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Perfusion Imaging of Meningioma by Using Continuous
Arterial Spin-Labeling: Comparison with Dynamic Susceptibility-Weighted
Contrast-Enhanced MR Images and Histopathologic Features.
Kimura
H, Takeuchi
H, Koshimoto
Y, Arishima
H, Uematsu
H, Kawamura
Y, Kubota
T, Itoh
H.
Department of Radiology, Faculty of Medical Science, University of Fukui,
Fukui, Japan.
PURPOSE: The goal of the present study was to determine the utility of
continuous arterial spin labeling (CASL) for characterization of meningioma
by MR perfusion imaging and to compare these results with those obtained
from the T2 dynamic susceptibility contrast (T2DSC) method and from
histopathologic examination. METHODS: Twenty-one cases of meningiomas were
examined at 1.5T. CASL perfusion imaging was implemented on the basis of
multisection single-shot echo-planar imaging with velocity-driven adiabatic
spin-inversion preparation. T2DSC perfusion imaging was also performed by
using a double-echo spoiled gradient echo sequence in a section containing
the tumor. By focusing on the regions of interest, maps of % signal
intensity change and cerebral blood flow (CBF) were determined from CASL and
cerebral blood volume (CBV). CBF and mean transit time (MTT) were obtained
from T2DSC. The microvessel area (MVA) was determined from specimens
immunostained with anti-CD31 in 14 cases by measuring the total amount of
staining in each histologic section. Linear regression analysis was
performed for rCBF values from both perfusion methods and for % signal
intensity change and MVA. RESULTS: There was a significant correlation
between CBF values determined from both perfusion methods (r(2) = 0.73; P
< .001); however, the slope from T2DSC to CASL was less than unity,
likely because of the different vascular weighting used for each method.
There was also a significant correlation between CASL-% signal intensity
change and MVA determined by histopathology (r(2) = 0.91; P < .00001).
Perfusion values were the greatest for angiomatous meningioma and lowest for
fibrous meningioma when using either perfusion method. CONCLUSIONS: CASL and
T2DSC perfusion methods are comparable in the characterization of
meningiomas. Further, CASL is of use in assessing tumor microcirculation.
PMID: 16418363 [PubMed - in process]
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Therapeutic potential of small interfering RNA for
central nervous system diseases.
Lovett-Racke
AE, Cravens
PD, Gocke
AR, Racke
MK, Stuve
O.
Department of Neurology, UT Southwestern Medical Center, Dallas, Tex
75390-9036, USA. Amy.Lovett-Racke@UTSouthwestern.edu
Publication Types:
PMID: 16344338 [PubMed - indexed for MEDLINE]
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| 3: Cancer.
2005 Dec 15;104(12):2862-71. |
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Phase II study of high-dose chemotherapy before radiation
in children with newly diagnosed high-grade astrocytoma: final analysis of
Children's Cancer Group Study 9933.
MacDonald
TJ, Arenson
EB, Ater
J, Sposto
R, Bevan
HE, Bruner
J, Deutsch
M, Kurczynski
E, Luerssen
T, McGuire-Cullen
P, O'Brien
R, Shah
N, Steinbok
P, Strain
J, Thomson
J, Holmes
E, Vezina
G, Yates
A, Phillips
P, Packer
R.
Department of Hematology-Oncology, Children's National Medical Center,
Washington, DC 20010, USA. tmacdona@cnmc.org
BACKGROUND: High-grade astrocytomas (HGA) carry a dismal prognosis and
compose nearly 20% of all childhood brain tumors. The role of high-dose
chemotherapy (HDCT) in the treatment of HGA remains unclear. METHODS: In a
nationwide study, The Children's Cancer Group (CCG) prospectively evaluated
102 children with HGA and postoperative residual disease for efficacy and
toxicity of four courses of HDCT before radiotherapy (RT). Patients were
randomly assigned to one of three couplets of drugs: carboplatin/etoposide
(Regimen A), ifosfamide/etoposide (Regimen B), or cyclophosphamide/etoposide
(Regimen C). After HDCT, all patients were to receive local RT followed by
lomustine and vincristine. Twenty-six patients were excluded after central
neuroradiographic review (n = 8) or pathology review (n = 18). RESULTS: Of
76 evaluable patients (median age, 11.95 yrs; range, 3-20 yrs), 30 patients
relapsed during HDCT, and 11 others did not complete HDCT because of
toxicity. Nonhematologic serious toxicities were common (29%), and 21% of
patients did not receive RT. Objective response rates were not associated
with amount of residual disease and did not statistically differ between
regimens: 27% (Regimen A), 8% (Regimen B), and 29% (Regimen C). Overall
survival (OS) was 24% +/- 5% at 5 years and did not differ between groups.
Median time to an event was longest for Regimen A (283 days compared with 83
and 91 days for Regimens B and C, respectively). The five-year, event-free
survival (EFS) rate for all patients was 8% +/- 3% and 14% +/- 7% for
Regimen A (P = 0.07). CONCLUSIONS: OS and EFS were not affected by
histologic grade. Patients who responded to HDCT had a nominally higher
survival rate (P = 0.03 for trend). The authors conclude that these commonly
used HDCT regimens provide no additional clinical benefit to conventional
treatment in HGA, regardless of the amount of measurable residual tumor.
Copyright 2005 American Cancer Society.
Publication Types:
PMID: 16315242 [PubMed - indexed for MEDLINE]
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Intracellular signaling pathways involved in the cell
growth inhibition of glioma cells by melatonin.
Martin
V, Herrera
F, Carrera-Gonzalez
P, Garcia-Santos
G, Antolin
I, Rodriguez-Blanco
J, Rodriguez
C.
Departamento de Morfologia y Biologia Celular and Instituto Universitario de
Oncologia del Principado de Asturias, Facultad de Medicina de la Universidad
de Oviedo, Oviedo, Spain.
Melatonin is an indolamine mostly produced in the pineal gland, soluble in
water, and highly lipophilic, which allows it to readily cross the
blood-brain barrier. Melatonin possesses antioxidant properties and its
long-term administration in rodents has not been found to cause noteworthy
side effects. In the present work, we found that millimolar concentrations
of this indolamine reduced cell growth of C6 glioma cells by 70% after 72
hours of treatment, inhibiting cell progression from G(1) to S phase of the
cell cycle. Intraperitoneal administration of 15 mg/kg body weight of
melatonin to rats previously injected in the flank with C6 glioma cells
reduces tumor growth by 50% 2 weeks after the implant. Inhibition of cell
growth does not depend on melatonin membrane receptor activation whereas it
seemingly relates to the reduction of intracellular basal free radical
levels by 30%. Increase of basal redox state of the cells and constitutive
activation of tyrosine kinase receptor [receptor tyrosine kinase (RTK)]
pathways, including the extracellular signal-regulated kinase 1/2 (ERK1/2)
and the Akt and protein kinase C (PKC) signaling pathways, contribute to the
progression of the gliomas leading to the constitutive activation of the
redox-dependent survival transcription factor nuclear factor kappaB (NF-kappaB).
The antioxidant effect of melatonin in C6 cells is associated to inhibition
of NF-kappaB and Akt, but not of ERK1/2. The antiproliferative effect of the
indolamine on these cells is partially abolished when coincubated with the
PKC activator 12-O-tetradecanoylphorbol-13-acetate, thus indicating that the
ability of melatonin to change cellular redox state may be inactivating the
pathway RTK/PKC/Akt/NF-kappaB. (Cancer Res 2006; 66(2): 1081-8).
PMID: 16424044 [PubMed - in process]
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Differential Gene Expression Analysis Reveals Generation
of an Autocrine Loop by a Mutant Epidermal Growth Factor Receptor in Glioma
Cells.
Ramnarain
DB, Park
S, Lee
DY, Hatanpaa
KJ, Scoggin
SO, Otu
H, Libermann
TA, Raisanen
JM, Ashfaq
R, Wong
ET, Wu
J, Elliott
R, Habib
AA.
Departments of Neurology and Pathology, Annette G. Strauss Center in Neuro-Oncology,
and Harold C. Simmons Comprehensive Cancer Center, University of Texas
Southwestern Medical Center, Dallas, Texas and Departments of Neurology and
Neurosurgery and Genomics Center, Beth Israel Deaconess Medical Center and
Harvard Medical School, Boston Massachusetts.
The epidermal growth factor receptor (EGFR) gene is commonly amplified and
rearranged in glioblastoma multiforme leading to overexpression of wild-type
and mutant EGFRs. Expression of wild-type EGFR ligands, such as transforming
growth factor-alpha (TGF-alpha) or heparin-binding EGF (HB-EGF), is also
often increased in gliomas resulting in an autocrine loop that contributes
to the growth autonomy of glioma cells. Glioblastoma multiformes express a
characteristic EGFR mutant (EGFRvIII, de 2-7) that does not bind ligand,
signals constitutively, and is more tumorigenic than the wild-type receptor.
However, the downstream signals that mediate this increased tumorigenicity
are not well understood. We hypothesized that signals induced specifically
by EGFRvIII and not the wild-type receptor are more likely to mediate its
increased tumorigenic activity and examined the gene expression profiles
resulting from inducible expression of comparable levels of either wild-type
EGFR or EGFRvIII in a U251-MG glioma cell line. Expression of EGFRvIII
resulted in specific up-regulation of a small group of genes. Remarkably,
all these genes, which include TGFA, HB-EGF, EPHA2, IL8, MAP4K4, FOSL1,
EMP1, and DUSP6, influence signaling pathways known to play a key role in
oncogenesis and function in interconnected networks. Increased expression of
EGFRvIII-induced genes was validated by real-time PCR. The mutant receptor
does not bind ligand, and EGFRvIII-induced expression of TGF-alpha and
HB-EGF suggests that EGFRvIII plays a role in generating an autocrine loop
using the wild-type EGFR in glioma. It also raises the possibility that
EGFRvIII may signal, at least in part, through the wild-type receptor.
Indeed, we show that inhibiting the activity of HB-EGF, a potent mitogen,
with neutralizing antibodies reduces cell proliferation induced by
expression of EGFRvIII. This suggests that the EGFRvIII-HB-EGF-wild-type
EGFR autocrine loop plays an important role in signal transduction by
EGFRvIII in glioma cells. We also show by immunohistochemistry that HB-EGF
expression correlates with the presence of EGFRvIII in glioblastoma
multiforme. Thus, our study provides a new insight into oncogenic signaling
by EGFRvIII and improves our understanding of how autocrine loops are
generated in glioma. (Cancer Res 2006; 66(2): 867-74).
PMID: 16424019 [PubMed - as supplied by publisher]
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Angiopoietin 2 Induces Glioma Cell Invasion by
Stimulating Matrix Metalloprotease 2 Expression through the {alpha}v{beta}1
Integrin and Focal Adhesion Kinase Signaling Pathway.
Hu
B, Jarzynka
MJ, Guo
P, Imanishi
Y, Schlaepfer
DD, Cheng
SY.
University of Pittsburgh Cancer Institute and Departments of Medicine and
Pathology, Research Pavilion at the Hillman Cancer Center, Pittsburgh,
Pennsylvania.
Accumulating evidence reveals a significant correlation between angiopoietin
2 (Ang2) expression and tumor invasion and metastasis in various human
cancers, but the major focus of recent studies has been on the angiogenic
effects of Ang2. We recently reported that Ang2-stimulated glioma cell
invasion results from the up-regulation and activation of matrix
metalloprotease 2 (MMP-2) in tumor cells. In this study, we identify a novel
mechanism by which Ang2 stimulates MMP-2 expression leading to glioma cell
invasion. We show that Ang2 interacts with alpha(v)beta(1) integrin in
Tie2-deficient human glioma cells, activating focal adhesion kinase (FAK),
p130(Cas), extracellular signal-regulated protein kinase (ERK) 1/2, and c-jun
NH(2)-terminal kinase (JNK) and substantially enhancing MMP-2 expression and
secretion. The Ang2/alpha(v)beta(1) integrin signaling pathway was
attenuated by functional inhibition of beta(1) and alpha(v) integrins, FAK,
p130(Cas), ERK1/2, and JNK. Furthermore, expression of a negative regulator
of FAK, FAK-related nonkinase, by U87MG/Ang2-expressing glioma xenografts
suppressed Ang2-induced MMP-2 expression and glioma cell infiltration in the
murine brain. These data establish a functional link between Ang2
interaction with alpha(v)beta(1) integrin and glioma cell invasion through
the FAK/p130(Cas)/ERK1/2 and JNK-mediated signaling pathway. (Cancer Res
2006; 66(2): 775-83).
PMID: 16424009 [PubMed - in process]
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c-Myc Overexpression Causes Anaplasia in Medulloblastoma.
Stearns
D, Chaudhry
A, Abel
TW, Burger
PC, Dang
CV, Eberhart
CG.
Departments of Neuropathology and Hematology, Johns Hopkins University
School of Medicine, Baltimore, Maryland and Department of Pediatrics, Drexel
University School of Medicine, Philadelphia, Pennsylvania.
Both anaplasia and increased c-myc gene expression have been shown to be
negative prognostic indicators for survival in medulloblastoma patients. myc
gene amplification has been identified in many large cell/anaplastic
medulloblastoma, but no causative link between c-myc and anaplastic changes
has been established. To address this, we stably overexpressed c-myc in two
medulloblastoma cell lines, DAOY and UW228, and examined the changes in
growth characteristics. When analyzed in vitro, cell lines with increased
levels of c-myc had higher rates of growth and apoptosis as well as
significantly improved ability to form colonies in soft agar compared with
control. When injected s.c. into nu/nu mice, flank xenograft tumors with
high levels of c-myc in DAOY cell line background were 75% larger than those
derived from control. Overexpression of c-myc was required for tumor
formation by UW228 cells. Most remarkably, the histopathology of the Myc
tumors was severely anaplastic, with large areas of necrosis/apoptosis,
increased nuclear size, and macronucleoli. Indices of proliferation and
apoptosis were also significantly higher in Myc xenografts. Thus, c-myc
seems to play a causal role in inducing anaplasia in medulloblastoma.
Because anaplastic changes are often observed in recurrent medulloblastoma,
we propose that c-myc dysregulation is involved in the progression of these
malignant embryonal neoplasms. (Cancer Res 2006; 66(2): 673-81).
PMID: 16423996 [PubMed - in process]
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Interleukin-8 differentially regulates migration of
tumor-associated and normal human brain endothelial cells.
Charalambous
C, Pen
LB, Su
YS, Milan
J, Chen
TC, Hofman
FM.
Department of Molecular Microbiology and Immunology, University of Southern
California Keck School of Medicine, Los Angeles, California 90033, USA.
Interleukin-8 (IL-8) is a chemokine involved in angiogenesis, a process
vital to tumor growth. Previously, we showed that endothelial cells derived
from human tumor tissue have different functional and phenotypic properties
compared with normal endothelial cells. This study analyzes the role of IL-8
in regulating angiogenesis of tumor-associated brain endothelial cells (TuBEC).
Results show that TuBECs have a higher baseline migration rate compared with
normal brain endothelial cells (BEC). TuBECs are unaffected when stimulated
with IL-8 whereas BECs are activated. This lack of response of TuBECs to
IL-8 is due to the constitutive production of IL-8. Endogenously produced
IL-8 activates TuBECs in an autocrine manner as shown by IL-8 receptor
inhibition. Blocking either CXCR1 or CXCR2 partially reduces TuBEC
migration, whereas blocking both receptors further reduces migration.
Treatment with antibody against vascular endothelial growth factor (VEGF)
shows that production of IL-8 by TuBECs is dependent on VEGF. Transforming
growth factor-beta1 (TGF-beta1), shown to down-regulate IL-8 production in
BECs, does not inhibit IL-8 production in TuBECs. In summary, these studies
show that TuBECs constitutively secrete IL-8 and autocrine activation by
IL-8 is the result of VEGF stimulation. Furthermore, TuBECs do not respond
to the feedback inhibition normally induced by TGF-beta1. These data
emphasize the functional uniqueness of TuBECs. Understanding the functions
and regulatory processes of tumor-associated endothelial cells is critical
for developing appropriate antiangiogenic therapies.
PMID: 16288024 [PubMed - indexed for MEDLINE]
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Novel molecular signaling and classification of human
clinically nonfunctional pituitary adenomas identified by gene expression
profiling and proteomic analyses.
Moreno
CS, Evans
CO, Zhan
X, Okor
M, Desiderio
DM, Oyesiku
NM.
Department of Pathology and Laboratory Medicine and Winship Cancer
Institute, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Pituitary adenomas comprise 10% of intracranial tumors and occur in about
20% of the population. They cause significant morbidity by compression of
regional structures or the inappropriate expression of pituitary hormones.
Their molecular pathogenesis is unclear, and the current classification of
clinically nonfunctional tumors does not reflect any molecular distinctions
between the subtypes. To further elucidate the molecular changes that
contribute to the development of these tumors and reclassify them according
to the molecular basis, we investigated 11 nonfunctional pituitary adenomas
and eight normal pituitary glands, using 33 oligonucleotide GeneChip
microarrays. We validated microarray results with the reverse transcription
real-time quantitative PCR, using a larger number of nonfunctional adenomas.
We also used proteomic analysis to examine protein expression in these
nonfunctional adenomas. Microarray analysis identified significant increases
in the expression of 115 genes and decreases in 169 genes, whereas proteomic
analysis identified 21 up-regulated and 29 down-regulated proteins. We
observed changes in expression of SFRP1, TLE2, PITX2, NOTCH3, and DLK1,
suggesting that the developmental Wnt and Notch pathways are activated and
important for the progression of nonfunctional pituitary adenomas. We
further analyzed gene expression profiles of all nonfunctional pituitary
subtypes to each other and identified genes that were affected uniquely in
each subtype. These results show distinct gene and protein expression
patterns in adenomas, provide new insight into the pathogenesis and
molecular classification of nonfunctional pituitary adenomas, and suggest
that therapeutic targeting of the Notch pathway could be effective for these
tumors.
PMID: 16288009 [PubMed - indexed for MEDLINE]
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Radiotherapy in Pediatric Medulloblastoma: Quality
Assessment of Pediatric Oncology Group Trial 9031.
Miralbell
R, Fitzgerald
TJ, Laurie
F, Kessel
S, Glicksman
A, Friedman
HS, Urie
M, Kepner
JL, Zhou
T, Chen
Z, Barnes
P, Kun
L, Tarbell
NJ.
Quality Assurance Review Committee, Providence, RI, USA; Department of
Radiation Oncology, University Hospital, Geneva, Switzerland.
PURPOSE: To evaluate the potential influence of radiotherapy quality on
survival in high-risk pediatric medulloblastoma patients. METHODS AND
MATERIALS: Trial 9031 of the Pediatric Oncology Group (POG) aimed to study
the relative benefit of cisplatin and etoposide randomization of high-risk
patients with medulloblastoma to preradiotherapy vs. postradiotherapy
treatment. Two-hundred and ten patients were treated according to protocol
guidelines and were eligible for the present analysis. Treatment volume
(whole brain, spine, posterior fossa, and primary tumor bed) and dose
prescription deviations were assessed for each patient. An analysis of first
site of failure was undertaken. Event-free and overall survival rates were
calculated. A log-rank test was used to determine the significance of
potential survival differences between patients with and without major
deviations in the radiotherapy procedure. RESULTS: Of 160 patients who were
fully evaluable for all treatment quality parameters, 91 (57%) had 1 or more
major deviations in their treatment schedule. Major deviations by treatment
site were brain (26%), spinal (7%), posterior fossa (40%), and primary tumor
bed (17%). Major treatment volume or total dose deviations did not
significantly influence overall and event-free survival. CONCLUSIONS:
Despite major treatment deviations in more than half of fully evaluable
patients, underdosage or treatment volume misses were not associated with a
worse event-free or overall survival.
PMID: 16413699 [PubMed - as supplied by publisher]
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Parkinsonism and dementia due to gliomatosis cerebri
mimicking sporadic Creutzfeldt-Jakob disease (CJD).
Slee
M, Pretorius
P, Ansorge
O, Stacey
R, Butterworth
R.
c/o Neurology Department, Austin Health, Heidelberg, Melbourne, VIC 3084,
Australia. markslee@doctors.org.uk.
PMID: 16421148 [PubMed - in process]
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Genetic Alterations in Primary Glioblastomas in Japan.
Fukushima
T, Favereaux
A, Huang
H, Shimizu
T, Yonekawa
Y, Nakazato
Y, Ohagki
H.
From the International Agency for Research on Cancer (TF, AF, HH, HO), Lyon,
France; Kanto Neurosurgical Hospital (TS), Kumagaya, Saitama, Japan;
Department of Neurosurgery (YY), University Hospital Zurich, Zurich,
Switzerland; and Department of Human Pathology (YN), Gunma University
Graduate School of Medicine, Maebashi, Gunma, Japan.
ABSTRACT: Current knowledge of genetic alterations in glioblastomas is based
largely on genetic analyses of tumors from mainly caucasian patients in the
United States and Europe. In the present study, screening for several key
genetic alterations was performed on 77 primary (de novo) glioblastomas in
Japanese patients. SSCP followed by DNA sequencing revealed TP53 mutations
in 16 of 73 (22%) glioblastomas and PTEN mutations in 13 of 63 (21%) cases
analyzed. Polymerase chain reaction (PCR) showed EGFR amplification in 25 of
77 (32%) cases and p16 homozygous deletion in 32 of 77 (42%) cases.
Quantitative microsatellite analysis revealed LOH 10q in 41 of 59 (69%)
glioblastomas. The frequencies of these genetic alterations were similar to
those reported for primary glioblastomas at the population level in
Switzerland. As previously observed for glioblastomas in Europe, there was a
positive association between EGFR amplification and p16 deletion (p =
0.009), whereas there was an inverse association between TP53 mutations and
p16 deletion (p = 0.049) in glioblastomas in Japan. Multivariate analyses
showed that radiotherapy was significantly predictive for longer survival of
glioblastoma patients (p = 0.002). SSCP followed by DNA sequencing of the
kinase domain (exons 18-21) of the EGFR gene revealed mutations in 2 ou of
69 (3%) glioblastomas in Japan and in 4 of 81 (5%) glioblastomas in
Switzerland. The allele frequencies of polymorphisms at codon 787 CAG/CAA (Gln/Gln)
in glioblastomas in Japan were G/G (82.4%), G/A (10.8%), A/A (6.8%),
corresponding to G 0.878 versus A 0.122, significantly different from those
in glioblastomas in Switzerland: G/G (27.2%), G/A (28.4%), A/A (44.4%),
corresponding to G 0.414 versus A 0.586 (p < 0.0001). These results
suggest that primary glioblastomas in Japan show genetic alterations similar
to those in Switzerland, suggesting a similar molecular basis in caucasians
and Asians, despite different genetic backgrounds, including different
status of a polymorphism in the EGFR gene.
PMID: 16410744 [PubMed - as supplied by publisher]
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Preoperative Grading of Gliomas by Using Metabolite
Quantification with High-Spatial-Resolution Proton MR Spectroscopic Imaging.
Stadlbauer
A, Gruber
S, Nimsky
C, Fahlbusch
R, Hammen
T, Buslei
R, Tomandl
B, Moser
E, Ganslandt
O.
1 Department of Neurosurgery, Neurocenter, University of Erlangen-Nuremberg,
Erlangen, Germany.
Purpose: To evaluate proton magnetic resonance (MR) spectroscopic imaging
with high spatial resolution for preoperative grading of suspected World
Health Organization grades II and III gliomas. Materials and Methods:
Institutional ethics committee approval and informed consent were obtained
for control subjects but were not required for the retrospective component
involving patients. Twenty-six patients (10 women, 16 men; mean age, 37.5
years) suspected of having gliomas and 26 age- and sex-matched control
subjects underwent proton MR spectroscopy. Absolute metabolite
concentrations for choline-containing compounds (Cho), creatine (Cr), and N-acetylaspartate
(NAA)-N-acetylaspartylglutamate (total NAA [tNAA]) were calculated by using
a user-independent spectral fit program. Metabolic maps of Cho/tNAA ratios
were calculated, segmented, and used for MR spectroszpcopy-guided
stereotactic brain biopsy. Two-sided paired Student t tests were used to
test for statistical significance. Results: Significantly lower Cho levels
(P = .002) and higher tNAA levels (P = .010) were found in grade II tumors
(n = 9) compared with grade III tumors (n = 17). The average Cho/tNAA ratio
over the voxels in the tumor center showed a distinct difference (P <
.001) between grade II and III gliomas at a threshold of 0.8 (with ratios
<0.8 for grade II). The maximum Cr concentration in the tumor showed a
clear-cut threshold between grade III oligodendrogliomas and
oligoastrocytomas (Cr level, <7 mmol/L) and grade III astrocytomas (Cr
level, >7 mmol/L; P = .020). Comparison between the histopathologic
findings from the MR spectroscopy-guided biopsy samples (76 biopsies from 26
patients) and molar metabolite values in corresponding voxels located at the
biopsy sampling points showed a negative linear correlation for tNAA (r =
-0.905) and a positive exponential correlation for Cho (r = 0.769) and Cho/tNAA
(r = 0.885). Conclusion: Proton MR spectroscopic imaging with high spatial
resolution allows preoperative grading of gliomas. (c) RSNA, 2006.
PMID: 16424238 [PubMed - as supplied by publisher]
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Volume 5, Number 4 - 22 January 2006