no instances
of visual deterioration. Simpson Grade 1 to 2 removal was possible in all
patients with primary surgery, whereas recurrent cases could only be treated
with lower grades of radicality. Radical removal, however, required
readiness to reoperate for cerebrospinal fluid leakage at the site of the
drilled tumor origin in bone.
PMID: 16955039 [PubMed - in process]2
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Volume 5, Number 37 - 11 September 2006