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| 1: AJNR
Am J Neuroradiol. 2005 Mar;26(3):642-5. |
|
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Lymphocytic vasculitis mimicking aggressive multifocal
cerebral neoplasm: mr imaging and MR spectroscopic appearance.
Panchal NJ, Niku S, Imbesi SG.
Department of Radiology, University of California, San Diego Medical Center,
San Diego, CA 92103, USA.
We present a case of multifocal enhancing lesions confined to the right
cerebral hemisphere that mimicked diffuse neoplasm. MR spectroscopy revealed
not only minimal elevation of the choline peak, but also marked elevation of
the glutamate and glutamine peaks, findings that are more suggestive of an
inflammatory process. Biopsy showed lymphocytic vasculitis, a rare variant
of primary angiitis of the CNS. Following appropriate medical therapy, MR
imaging demonstrated complete resolution of the lesions.
Publication Types:
PMID: 15760879 [PubMed - indexed for MEDLINE]
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| 2: AJNR
Am J Neuroradiol. 2005 Mar;26(3):635-41. |
|
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3D-CT arteriography and 3D-CT venography: the separate
demonstration of arterial-phase and venous-phase on 3D-CT angiography in a
single procedure.
Matsumoto M, Kodama N, Sakuma J, Sato S, Oinuma M, Konno Y, Suzuki K,
Sasaki T, Suzuki K, Katakura T, Shishido F.
Department of Neurosurgery, Fukushima Medical University, Fukushima, Japan.
Although 3D-CT angiography provides valuable anatomic information regarding
lesion and their surrounding vessels and bony structures, it cannot
demonstrate lesions, arteries, and veins, separately. The separate
demonstration of arterial-phase 3D-CT angiography (3D-CT arteriography) and
venous-phase 3D-CT angiography (3D-CT venography) will facilitate the
understanding of the vascular anatomy within lesions, thus, allowing
improvement of diagnostic accuracy and potentially a safer surgical
approach. We describe 3D-CT arteriography and 3D-CT venography by using a
multidetector row helical CT.
Publication Types:
PMID: 15760878 [PubMed - indexed for MEDLINE]
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| 3: Cancer.
2005 Mar 15;103(6):1314-5; author reply 1315. |
|
Comment on:
The risk of central nervous system metastases after
trastuzumab therapy in patients with breast carcinoma.
Montemurro F, Aglietta M.
Publication Types:
PMID: 15674855 [PubMed - indexed for MEDLINE]
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| 4: Cancer.
2005 Mar 15;103(6):1234-44. |
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Is older age associated with a worse prognosis due to
different patterns of care? A long-term study of 1346 patients with
glioblastomas or brain metastases.
Lutterbach J, Bartelt S, Momm F, Becker G, Frommhold H, Ostertag C.
Department of Radiotherapy, Cancer Center Freiburg, Freiburg, Germany.
lutterba@mst1.ukl.uni-freiburg.de
BACKGROUND: The objective of this study was to find out whether the worse
prognosis of older patients with primary or metastatic brain tumors can be
explained by different patterns of care compared with younger patients.
METHODS: A data base that included 430 patients with glioblastomas and 916
patients with brain metastases who underwent radiotherapy at the author's
hospital between 1980 and 2000 was analyzed. Patterns of care were compared
for different age groups using the chi-square test. RESULTS: In both patient
groups, age turned out to be an independent risk factor. Older age was
associated with worse overall survival. Independent of the cut-off age (<
50 years vs. > or = 50 years, < 60 years vs. > or = 60 years, <
65 years vs. > or = 65 years, and < 70 years vs. > or = 70 years),
there were no statistically significant differences between the age groups
concerning the use of different imaging modalities (computed tomography
scans vs. magnetic resonance imaging), type of surgery (none vs. biopsy vs.
resection), waiting time for radiotherapy (< median vs. > or =
median), radiotherapy treatment planning (simulator-based vs.
computer-based), use of radiation sources (cobalt unit vs. linear
accelerator), and fractionation protocols (conventional vs. modified). When
the recruitment period of 21 years was divided into 3 intervals, impressive
changes with regard to the patterns of care became apparent. However, the
changes were seen similarly throughout the different age groups.
CONCLUSIONS: Older age did not limit access to state-of-the-art patterns of
care in neurooncology. Patients participated in medical progress
irrespective of their age. The worse prognosis of older patients with
glioblastomas or brain metastases was not determined by age-related
differences in access to health care.
PMID: 15666327 [PubMed - indexed for MEDLINE]
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| 5: Cancer
Res. 2005 Apr 15;65(8):3336-46. |
|
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Synergistic augmentation of rapamycin-induced autophagy
in malignant glioma cells by phosphatidylinositol 3-kinase/protein kinase B
inhibitors.
Takeuchi H, Kondo Y, Fujiwara K, Kanzawa T, Aoki H, Mills GB, Kondo S.
Department of Neurosurgery, University of Texas M.D. Anderson Cancer Center,
1515 Holcombe Boulevard, Houston, TX 77030, USA.
The mammalian target of rapamycin (mTOR) is a downstream effector of the
phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling
pathway and a central modulator of cell proliferation in malignant gliomas.
Therefore, the targeting of mTOR signaling is considered a promising therapy
for malignant gliomas. However, the mechanisms underlying the cytotoxic
effects of a selective mTOR inhibitor, rapamycin, on malignant glioma cells
are poorly understood. The purpose of this study was thus to elucidate how
rapamycin exerts its cytotoxic effects on malignant glioma cells. We showed
that rapamycin induced autophagy but not apoptosis in rapamycin-sensitive
malignant glioma U87-MG and T98G cells by inhibiting the function of mTOR.
In contrast, in rapamycin-resistant U373-MG cells, the inhibitory effect of
rapamycin was minor, although the phosphorylation of p70S6 kinase, a
molecule downstream of mTOR, was remarkably inhibited. Interestingly, a PI3K
inhibitor, LY294002, and an Akt inhibitor, UCN-01 (7-hydroxystaurosporine),
both synergistically sensitized U87-MG and T98G cells as well as U373-MG
cells to rapamycin by stimulating the induction of autophagy. Enforced
expression of active Akt in tumor cells suppressed the combined effects of
LY294002 or UCN-01, whereas dominant-negative Akt expression was sufficient
to increase the sensitivity of tumor cells to rapamycin. These results
indicate that rapamycin exerts its antitumor effect on malignant glioma
cells by inducing autophagy and suggest that in malignant glioma cells a
disruption of the PI3K/Akt signaling pathway could greatly enhance the
effectiveness of mTOR inhibitors.
PMID: 15833867 [PubMed - in process]
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| 6: Cancer
Res. 2005 Apr 15;65(8):3307-18. |
|
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Human bone marrow-derived mesenchymal stem cells in the
treatment of gliomas.
Nakamizo A, Marini F, Amano T, Khan A, Studeny M, Gumin J, Chen J,
Hentschel S, Vecil G, Dembinski J, Andreeff M, Lang FF.
Department of Neurosurgery, Brain Tumor Center, University of Texas M.D.
Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
The poor survival of patients with human malignant gliomas relates partly to
the inability to deliver therapeutic agents to the tumor. Because it has
been suggested that circulating bone marrow-derived stem cells can be
recruited into solid organs in response to tissue stresses, we hypothesized
that human bone marrow-derived mesenchymal stem cells (hMSC) may have a
tropism for brain tumors and thus could be used as delivery vehicles for
glioma therapy. To test this, we isolated hMSCs from bone marrow of normal
volunteers, fluorescently labeled the cells, and injected them into the
carotid artery of mice bearing human glioma intracranial xenografts (U87,
U251, and LN229). hMSCs were seen exclusively within the brain tumors
regardless of whether the cells were injected into the ipsilateral or
contralateral carotid artery. In contrast, intracarotid injections of
fibroblasts or U87 glioma cells resulted in widespread distribution of
delivered cells without tumor specificity. To assess the potential of hMSCs
to track human gliomas, we injected hMSCs directly into the cerebral
hemisphere opposite an established human glioma and showed that the hMSCs
were capable of migrating into the xenograft in vivo. Likewise, in vitro
Matrigel invasion assays showed that conditioned medium from gliomas, but
not from fibroblasts or astrocytes, supported the migration of hMSCs and
that platelet-derived growth factor, epidermal growth factor, or stromal
cell-derived factor-1alpha, but not basic fibroblast growth factor or
vascular endothelial growth factor, enhanced hMSC migration. To test the
potential of hMSCs to deliver a therapeutic agent, hMSCs were engineered to
release IFN-beta (hMSC-IFN-beta). In vitro coculture and Transwell
experiments showed the efficacy of hMSC-IFN-beta against human gliomas. In
vivo experiments showed that treatment of human U87 intracranial glioma
xenografts with hMSC-IFN-beta significantly increase animal survival
compared with controls (P < 0.05). We conclude that hMSCs can integrate
into human gliomas after intravascular or local delivery, that this
engraftment may be mediated by growth factors, and that this tropism of
hMSCs for human gliomas can be exploited to therapeutic advantage.
PMID: 15833864 [PubMed - in process]
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| 7: Int
J Radiat Oncol Biol Phys. 2005 Mar 15;61(4):1173-82. |
|
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Enhanced delivery of iodine for synchrotron stereotactic
radiotherapy by means of intracarotid injection and blood-brain barrier
disruption: quantitative iodine biodistribution studies and associated
dosimetry.
Adam JF, Biston MC, Joubert A, Charvet AM, Le Bas JF, Esteve F, Elleaume
H.
Unite INSERM U647 Rayonnement synchrotron et recherche medicale, Universite
Joseph Fourier, European Synchrotron Radiation Facility Medical Beamline
(ESRF-ID17), Grenoble, France.
PURPOSE: Synchrotron stereotactic radiotherapy (SSR) is a binary cancer
treatment modality that involves the selective accumulation of a high Z
element, such as iodine, in tumors, followed by stereotactic irradiation
with kilovoltage X-rays from a synchrotron source. The success of SSR is
directly related to the absolute amount of iodine achievable in the tumor.
The purposes of this preclinical study were to determine whether the
delivery of iodine to brain tumor models in rats could be enhanced by the
means of its intracarotid injection with or without a hyperosmotic solution
and to evaluate corresponding absorbed X-ray doses. METHODS AND MATERIALS:
Experiments were performed on four groups of F98 glioma-bearing rats, which
received either intracarotid (IC) or intravenous (IV) infusions of a mixture
(6 mL in 12 min) of an iodinated contrast agent associated or not with a
transient blood-brain barrier opener (mannitol). The mixture volumetric
proportions were 8/13 of Iomeron (C = 350 mg/mL) for 5/13 of mannitol or
saline, respectively. Absolute iodine concentration kinetic was measured in
vivo in the tumor, blood, contralateral and ipsilateral brain, and muscle by
monochromatic computed tomography. Associated dosimetry was performed by
computing the iodine dose enhancement factor (DEF) in each region and
building dose distribution maps by analytical simulations. RESULTS: Infusion
of mannitol significantly enhanced iodine tumor uptake compared with the
control values (p < 0.0001 and p = 0.0138, for IC and IV protocols,
respectively). The mean iodine concentrations (C) reached 20.5 +/- 0.98
mg/mL (DEF = 4.1) after administration of iodine and mannitol vs. 4.1 +/-
1.2 mg/mL i.c. with serum (DEF = 1.6). The tumor iodine uptakes after
jugular injection with mannitol (C = 4.4 +/- 2.1 mg/mL, DEF = 1.7) were not
significantly different from IC injection of iodine without mannitol (p =
0.8142). The IV injection of iodine with saline led to an iodine
concentration in the tumor of 1.2 +/- 0.98 mg/mL and a DEF of 1.2.
CONCLUSIONS: This study established that optimizing the delivery of iodine
by means of IC injection combined with a blood-brain barrier opener
(mannitol) significantly increases the iodine uptake of F98 rat gliomas.
This infusion protocol could potentially enhance the efficacy of SSR
treatment, because the radiation dose is proportional to the iodine amount
present in the irradiation bed.
PMID: 15752899 [PubMed - indexed for MEDLINE]
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| 8: J
Clin Oncol. 2005 Apr 20;23(12):2869-70. |
|
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What is the appropriate radiotherapy protocol for older
patients with newly diagnosed glioblastoma?
Lutterbach J, Ostertag C.
Publication Types:
PMID: 15838008 [PubMed - in process]
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| 9: J
Clin Oncol. 2005 Apr 1;23(10):2437-8; author reply 2438. |
|
Comment on:
Rationing and decision making.
Abratt RP.
Publication Types:
PMID: 15800346 [PubMed - indexed for MEDLINE]
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| 10: J
Clin Oncol. 2005 Apr 1;23(10):2256-63. |
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Serial evaluation of academic and behavioral outcome
after treatment with cranial radiation in childhood.
Mabbott DJ, Spiegler BJ, Greenberg ML, Rutka JT, Hyder DJ, Bouffet E.
Paediatric Brain Tumor Program, The Hospital for Sick Children, 555
University Ave, Toronto, Ontario, M5G 1X8, Canada.
donald.mabbott@sickkids.ca
PURPOSE: To evaluate academic and behavioral outcome in radiated survivors
of posterior fossa (PF) tumors. PATIENTS AND METHODS: Fifty-three patients
(36 males) treated for malignant PF tumors were seen for evaluation of
academics and/or behavioral functioning. Forty-six patients were treated for
medulloblastoma, and seven patients were treated for ependymoma. Fourteen
patients were treated with reduced-dose cranial radiation, and 34 patients
were treated with standard-dose cranial radiation (dose was not available
for four patients). All patients received an additional boost to the PF. One
patient was treated with PF radiation only. Standardized achievement tests
and behavioral questionnaires were administered at different times after
diagnosis for each child. First, the influence of demographic and medical
variables on outcome was examined. Second, the rate of change in scores was
determined using mixed model regression for patients seen for serial
assessment. RESULTS: The presence of hydrocephalus was related to poorer
academics, but outcome was not related to radiation dose, extent of surgery,
or treatment with chemotherapy. Younger age predicted poor reading ability
and lower parent rating of academic achievement. Children's performance
declined for spelling, mathematics, and reading. Significant declines were
also evident in parent and teacher's ratings of academic ability. Behavioral
functioning was generally not related to medical and demographic variables,
and few clinically significant problems in externalizing behavior were
evident. Increases in social and attention problems emerged over time.
CONCLUSION: Cranial radiation is associated with declines in academic
ability, social skills, and attention. However, neither psychological
distress nor behavior problems were a significant concern for this sample.
PMID: 15800316 [PubMed - indexed for MEDLINE]
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| 11: J
Clin Oncol. 2005 Apr 1;23(10):2233-9. |
|
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Primary CNS lymphoma of T-cell origin: a descriptive
analysis from the international primary CNS lymphoma collaborative group.
Shenkier TN, Blay JY, O'Neill BP, Poortmans P, Thiel E, Jahnke K, Abrey
LE, Neuwelt E, Tsang R, Batchelor T, Harris N, Ferreri AJ, Ponzoni M,
O'Brien P, Rubenstein J, Connors JM.
British Columbia Cancer Agency, 600 W 10th Ave, Vancouver, BC, V5Z 4E6,
Canada. tshenkier@bccancer.bc.ca
PURPOSE: To describe the demographic and tumor related characteristics and
outcomes for patients with primary T-cell CNS lymphoma (TPCNSL). PATIENTS
AND METHODS: A retrospective series of patients with TPCNSL was compiled
from twelve cancer centers in seven countries. RESULTS: We identified 45
patients with a median age of 60 years (range, 3 to 84 years). Twenty (44%)
had Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 0
or 1. Twenty-six (58%) had involvement of a cerebral hemisphere and sixteen
(36%) had lesions of deeper sites in the brain. Serum lactate dehydrogenase
was elevated in 7 (32%) of 22 patients, and CSF protein was elevated in 19
of 24 patients (79%) with available data. The median disease-specific
survival (DSS) was 25 months (95% CI, 11 to 38 months). The 2- and 5-year
DSS were 51% (95% CI, 35% to 66%) and 17% (95% CI, 6% to 34%), respectively.
Univariate and multivariate analyses were conducted for age (</= 60 v
> 60 years), PS (0 or 1 v 2, 3, or 4), involvement of deep structures of
the CNS (no v yes), and methotrexate (MTX) use in the primary treatment (yes
v no). Only PS and MTX use were significantly associated with better outcome
with hazard ratios of 0.2 (95% CI, 0.1 to 0.4) and 0.4 (95% CI, 0.2 to 0.8),
respectively. CONCLUSION: This is the largest series ever assembled of
TPCNSL. The presentation and outcome appear similar to that of B cell PCNSL.
PS 0 or 1 and administration of MTX are associated with better survival.
Publication Types:
PMID: 15800313 [PubMed - indexed for MEDLINE]
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| 12: J
Neurochem. 2005 May;93(3):513-25. |
|
Induction of hypoxia inducible factor-1 attenuates
metabolic insults induced by 3-nitropropionic acid in rat C6 glioma cells.
Yang YT, Ju TC, Yang DI.
Institute of Neuroscience, Tzu Chi University, Hualien, Taiwan.
Abstract Compromised mitochondrial function in neurons and glia has been
observed in several neurodegenerative disorders, including Huntington's
disease and Alzheimer's disease. Chemical/hypoxic preconditioning may afford
protection against subsequently more severe oxidative damages. In this
study, we tested whether induction of hypoxia inducible factor-1 (HIF-1) may
exert cytoprotective effects against mitochondrial dysfunction caused by
3-nitropropionic acid (3-NP) in glial cells. Preconditioning of C6
astroglial cells with cobalt chloride, mimosine (MIM), and desferrioxamine
(DFO), all of which known to activate HIF-1, significantly attenuated
cytotoxicity induced by 3-NP, an irreversible inhibitor of mitochondrial
complex II, and antimycin A, a mitochondrial complex III inhibitor.
Application of cadmium chloride capable of neutralizing cobalt-induced HIF-1
activation, HIF-specific oligodeoxynucleotide (ODN) decoy, and antisense
phosphorothioate ODN against HIF-1alpha abolished the protective effect
mediated by preconditioning with cobalt chloride. Preloading of C6 cells
with SN50, PD98059, or SB202190, the respective inhibitor of nuclear
factor-kappaB (NF-kappaB), p44/p42 extracellular signal-regulated kinase
(ERK), and p38 mitogen-activated protein kinase (MAPK), failed to affect the
protection afforded by cobalt preconditioning. Taken together, these results
suggest that HIF-1 induction secondary to preconditioning with cobalt
chloride or iron chelators may mediate the protective effects against
metabolic insult induced by the mitochondrial inhibitor 3-NP in C6
astroglial cells.
PMID: 15836611 [PubMed - in process]
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| 13: J
Neuropathol Exp Neurol. 2005 Apr;64(4):312-22. |
|
Chromosomal instability in meningiomas.
van Tilborg AA, Al Allak B, Velthuizen SC, de Vries A, Kros JM, Avezaat
CJ, de Klein A, Beverloo HB, Zwarthoff EC.
Department of Pathology, Erasmus MC, Rotterdam, The Netherlands.
Approximately 60% of sporadic meningiomas are caused by inactivation of the
NF2 tumor suppressor gene on chromosome 22. No causative gene is known for
the remaining 40%. Cytogenetic analysis shows that meningiomas caused by
inactivation of the NF2 gene can be divided into tumors that show monosomy
22 as the sole abnormality and tumors with a more complex karyotype.
Meningiomas not caused by the NF2 gene usually have a diploid karyotype.
Here we report that, besides the clonal chromosomal aberrations, the
chromosome numbers in many meningiomas varied from one metaphase spread to
the other, a feature that is indicative of chromosomal instability.
Unexpectedly and regardless of genotype, a subgroup of tumors was observed
with an average number of 44.9 chromosomes and little variation in the
number of chromosomes per metaphase spread. In addition, a second subgroup
was recognized with a hyperdiploid number of chromosomes (average 48.5) and
considerable variation in numbers per metaphase. However, this numerical
instability resulted in a clonal karyotype with chromosomal gains and losses
in addition to loss of chromosome 22 only in meningiomas caused by
inactivation of the NF2 gene. In cultured cells of all tumor groups, bi- and
multinucleated cells were seen, as well as anaphase bridges, residual
chromatid strings, multiple spindle poles, and unseparated chromatids,
suggesting defects in the mitotic apparatus or kinetochore. Thus, we
conclude that even a benign and slow-growing tumor like a meningioma
displays chromosomal instability.
PMID: 15835267 [PubMed - in process]
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| 14: Neurol
Res. 2005 Apr;27(3):324-32. |
|
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Clinical and histological features of multiple
meningiomas compared with solitary meningiomas.
Huang H, Buhl R, Hugo HH, Mehdorn HM.
Department of Neurosurgery, First Affiliated Hospital of Zhejiang
University, Hangzhou, China.
Between 1991 and 2002, 456 patients with an intracranial meningioma were
treated. Thirty-nine of these had more than one meningioma (8.6%). The mean
age was 58 years (27-85 years). Sex distribution was 8.8:1 (35 female, four
male). There was no associated spinal meningioma. No patient had
neurofibromatosis. In 19 patients all meningiomas were removed. Twelve
showed the same histology, seven had different histological features. In the
remaining 20 patients only the symptomatic meningioma was removed.
Recurrences occurred in 11 patients (28.2%). Six patients died during
follow-up. Multiple meningiomas have their own clinical features. Besides a
high female preponderance, PR expression was stronger in multiple
meningiomas than in solitary meningiomas while p53 status and MIB-1 LI were
similar between the two groups. Progesterone receptor, p53 status and MIB-1
LI were valuable markers for predicting a patient's outcome in multiple
meningiomas. The number of meningiomas is growing in patients with recurrent
meningiomas.
PMID: 15845217 [PubMed - in process]
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| 15: Neurosurg
Clin N Am. 2005 Apr;16(2):411-32, xi. |
|
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Preoperative embolization of central nervous system
tumors.
Deshmukh VR, Fiorella DJ, McDougall CG, Spetzler RF, Albuquerque FC.
Division of Neurological Surgery, Barrow Neurological Institute, St.
Joseph's Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ
85013, USA.
Publication Types:
PMID: 15694171 [PubMed - indexed for MEDLINE]
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| 16: Oncogene.
2005 Mar 17;24(12):1994-2007. |
|
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Survivin splice variants regulate the balance between
proliferation and cell death.
Caldas H, Jiang Y, Holloway MP, Fangusaro J, Mahotka C, Conway EM, Altura
RA.
Center for Childhood Cancer, Columbus Children's Research Institute, The
Ohio State University, Columbus, OH, USA.
Survivin is an inhibitor of apoptosis protein that also plays critical roles
in regulating the cell cycle and mitosis. Its prominent expression in
essentially all human malignancies, and low or absent expression in most
normal tissues, suggests that it would be an ideal target for
cancer-directed therapy. Impeding development of safe and effective survivin
antagonists for clinical use is a lack of understanding of the molecular
mechanisms by which survivin differentially affects apoptosis and cell
division, in normal and malignant cells. We show that the diverse functional
roles of survivin can be explained, in part, by its heterodimerization with
survivin splice variants in tumor cells. Survivin and survivin-DeltaEx3
interact within the mitochondria where they may inhibit
mitochondrial-dependent apoptosis. If the expression of all survivin forms
is eliminated by siRNA transfections, cells undergo both apoptosis and
defective cell division. Overall, we provide new insights suggesting that
targeting specific survivin isoforms, rather than survivin alone, may
selectively and effectively destroy tumor cells. These findings are likely
to have a significant impact in the design of biologic agents for clinical
therapy.
PMID: 15688031 [PubMed - indexed for MEDLINE]
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| 17: Radiology.
2005 Apr 15; [Epub ahead of print] |
|
-
Apparent Diffusion Coefficient of Human Brain Tumors at
MR Imaging.
Yamasaki F, Kurisu K, Satoh K, Arita K, Sugiyama K, Ohtaki M, Takaba J,
Tominaga A, Hanaya R, Yoshioka H, Hama S, Ito Y, Kajiwara Y, Yahara K, Saito
T, Thohar MA.
Depts of Neurosurgery and Radiology, Graduate School of Biomedical Sciences,
Hiroshima Univ, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan; Dept of
Environmetrics and Biometrics, Research Inst for Radiation Biology and
Medicine, Hiroshima Univ, Japan.
PURPOSE: To determine if apparent diffusion coefficient (ADC) can be used to
differentiate brain tumors at magnetic resonance (MR) imaging. MATERIALS AND
METHODS: Institutional review board approval or informed patient consent was
not required. MR images were reviewed retrospectively in 275 patients with
brain tumors: 147 males and 128 females 1-81 years old, treated between
September 1997 and July 2003. Regions of interest were placed manually in
tumor regions on MR images, and ADC was calculated with a five-point
regression method at b values of 0, 250, 500, 750, and 1000 sec/mm(2). ADC
values were average values in tumor. All brain tumor subgroups were
analyzed. Logistic discriminant analysis was performed by using ADC, age,
and patient sex as independent variables to discriminate among tumor groups.
RESULTS: A significant negative correlation existed between ADC and
astrocytic tumors of World Health Organization grades 2-4 (grade 2 vs grades
3 and 4, accuracy of 91.3% [P < .01]; grade 3 vs 4, accuracy of 82.4% [P
< .01]). ADC of dysembryoplastic neuroepithelial tumors (DNTs) was higher
than that of astrocytic grade 2 tumors (accuracy, 100%) and other
glioneuronal tumors. ADC of malignant lymphomas was lower than that of
glioblastomas and metastatic tumors (accuracy, 83.6%; P < .01). ADC of
primitive neuroectodermal tumors (PNETs) was lower than that of ependymomas
(accuracy, 100%). ADC of meningiomas was lower than that of schwannomas
(accuracy, 92.4%; P < .01). ADC of craniopharyngiomas was higher than
that of pituitary adenomas (accuracy, 85.2%; P < .05). ADC of epidermoid
tumors was lower than that of chordomas (accuracy, 100%). In meningiomas,
ADC was not indicative of malignancy grade or histologic subtype.
CONCLUSION: ADC is useful for differentiation of some human brain tumors,
particularly DNT, malignant lymphomas versus glioblastomas and metastatic
tumors, and ependymomas versus PNETs. (c) RSNA, 2005.
PMID: 15833979 [PubMed - as supplied by publisher]
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| 18: Arq
Neuropsiquiatr. 2005 Mar;63(1):171-2. Epub 2005 Apr 13. |
|
[Transient lesion in the splenium of the corpus callosum
in epileptic child with cerebral low grade glioma]
[Article in Portuguese]
Assencio-Ferreira VJ, Mussi ML, Guirado VM, Veiga JC.
Universidade de Sao Paulo, Brazil. vicasfer@iconet.com.br
We report on a seven years-old boy with complex partial seizures and the
presence of low grade glioma in left fronto-parietal region. The magnetic
resonance imaging showed focal non-hemorrhagic lesion in the splenium of the
corpus callosum. The description of the transient lesion in the splenium of
the corpus callosum was related in three previous studies, in patients with
epilepsy. Thus, the observed transient focal lesion in the splenium of the
corpus callosum of this child, probably, has correlation with to prolonged
focal partial seizures and not to the presence of glioma low grade.
PMID: 15830087 [PubMed - in process]
-
| 19: Neurology.
2005 Apr 12;64(7):1189-95. |
|
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Cellular telephones and risk for brain tumors: a
population-based, incident case-control study.
Christensen HC, Schuz J, Kosteljanetz M, Poulsen HS, Boice JD Jr,
McLaughlin JK, Johansen C.
Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen,
Denmark. hcollatz@dadlnet.dk
OBJECTIVE: To evaluate a possible association of glioma or meningioma with
use of cellular telephones, using a nationwide population-based case-control
study of incident cases of meningioma and glioma. METHODS: The authors
ascertained all incident cases of glioma and meningioma diagnosed in Denmark
between September 1, 2000, and August 31, 2002. They enrolled 252 persons
with glioma and 175 persons with meningioma aged 20 to 69. The authors also
enrolled 822 randomly sampled, population-based controls matched for age and
sex. Information was obtained from personal interviews, medical records
containing diagnoses, and the results of radiologic examinations. For a
small number of cases and controls, the authors obtained the numbers of
incoming and outgoing calls. They evaluated the memory of the respondents
with the Mini-Mental State Examination and obtained data on socioeconomic
factors from Statistics Denmark. RESULTS: There were no material
socioeconomic differences between cases and controls or participants and
non-participants. Use of cellular telephone was associated with a low risk
for high-grade glioma (OR, 0.58; 95% CI, 0.37 to 0.90). The risk estimates
were closer to unity for low-grade glioma (1.08; 0.58 to 2.00) and
meningioma (1.00; 0.54 to 1.28). CONCLUSION: The results do not support an
association between use of cellular telephones and risk for glioma or
meningioma.
PMID: 15824345 [PubMed - in process]
-
| 20: Lancet
Oncol. 2005 Apr;6(4):240-4. |
|
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Lessons learned from randomised clinical trials in adult
low grade glioma.
Papagikos MA, Shaw EG, Stieber VW.
Department of Radiation Oncology, Comprehensive Cancer Center, Wake Forest
University Baptist Medical Center, Winston-Salem, NC 27157, USA.
"Lesson" is a Middle English word that has been defined as "a
passage from sacred writings read in a service of worship" as well as
"something learned by study or experience". The term is quite
appropriate in assessment of what has been learned from randomised trials in
adult low-grade gliomas, since the treatment of these tumours has
traditionally been guided as much by belief as by fact. Therefore, when
assessing these trials we can apply the principles of hermeneutics. Thus,
the first meaning of "lesson" given here can be described as
literal, whereas the second may be seen as figurative. Since hermeneutics
may also refer to an in-depth analysis of a particular text, the
investigators will present their interpretation of data from randomised
trials. The goal is to show that the lessons learned are not necessarily
literal or dogmatic but can be much more allegorical in nature.
PMID: 15811619 [PubMed - in process]
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Volume 4, Number 19 - 26 April 2005