-
Edema is a precursor to central nervous system
peritumoral cyst formation.
Lonser
RR, Vortmeyer
AO, Butman
JA, Glasker
S, Finn
MA, Ammerman
JM, Merrill
MJ, Edwards
NA, Zhuang
Z, Oldfield
EH.
Surgical Neurology Branch, National Institute of Neurological Disorders and
Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
lonserr@ninds.nih.gov
Despite the common occurrence and frequent clinical effects of peritumoral
cysts in the central nervous system (CNS), the mechanism underlying their
development and evolution is not understood. Because they commonly produce
peritumoral cysts and because serial magnetic resonance imaging (MRI) is
obtained in von Hippel-Lindau disease patients, hemangioblastomas provide an
opportunity to examine the pathophysiology of CNS peritumoral cyst
formation. Serial MRI was correlated with the clinical findings in 16 von
Hippel-Lindau disease patients with 22 CNS hemangioblastomas (11 spinal
cord; 11 cerebellar) that were associated with the appearance and evolution
of peritumoral cysts. Hemangioblastoma-associated cyst wall
histomorphological analysis was performed on postmortem tissues from three
von Hippel-Lindau disease patients (not in the clinical series). Comparative
proteomic profiling was performed on peritumoral cyst fluid and serum.
Vascular endothelial growth factor levels were determined in peritumoral
cysts. MRI clearly showed peritumoral edema that developed and slowly and
progressively evolved into enlarging hemangioblastoma-associated cysts in
all tumors (mean follow-up, 130 +/- 38 months; mean +/- standard deviation).
Postcontrast MRI demonstrated convective leakage of gadolinium into cysts.
Mean time required for edema to evolve into a cyst was 36 +/- 23 months
(range, 8-72 months). Thirteen (59%) hemangioblastoma-cysts became
symptomatic (mean time to symptom formation after cyst development, 35 +/-
32 months; range, 3-102 months) and required resection. Protein profiles of
cyst fluid and serum were similar. Mean cyst fluid vascular endothelial
growth factor concentration was 1.5 ng/ml (range, 0-5.4 ng/ml). Histology of
the cyst walls was consistent with reactive gliosis. CNS peritumoral cyst
formation is initiated by increased tumor vascular permeability, increased
interstitial pressure in the tumor, and plasma extravasation with convective
distribution into the surrounding tissue. When the delivery of plasma from
the tumor exceeds the capacity of the surrounding tissue to absorb the
extravasated fluid, edema (with its associated increased interstitial
pressure) and subsequent cyst formation occur.
PMID: 16130092 [PubMed - indexed for MEDLINE]
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EGFR intragenic loss and gene amplification in astrocytic
gliomas.
Arjona
D, Bello
MJ, Rey
JA.
Unidad de Investigacion, Laboratorio de Oncogenetica Molecular, Hospital
Universitario La Paz, Paseo Castellana 261, 28046 Madrid, Spain.
We have studied EGFR gene amplification and allelic status of chromosome 7
in 68 tumors consisting of 34 WHO grade IV glioblastomas (26 primary and 8
secondary), 14 WHO grade III anaplastic astrocytomas, and 20 WHO grade II
astrocytomas, by polymerase chain reaction-single-strand conformation
polymorphism (PCR-SSCP), quantitative PCR, and microsatellite analysis. EGFR
gene amplification was present in 27 of these tumors (40%), and we
identified allelic losses at 7p11 approximately p14 in 38 of the 68 cases
(56%), including 17 tumors displaying loss for EGFR intragenic markers. The
positive correlation (P < 0.05, chi(2)) between tumors with EGFR
intragenic loss and EGFR gene amplification, frequently displaying the EGFR
vIII form, suggests that EGFR gene rearrangement leading to intragenic loss
is a molecular event that participates in the amplification process of this
gene.
PMID: 16364761 [PubMed - in process]
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-
Host lymphodepletion augments T cell adoptive
immunotherapy through enhanced intratumoral proliferation of effector cells.
Wang
LX, Shu
S, Plautz
GE.
Center for Surgery Research, Division of Surgery, Cleveland Clinic
Foundation, Cleveland, OH 44195, USA.
T-cell adoptive immunotherapy for stringent murine tumor models, such as
intracranial, s.c., or advanced pulmonary metastases, routinely uses
lymphodepletive conditioning regimens before T-cell transfer, like recent
clinical protocols. In this study, we examined whether host lymphodepletion
is an obligatory component of curative T-cell therapy; we also examined the
mechanism by which it augments therapy. Mice bearing intracranial, s.c., or
10-day pulmonary metastases of MCA 205 received total body irradiation
conditioning or were nonirradiated before i.v. transfer of tumor-reactive T
cells. Total body irradiation was not required for immunologically specific
curative therapy and induction of memory provided that a 3- to 12-fold
higher T-cell dose was administered. The mechanism involved enhanced
intratumoral proliferation of T-effector cells in total body
irradiation-conditioned recipients. In this tumor model, intratumoral T(reg)
cells were not detected; consequently, intratumoral T-effector cells
produced identical amounts of IFN-gamma upon ex vivo antigen stimulation
irrespective of total body irradiation conditioning. Thus, host
lymphodepletion augments T-cell immunotherapy through enhanced
antigen-driven proliferation of T-effector cells, but curative therapy can
be achieved in nonconditioned hosts by escalation of T-cell dose. These data
provide a rationale for dose escalation of T-effector cells in situations
where single or repeated lymphodepletion regimens are contraindicated.
PMID: 16230420 [PubMed - indexed for MEDLINE]
-
-
The scatter factor/hepatocyte growth factor: c-met
pathway in human embryonal central nervous system tumor malignancy.
Li
Y, Lal
B, Kwon
S, Fan
X, Saldanha
U, Reznik
TE, Kuchner
EB, Eberhart
C, Laterra
J, Abounader
R.
Department of Neurology, Johns Hopkins University School of Medicine, MD
21205, USA.
Embryonal central nervous system (CNS) tumors, which comprise
medulloblastoma, are the most common malignant brain tumors in children. The
role of the growth factor scatter factor/hepatocyte growth factor (SF/HGF)
and its tyrosine kinase receptor c-Met in these tumors has been until now
completely unknown. In the present study, we show that human embryonal CNS
tumor cell lines and surgical tumor specimens express SF/HGF and c-Met.
Furthermore, c-Met mRNA expression levels statistically significantly
correlate with poor clinical outcome. Treatment of medulloblastoma cells
with SF/HGF activates c-Met and downstream signal transduction as evidenced
by c-Met, mitogen-activated protein kinase, and Akt phosphorylation. SF/HGF
induces tumor cell proliferation, anchorage-independent growth, and cell
cycle progression beyond the G1-S checkpoint. Using dominant-negative Cdk2
and a degradation stable p27 mutant, we show that cell cycle progression
induced by SF/HGF requires Cdk2 function and p27 inhibition. SF/HGF also
protects medulloblastoma cells against apoptosis induced by chemotherapy.
This cytoprotective effect is associated with reduction of proapoptotic
cleaved poly(ADP-ribose) polymerase and cleaved caspase-3 proteins and
requires phosphoinositide 3-kinase activity. SF/HGF gene transfer to
medulloblastoma cells strongly enhances the in vivo growth of s.c. and
intracranial tumor xenografts. SF/HGF-overexpressing medulloblastoma
xenografts exhibit increased invasion and morphologic changes that resemble
human large cell anaplastic medulloblastoma. This first characterization
establishes SF/HGF:c-Met as a new pathway of malignancy with multifunctional
effects in human embryonal CNS tumors.
PMID: 16230398 [PubMed - indexed for MEDLINE]
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-
Effect of repetitive administration of
Doxorubicin-containing liposomes on plasma pharmacokinetics and drug
biodistribution in a rat brain tumor model.
Arnold
RD, Mager
DE, Slack
JE, Straubinger
RM.
Authors' Affiliation: Department of Pharmaceutical Sciences, University at
Buffalo, State University of New York, Amherst, New York.
PURPOSE: The incorporation of doxorubicin in long-circulating sterically
stabilized liposomes (SSL-DXR) alters the pharmacokinetics and
biodistribution of doxorubicin and therefore has the potential to alter the
pharmacologic properties of doxorubicin. Previously, we showed that
repetitive administration of SSL-DXR alters tumor vascular
permeability.EXPERIMENTAL DESIGN: Here, we investigated the effect of weekly
i.v. injections of SSL-DXR on plasma pharmacokinetics and drug
biodistribution in the orthotopic 9L rat brain tumor model.Results and
CONCLUSIONS: The pharmacokinetics of free doxorubicin (5.67 mg/kg) did not
change with repeat dosing. In contrast, drug concentrations in plasma and
brain tumor increased and deposition in liver and spleen decreased after
administration of the second of two weekly doses of SSL-DXR.
Noncompartmental analysis and descriptive pharmacokinetic models were
created to test hypotheses relating to the mechanisms responsible for
alterations in SSL-DXR deposition. The analysis suggested that weekly
administration of SSL-DXR significantly (P < 0.05) decreased the plasma
elimination rate of SSL-DXR (34%) and decreased drug deposition in liver
(2-fold) and spleen (3.5-fold). The pharmacokinetic model that best captured
the observed 2.5-fold increase in tumor uptake of SSL-DXR mediated by repeat
dosing was one that hypothesized that the rates of drug influx/efflux into
tumor were increased by the first dose of SSL-DXR. Models that accounted
only for residual drug deposited in the tissue or blood by the first weekly
injection provided inferior fits to the data. Thus, the effects of
repetitive dosing on SSL-DXR deposition in tumor are consistent with a
treatment-mediated alteration of tumor vascular permeability.
PMID: 16361575 [PubMed - in process]
-
-
Magnetic resonance imaging characteristics predict
epidermal growth factor receptor amplification status in glioblastoma.
Aghi
M, Gaviani
P, Henson
JW, Batchelor
TT, Louis
DN, Barker
FG 2nd.
Authors' Affiliations: Neurosurgical Service; Departments of Neurology,
Neuroradiology, and Pathology.
PURPOSE: Two clinical-molecular glioblastoma subtypes have been described:
"primary" glioblastomas arise de novo in older patients and often
overexpress epidermal growth factor receptor (EGFR); "secondary"
glioblastomas progress from lower-grade tumors in younger patients and
commonly have TP53 mutations. EGFR overexpression correlates in experimental
gliomas with increased angiogenesis, edema, and invasion. No radiographic
predictors of molecular glioblastoma subtype are known.EXPERIMENTAL DESIGN:
We retrospectively reviewed 75 glioblastomas, classified as TP53-mutated (n
= 11), EGFR-amplified (n = 31), or neither (non-TP53/non-EGFR; n = 33). Four
variables were derived from preoperative magnetic resonance imaging: (a)
T2/T1, the ratio of T2-bright volume to enclosed T1-enhancing volume; (b)
percentage of tumor volume that was necrosis; and (c and d) T1 and T2 border
sharpness coefficients (BSC), the rates of change in grayscale intensity of
adjacent 0.02-cm(2) voxels traversing the anterior, posterior, and lateral
borders on T1-enhanced and T2 images.Results and CONCLUSIONS: Mean T2/T1 was
4.7 for EGFR-amplified glioblastomas, greater than that of TP53-mutated
glioblastomas (2.3) or non-TP53/non-EGFR glioblastomas (2.6; P <
0.00005). All four tumors with T2/T1 > 7.2 were EGFR-amplified; 0 of 15
with T2/T1 < 4.7 underwent gross total resection. The mean T2 BSC of
EGFR-amplified glioblastomas was 33.7, less sharp (P < 0.0000005) than
TP53-mutated (72.2) and non-TP53/non-EGFR glioblastomas (81.2). All 15
glioblastomas with T2 BSC < 30.8 were EGFR-amplified. Percentage necrosis
and T1 BSC did not differ between glioblastoma subtypes. The increased T2/T1
ratio and decreased T2 BSC in EGFR-overexpressing tumors are the first
radiographic distinctions described between glioblastoma molecular subtypes.
These findings may reflect increased angiogenesis, edema, and/or invasion in
EGFR-overexpressing tumors.
PMID: 16361543 [PubMed - in process]
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Comment on:
Personalized, multivalent, and more affordable: the
globalization of vaccines.
Debinski
W.
Publication Types:
PMID: 16115899 [PubMed - indexed for MEDLINE]
-
-
Tumor Necrosis Factor-{alpha}-Induced Protein 3 As a
Putative Regulator of Nuclear Factor-{kappa}B-Mediated Resistance to
O6-Alkylating Agents in Human Glioblastomas.
Bredel
M, Bredel
C, Juric
D, Duran
GE, Yu
RX, Harsh
GR, Vogel
H, Recht
LD, Scheck
AC, Sikic
BI.
Division of Oncology, Center for Clinical Sciences Research, Institute for
Computational and Mathematical Engineering, Departments of Neurosurgery,
Pathology, and Neurology, Stanford University School of Medicine, Stanford,
CA; Ina Levine Brain Tumor Center, Neuro-Oncology Research and Neurosurgery
Research, Barrow Neurological Institute of St. Joseph's Hospital and Medical
Center, Phoenix, AZ; and the Department of General Neurosurgery,
Neurocenter, University of Freiburg, Freiburg, Germany.
PURPOSE: Pre-existing and acquired drug resistance are major obstacles to
the successful treatment of glioblastomas. METHODS: We used an integrated
resistance model and genomics tools to globally explore molecular factors
and cellular pathways mediating resistance to O(6)-alkylating agents in
glioblastoma cells. RESULTS: We identified a transcriptomic signature that
predicts a common in vitro and in vivo resistance phenotype to these agents,
a proportion of which is imprinted recurrently by gene dosage changes in the
resistant glioblastoma genome. This signature was highly enriched for genes
with functions in cell death, compromise, and survival. Modularity was a
predominant organizational principle of the signature, with functions being
carried out by groups of interacting molecules in overlapping networks. A
highly significant network was built around nuclear factor-kappaB
(NF-kappaB), which included the persistent alterations of various NF-kappaB
pathway elements. Tumor necrosis factor-alpha-induced protein 3 (TNFAIP3)
was identified as a new regulatory component of a putative cytoplasmic
signaling cascade that mediates NF-kappaB activation in response to DNA
damage caused by O(6)-alkylating agents. Expression of the corresponding
zinc finger protein A20 closely mirrored the expression of the TNFAIP3
transcript, and was inversely related to NF-kappaB activation status in the
resistant cells. A prediction model based on the resistance signature
enabled the subclassification of an independent, validation cohort of 31
glioblastomas into two outcome groups (P = .037) and revealed TNFAIP3 as
part of an optimized four-gene predictor associated significantly with
patient survival (P = .022). CONCLUSION: Our results offer strong evidence
for TNFAIP3 as a key regulator of the cytoplasmic signaling to activate
NF-kappaB en route to O(6)-alkylating agent resistance in glioblastoma
cells. This pathway may be an attractive target for therapeutic modulation
of glioblastomas.
PMID: 16365179 [PubMed - as supplied by publisher]
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-
Phase II Study of Imatinib Mesylate Plus Hydroxyurea in
Adults With Recurrent Glioblastoma Multiforme.
Reardon
DA, Egorin
MJ, Quinn
JA, Rich
JN Sr, Gururangan
I, Vredenburgh
JJ, Desjardins
A, Sathornsumetee
S, Provenzale
JM, Herndon
JE 2nd, Dowell
JM, Badruddoja
MA, McLendon
RE, Lagattuta
TF, Kicielinski
KP, Dresemann
G, Sampson
JH, Friedman
AH, Salvado
AJ, Friedman
HS.
the Brain Tumor Center at Duke, Duke University Medical Center, Box 3624,
Durham, NC 27710; e-mail: reard003@mc.duke.edu.
PURPOSE We performed a phase II study to evaluate the combination of
imatinib mesylate, an adenosine triphosphate mimetic, tyrosine kinase
inhibitor, plus hydroxyurea, a ribonucleotide reductase inhibitor, in
patients with recurrent glioblastoma multiforme (GBM). PATIENTS AND METHODS
Patients with GBM at any recurrence received imatinib mesylate plus
hydroxyurea (500 mg twice a day) orally on a continuous, daily schedule. The
imatinib mesylate dose was 500 mg twice a day for patients on
enzyme-inducing antiepileptic drugs (EIAEDs) and 400 mg once a day for those
not on EIAEDs. Assessments were performed every 28 days. The primary end
point was 6-month progression-free survival (PFS). Results Thirty-three
patients enrolled with progressive disease after prior radiotherapy and at
least temozolomide-based chemotherapy. With a median follow-up of 58 weeks,
27% of patients were progression-free at 6 months, and the median PFS was
14.4 weeks. Three patients (9%) achieved radiographic response, and 14 (42%)
achieved stable disease. Cox regression analysis identified concurrent EIAED
use and no more than one prior progression as independent positive
prognostic factors of PFS. The most common toxicities included grade 3
neutropenia (16%), thrombocytopenia (6%), and edema (6%). There were no
grade 4 or 5 events. Concurrent EIAED use lowered imatinib mesylate
exposure. Imatinib mesylate clearance was decreased at day 28 compared with
day 1 in all patients, suggesting an effect of hydroxyurea. CONCLUSION
Imatinib mesylate plus hydroxyurea is well tolerated and associated with
durable antitumor activity in some patients with recurrent GBM.
PMID: 16361636 [PubMed - in process]...
-
-
Secondary analysis of Radiation Therapy Oncology Group
study (RTOG) 9310: an intergroup phase II combined modality treatment of
primary central nervous system lymphoma.
Fisher
B, Seiferheld
W, Schultz
C, DeAngelis
L, Nelson
D, Schold
SC, Curran
W, Mehta
M.
Department of Radiation Oncology, London Regional Cancer Program and
University of Western Ontario, 790 Commissioners Road East, London N6A 4L6,
Ontario, Canada. barb.fisher@lrcc.on.ca
PURPOSE: To determine whether a lower dose of hyperfractionated whole brain
radiation reduces central nervous system morbidity without compromising
survival for primary CNS lymphoma (PCNSL) patients receiving combined
modality treatment. MATERIALS AND METHODS: One hundred and two patients
received a course of pre-radiation chemotherapy, followed by whole brain
radiation, followed by cytosine-arabinoside. Initial radiation dose was 45
Gy/25 fractions (RT) then the study was amended to reduce this dose for
complete responders to induction chemotherapy to 36 Gy/30 fractions/3 weeks
(HFX). Eighty-two patients received radiotherapy and were evaluable for
toxicity analysis (66 RT patients and 16 HFX patients). MMSE scores and
survival for the 40 patients who received radiotherapy after complete
response to chemotherapy (27 RT and 13 HFX) were compared. There were no
notable differences in pre-treatment patient characteristics between the RT
and HFX groups. RESULTS: Neurotoxicity: By 4 years, there were 8/82 (10%)
grade 5 neurotoxicities which included 2/16 (13%) grade 5 encephalopathies
and 0/27 in the RT group of complete responders to chemotherapy. Survival:
There was no statistically significant difference in overall or
progression-free survival (PFS) between the chemotherapy-complete responders
who received RT and HFX. Cognitive function testing: MMSE scores improved at
8 months across both treatment groups. Analysis of the area under the MMSE
curve at 8 months showed no statistically significant difference between RT
and HFX groups (P=0.81). Leukoencephalopathy occurred later in the HFX group
than in the RT patients. CONCLUSION: Although the HFX schedule represented a
25% reduction in biologically effective tumor dose in comparison, PFS and
overall survival were not significantly affected. The HFX regimen delayed
but did not eliminate severe neurotoxicity from chemoradiation in PCNSL
patients.
Publication Types:
PMID: 16193393 [PubMed - indexed for MEDLINE]
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-
Malignant transformation of intra-cranial epithelial
cysts: systematic article review.
Hamlat
A, Hua
ZF, Saikali
S, Laurent
JF, Gedouin
D, Ben-Hassel
M, Guegan
Y.
Department of Neurosurgery, Service de Neurochirurgie, CHRU Pontchaillou,
Rue Henry Le Guilloux, 35000 Rennes Cedex 2, France. hamlat.abd@wanadoo.fr
INTRODUCTION: Epidermoid and dermoid cysts are among the most benign intra
cranial tumors. Their malignant transformation into squamous cell carcinoma
is rare. The authors reviewed the literature. MATERIALS AND METHODS: MEDLINE
and SCIENCE DIRECT searches, and examination of the references in the
selected articles yielded 74 patients, 52 of whom fulfilled Garcia's
criteria and were selected for the study. Survival analyses were performed
to determine whether survival differences were of statistical significance,
and P < 0.05 was considered as significant. RESULTS: Malignant
transformation is characterized by a rapid onset of symptoms, recurrence,
leptomeningeal carcinomatosis (LC), and tumor enhancement at Computed
Tomography Scan or Magnetic Resonance Imaging (87.8 showed this radiological
feature). In this review, the SCCs were classified in five groups: (1)
Initial malignant transformation of a benign cyst; (2) malignant
transformation from a remnant cyst; (3) malignant transformation of a
dermoid and epithelial cyst; (4) malignant transformation with
leptomeningeal carcinomatosis; (5) other malignancies arising from benign
cysts. The median survival was 9 months. Statistics show that LC was of poor
prognosis and radiotherapy, although not statistically significant, seems
effective against such lesions, with a median survival of 26 months as
opposed to 3 months (P=0.077). CONCLUSION: Although rare, malignant
transformation of intracranial epithelial cysts has a poor prognosis and
surgery followed by radiotherapy seems to be the best therapeutic modality.
Publication Types:
PMID: 16193391 [PubMed - indexed for MEDLINE]
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Spinal cord metastasis of a non-neurofibromatosis type-1
malignant peripheral nerve sheath tumor: an unusual manifestation of a rare
tumor.
Baek
WS, Pytel
P, Undevia
SD, Rubeiz
H.
The Department of Neurology, The University of Chicago School of Medicine
and Medical Center, 5841 S. Maryland Street, Chicago, IL 60637, USA.
Malignant peripheral nerve sheath tumors are rare spindle-cell sarcomas
derived from Schwann cells or pluripotent cells of the neural crest. They
arise from the spinal roots, peripheral nerves, brachial and lumbosacral
plexi, cranial nerves and terminal nerve fibers within soft tissue,
intestine, lung and bone. These tumors recur either locally, or metastasize
distally. Most of these tumors occur in association with neurofibromatosis
type 1. Spinal cord metastasis from malignant nerve sheath tumors associated
with neurofibromatosis type 1 is very rare. We describe a rare case of
near-total spinal cord metastasis in a patient with malignant nerve sheath
tumor in the absence of neurofibromatosis, and highlight the microscopic
findings and natural history of this disease process.
Publication Types:
PMID: 16193390 [PubMed - indexed for MEDLINE]
-
-
Unusual radiological presentation of PCNSL.
Agrawal
D, Mahapatra
AK.
Department of Neurosurgery, Neurosciences Center, All India Institute of
Medical Sciences, New Delhi, India.
Publication Types:
PMID: 16193386 [PubMed - indexed for MEDLINE]
-
Cystic cavernous malformation of the cerebellopontine
angle. Case illustration.
Stevenson
CB, Johnson
MD, Thompson
RC.
Department of Neurological Surgery, Vanderbilt University Medical Center,
Nashville, Tennessee 37232-2380, USA.
Publication Types:
PMID: 16305001 [PubMed - indexed for MEDLINE]
-
Ultrastructural characteristics of hemorrhagic,
nonhemorrhagic, and recurrent cavernous malformations.
Tu
J, Stoodley
MA, Morgan
MK, Storer
KP.
Prince of Wales Medical Research Institute, University of New South Wales,
New South Wales, Australia.
OBJECT: Ultrastructural characteristics of hemorrhagic, nonhemorrhagic,
primary, and recurrent central nervous system cavernous malformations (CMs)
were examined in an attempt to clarify their pathological mechanisms.
METHODS: Thirteen specimens (nine from samples of CMs and four from healthy
control tissue) were processed for ultrastructural study immediately after
surgical or postmortem removal, by fixation in glutaraldehyde/formalin and
postfixation in OsO4. Transmission electron microscopy was used to examine
the vascular walls, endothelium, subendothelium, and cytoplasmic organelles.
The vascular walls in CMs demonstrated abnormal ultrastructure with no
basement membranes and astrocytic foot processes. Pericytes were rarely
seen. Single-layer lining endothelial cells showed fenestrated luminal
surfaces. Large gaps were observed at intercellular junctions between
endothelial cells, and large vesicles with extremely thin plasma membranes
bordering the lumen were common in the lesions that had previously
hemorrhaged. Endothelial cells of recurrent CMs had more Weibel-Palade
bodies, filopodia, cytoplasmic processes, micropinocytotic vesicles, and
filaments than those in primary lesions and normal control tissues.
CONCLUSIONS: The absence of the blood-brain barrier, normal supporting wall
structure, and large vesicles bordering the lumen of CM vessels may explain
leakage of red blood cells into surrounding brain in the absence of major
hemorrhage. Proliferation of residual abnormal endothelial cells may
contribute to the recurrence of surgically removed CMs.
PMID: 16304995 [PubMed - indexed for MEDLINE]
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Rathke cleft cyst intracystic nodule: a characteristic
magnetic resonance imaging finding.
Binning
MJ, Gottfried
ON, Osborn
AG, Couldwell
WT.
Departments of Neurosurgery and Radiology, University of Utah, Salt Lake
City, Utah 84132, USA.
OBJECT: The fluid content of Rathke cleft cysts (RCCs) displays variable
appearances on magnetic resonance (MR) images and can appear
indistinguishable from other intrasellar or suprasellar cystic lesions.
Intracystic nodules associated with individual RCCs have been noted, but to
date their significance has not been fully explored. METHODS: The authors
retrospectively reviewed MR imaging studies obtained in patients harboring
intrasellar or suprasellar lesions that were consistent with RCCs to
identify the presence and imaging characteristics of intracystic nodules. An
intracystic nodule was present in nine (45%) of 20 patients with an RCC. All
intracystic nodules were clearly visible and displayed a characteristic low
signal intensity on T2-weighted MR images. The nodule was only visualized on
T1-weighted images in four cases, in which it exhibited a consistent high
signal intensity similar to that of the cyst fluid. The nodules did not
enhance following the intravenous administration of a contrast agent.
CONCLUSIONS: Although it is difficult to differentiate RCCs from other
sellar cystic lesions because of the variable signal intensities displayed
on MR images, the intensity of the intracystic nodule seems consistent on
T1- and T2-weighted images, and the nodule is always clearly visible on
T2-weighted images. With a nonenhancing cystic lesion that does not cause
significant symptoms in the patient, the identification of an intracystic
nodule with a characteristic signal intensity will aid in the diagnosis of
RCC and the selection of conservative management.
PMID: 16304987 [PubMed - indexed for MEDLINE]
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Comment in:
Posterior subtemporal transtentorial approach to
intraparenchymal lesions of the anteromedial region of the superior
cerebellum.
Ammerman
JM, Lonser
RR, Oldfield
EH.
Surgical Neurology Branch, National Institute of Neurological Disorders and
Stroke, National Institutes of Health, Bethesda, Maryland 20892-1414, USA.
OBJECT: To overcome the limitations associated with surgical approaches that
have been described for accessing intraparenchymal lesions of the
anteromedial region of the superior cerebellum, the authors used a posterior
subtemporal transtentorial approach to remove tumors in this region. In this
paper they describe the surgical technique that they used as well as the
operative findings and clinical outcomes observed in patients who underwent
resection of tumors in the anteromedial superior cerebellum. METHODS: The
consecutive patients with anteromedial superior cerebellar tumors who
underwent resection performed using the posterior subtemporal transtentorial
approach at the National Institutes of Health were included in this study.
Clinical, neuroimaging, and operative results were analyzed. Three patients
(two men and one woman) with anteromedial superior cerebellar tumors (two
hemangioblastomas and one pilocytic astrocytoma) underwent resection via
this approach. All the tumors were larger than 3 cm in diameter (range
3.1-3.5 cm). This approach provided excellent surgical access and permitted
complete tumor resection in each case. The patients remained neurologically
unchanged compared with preoperative baseline findings at the last follow-up
examination (conducted at 4, 18, and 42 months postoperatively). One patient
displayed a mild transient confusion immediately after surgery, but it
resolved within 6 days. CONCLUSIONS: The posterior subtemporal
transtentorial approach provides excellent access to the anteromedial
superior cerebellar region. This approach permits resection of large lesions
in this location, while avoiding many of the limitations associated with
other approaches to this site.
Publication Types:
PMID: 16304980 [PubMed - indexed for MEDLINE]
-
Comment on:
Transtentorial approach.
Heros
RC.
Publication Types:
PMID: 16304978 [PubMed - indexed for MEDLINE]
-
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Large thalamic mass due to neuro-Behcet disease.
Schmolck
H.
Department of Neurology NB302, Baylor College of Medicine, 6501 Fannin
Street, Houston, TX 77030-2703, USA. schmolck@bcm.tmc.edu
Publication Types:
PMID: 16087909 [PubMed - indexed for MEDLINE]
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Volume 4, Number 53 - 27 December 2005