- Cancer Types
Information about risk, prevention, screening, symptoms, diagnosis, treatment, and support for all cancers Cancer A to Z - Cancer Treatment
Cancer Treatment
Information about cancer treatment, including surgery, chemotherapy, radiation therapy, clinical trials, proton therapy, complementary medicine, and cutting edge technologies.
- Risk and Prevention
- Cancer Drugs
- Support
Support
Ways for cancer patients and caregivers to cope with cancer, side effects, nutrition, general cancer support issues, grief/end of life issues, and shared survivor's experiences.
- Healthcare Professionals
- Clinical Trials
My Patient Treatment Binder
OncoLink Blogs
What's My Cancer Risk?
OncoPilot: Navigating Your Cancer Journey
Community Events Calendar
OncoLink eNews
Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Brain Tumor - October 2001
National Cancer Institute®
Last Modified: November 21, 2001
Table of Contents
1
UI - 21230236
AU - Moreno A; de Felipe J; Garcia Sola R; Navarro A; Ramon y Cajal S
TI -
Neuronal and mixed neuronal glial tumors associated to epilepsy. A
heterogeneous and related group of tumours.
SO - Histol Histopathol 2001 Apr;16(2):613-22
AD - Department of Pathology, Clinica Puerta de Hierro, Madrid, Spain.
The group of brain tumors with mature components encompasses several
pathological entities including: the ganglioneuroma; the gangliocytoma;
the ganglioglioma; the desmoplastic ganglioglioma; the neurocitoma and a
group of glioneuronal hamartomatous tumorous lesions, such as
meningoangiomatosis. The dysembryoplastic neuroepithelial tumor is
characterized by the presence of multiple cortical nodules made up of
small, oligo-like cells and a myxoid pattern rich in
mucopolysaccharides. Mature neuronal cells are frequently detected
throughout the tumor. Most of them are associated with microhamartias in
the adjacent brain and pharmacoresistant epilepsy. The excellent
prognosis of the majority of these tumors and the potential for
malignant transformation of the glial component in the ganglioglioma are
the two most remarkable findings. Histological signs of anaplasia and
greater mitotic and proliferative activities are associated with local
recurrences. Atypical neurocytomas occur only exceptionally. Treatment
choices are surgical resectioning and, in those cases presenting greater
proliferative activity and cytological atypia, postoperative
radiotherapy may be recommended. This paper reviews this heterogeneous
group of neoplasms and hamartomatous lesions, pointing out presumable
transitions among the different types of mixed neuronal and glial brain
tumors. A single term of "mixed neuronal-glial tumors" is defended,
distinguishing different subgroups of tumors, depending on the
predominant cellular component.
2
UI - 21236052
AU - Nishio S; Morioka T; Mihara F; Gondo K; Fukui M
TI -
Cerebral ganglioglioma with epilepsy: neuroimaging features and
treatment.
SO - Neurosurg Rev 2001 Mar;24(1):14-9
AD - Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu
University, Fukuoka, Japan. shunji@ns.med.kyushu-u.ac.jp
Gangliogliomas are an increasingly recognized cause of epilepsy in
children. In this study the clinical, neuroimaging, and
neurophysiological data of five patients with cerebral ganglioglioma and
epilepsy are reviewed retrospectively. The average age of these patients
was 4.4 years at onset and the average duration of seizures before
diagnosis was 11 months. Tumors were located in the frontal (3),
parietal (1), and occipital (1) lobes. While one cystic and four solid
tumors showed various densities on CT and MRI, one frontal lesion was
not demonstrated by CT scan but clearly shown by MRI. Scalp
electroencephalography (EEG) showed neither localized nor epileptiform
abnormalities in three patients, while the remaining two had these
abnormalities. In one patient, invasive chronic electrocorticography
(ECoG) recordings with subdural electrodes revealed an ictal onset zone
located in the hand motor area. In all patients, intraoperative ECoG
failed to reveal any epileptiform activities, and tumor removal alone
was performed. For a mean of 3.4 years after surgery, all patients are
alive and seizure-free, with stable imaging findings. Tumor resection
may be the most important factor for optimal seizure control and
prevention of tumor recurrence despite the fact that EEG and ECoG
findings may conflict on tumor location.
3
UI - 21355509
AU - Meyer K; Seidel G; Knopp U
TI -
Transcranial sonography of brain tumors in the adult: an in vitro and in
vivo study.
SO - J Neuroimaging 2001 Jul;11(3):287-92
AD - Department of Neurology, Medical University Lubeck, Germany.
BACKGROUND: Few reports indicate the potential of transcranial
sonography (TCS) in detecting human brain tumors. METHODS: With an
Agilent Sonos 2500 ultrasound device, the authors studied 4 brain tumor
phantoms and compared the findings with magnetic resonance imaging
(MRI). TCS was performed on 40 patients with intracranial tumors in a
follow-up design. Sonographic tumor volume and affection of the
ventricular system were compared with MRI findings. RESULTS: The authors
found a good correlation between TCS and MRI volumetry in the in vitro
study. TCS showed good intraobserver and interobserver reliability. A
new volumetric formula for TCS measurement was determined. TCS detection
rate of brain tumors in vivo was 40%. When the investigators were given
access to radiological findings, the rate of tumor identification was
80%. Despite a sufficient acoustic window, 40% of gliomas grade II and
III were not detected. One glioblastoma was not identified owing to an
insufficient temporal acoustic window. Tumor volumes measured with MRI
and TCS correlated well. MRI volumes exceeded TCS volumes by 41%. In the
postoperative examinations (mean = 8 days postoperative, n = 15), the
resection cavity was displayed as hyperechogenic. It appeared impossible
to differentiate between residual tumor tissue and normal repair
mechanisms or blood. In the follow-up examination (mean = 99 days
postoperative, n = 15) in 5 patients, neither MRI nor TCS showed tumor
regrowth. Ten patients had residual tumors that were detected by
sonography. CONCLUSIONS: The value of TCS for the diagnostics of brain
tumors is at present limited. Once the tumor has been identified,
sonographic results match well with those of MRI.
4
UI - 21356549
AU - Granone P; Margaritora S; D'Andrilli A; Cesario A; Kawamukai K; Meacci E
TI -
Non-small cell lung cancer with single brain metastasis: the role of
surgical treatment.
SO - Eur J Cardiothorac Surg 2001 Aug;20(2):361-6
AD - General Thoracic Surgery, Department of General Surgery, A. Gemelli
Hospital-Catholic University of Rome, Rome, Italy.
OBJECTIVE: The prognosis of non-small cell lung cancer (NSCLC) with
brain metastasis is very poor, with median survival rate below 6 months,
even if treated with palliative radio and/or chemotherapy. To assess the
effectiveness of surgical treatment for this kind of patients we
patients (26 males and four females; mean age: 58.7 years) with NSCLC
and single brain metastasis underwent surgical treatment of both primary
lung cancer and secondary cerebral lesion. Patients (pts) were divided
into two major groups. In group 1 (G1) 20 pts (18 males and two females)
presented a synchronous brain metastasis. In group 2 (G2) 10 pts (eight
males and two females) presented a metachronous brain metastasis during
the follow-up period (range 3-24 months since the primary tumor).
Patients selected in G1 had T1-2, N0-1 clinical staging, good
'performance status' (ECOG:0--1; Karnofsky index > 70%), age < 75 years.
Craniotomy has always been the first approach. In G2 also patients with
locally advanced tumors (T3 and/or N2) were included. Whole brain
radiotherapy and/or chemotherapy was the post-operative choice
treatment. RESULTS: Histologic findings have shown: adenocarcinoma in 17
cases (12 in G1; five in G2), squamous cell carcinoma in 10 cases (six
in G1; four in G2), large cell carcinoma in 2 (one in G1; one in G2) and
large cell neuroendocrine carcinoma in one (G1). Survival analysis
(Kaplan--Meier method) has shown an overall value of 80% at 1 year (95%
in G1; 50% in G2), 41% at 2 years (47% in G1; 30% in G2) and 17% at 3
years (14% in G1; 20% in G2). Overall median survival is 23 months (23
in G1; 11 in G2); mean survival 27.8 months (30.3 months in G1; 22.8
months in G2). According to univariate analysis prognosis is
definitively better in N0 tumors compared to N1-2 tumors and in
adenocarcinoma cases compared to other histotypes (P < 0.05).
CONCLUSIONS: We can conclude that combined surgical therapy is,
nowadays, the choice treatment for this kind of patients, even though
restricted to selected cases. The knowledge of prognostic factors may
optimize indications for surgery.
5
UI - 21370160
AU - Nelson SJ
TI -
Analysis of volume MRI and MR spectroscopic imaging data for the
evaluation of patients with brain tumors.
SO - Magn Reson Med 2001 Aug;46(2):228-39
AD - Magnetic Resonance Science Center, Department of Radiology, University
of California, San Francisco, California 94143, USA.
nelson@mrsc.ucsf.edu
The combination of volumetric MRI and multivoxel localized MR
spectroscopic imaging (MRSI) data provides the potential for quantifying
variations in tissue morphology and function. These techniques have
numerous applications for the evaluation of neurological diseases. While
state-of-the-art whole-body MR scanners are able to acquire both types
of data, there have been relatively few reports which have presented
clinical applications of the technology. One of the reasons for this has
been the need to develop software for reconstruction and reliable
interpretation of 3D imaging and spectral data. In this article, we
describe the strategy developed for quantitative analysis of combined
MRI and MRSI examinations from patients with brain tumors and evaluate
the key components of this procedure using both simulations and
empirical data from phantoms, normal volunteers, and patients. Important
factors are the use of volume or interleaved multislice anatomic images
as a reference, the reconstruction and correction of the spectral data
for frequency, phase, and baseline distortions and consideration of the
characteristics of the coil, RF pulses used for spatial selection, and
phase encoding procedures. These studies show that the metabolic
parameters most critical for distinguishing tumor from normal and
necrotic tissue were relative levels of choline and NAA. Levels of
creatine and lactate were found to be variable, both in terms of their
spatial distribution within individual lesions and between different
patients.
6
UI - 21385135
AU - Lilja A; Nordborg C; Brun A; Salford LG; Aman P
TI -
Expression of the IL-6 family cytokines in human brain tumors.
SO - Int J Oncol 2001 Sep;19(3):495-9
AD - Lundberg Laboratory for Cancer Research, Department of Pathology,
Sahlgrenska University Hospital, Goteborg University, Goteborg, Sweden.
In our RT-PCR screen for cytokine expression in human brain tumors we
discovered increased levels of oncostatin M (OSM), ciliary neurotrophic
factor (CNTF) and leukemia inhibitory factor (LIF), all belonging to the
interleukin-6 (IL-6) cytokine family, in most of the tumors. The
expression of these cytokines in normal adult brain tissue was found to
be very low or below detection limit. OSM expression was elevated in
most of the tumors and immunohistochemistry analysis showed that the
tumor cells contained OSM in their cytoplasm, suggesting they produce
this factor. Overexpression of OSM has not previously been reported in
primary human brain tumors. The IL-6 cytokine family acts through a
common gp130 receptor subunit that activates the JAK/STAT signaling
pathway and therefore they have been suggested to have overlapping
effects. Tissue inhibitor of metalloproteinase-1 (TIMP-1), matrix
metalloproteinase 1 (MMP-1) and MMP-3 and IL-6 have been reported to be
regulated by OSM. IL-6 was low or absent in the tumors. TIMP-1, MMP-1
and MMP-3 was expressed in most tumors but with no strict correlation to
OSM levels.
7
UI - 21385152
AU - Alonso ME; Bello MJ; Lomas J; Gonzalez-Gomez P; Arjona D; De Campos JM;
TI -
Gutierrez M; Isla A; Vaquero J; Rey JA
Absence of mutation of the p73 gene in astrocytic neoplasms.
SO - Int J Oncol 2001 Sep;19(3):609-12
AD - Laboratorio de Oncogenetica Molecular, Departamento de C. Experimental,
Hospital Universitario La Paz, Paseo Castellana 261, 28046 Madrid,
Spain.
In subgroups of astrocytic neoplasms, including glioblastoma (GBM),
mutations of the p53 tumour suppressor gene lead to loss of
growth-suppressive properties. A p53-related gene termed p73 has
recently been identified; its gene product shows structural and
functional similarities to p53. After being mapped to chromosome region
1p36, p73 was proposed to act as a tumour suppressor gene, as this
region is frequently deleted in a variety of human cancers, including
astrocytic tumours. To determine whether p73 is involved in
astrocytoma/GBM development, we analysed 10 pilocytic astrocytomas, 15
WHO grade II astrocytomas, 15 WHO grade III anaplastic astrocytomas, and
20 GBM for p73 gene alterations. In parallel, we used six polymorphic
markers to determine the allelic status of region 1p36 in this tumour
series. Although loss of heterozygosity was evidenced in 12 of 60 cases
(20% of samples), PCR-SSCP and direct sequencing failed to detect any
gene mutation in the entire coding region and intronic sequences of p73.
Eight tumours displayed five distinct polymorphic nucleotide changes,
also present in the corresponding normal DNA. These variations consisted
of T-->C variation, with no change in Thr173; C-->T transition, with no
change in His197; exon 9 simultaneous double change C-->T and T-->C ,
with no variations in Ala336 and His349, respectively, and C-->T change
at exon 9/-24 position of intron 8. These results suggest that, in
astrocytic gliomas, p73 may not play a major role as a tumour
suppressor, but the relatively high incidence of LOH confirms the
presence at 1p36 of an as yet unidentified gene of this category, with a
key function in astrocytoma/GBM progression.
8
UI - 21424836
AU - Wharton SB; Chan KK; Anderson JR; Stoeber K; Williams GH
TI -
Replicative Mcm2 protein as a novel proliferation marker in
oligodendrogliomas and its relationship to Ki67 labelling index,
histological grade and prognosis.
SO - Neuropathol Appl Neurobiol 2001 Aug;27(4):305-13
AD - Academic Unit of Pathology, University of Sheffield, Medical School, UK.
s.wharton@sheffield.ac.uk
The grading and prognostic assessment of oligodendrogliomas is severely
constrained and there remains a need for improved diagnosis. Recently,
we have identified the minichromosome maintenance (MCM) family of
proteins as a novel class of proliferation markers. Mcm2 is a protein
which forms part of the prereplicative complex. It is necessary for this
complex to be assembled at origins of future DNA replication during the
G1 phase to allow genome replication in the subsequent S phase. Our aim
was to determine whether analysis of Mcm2 protein expression in
oligodendrogliomas is of diagnostic value. Immunohistochemical staining
for Mcm2 was performed on an archival series of 32 oligodendrogliomas.
These tumours have been previously characterized for Ki67, mitotic
labelling index and outcome. Cells showing expression of Mcm2 were
quantified as a percentage to provide an Mcm2 labelling index. We have
demonstrated a good correlation between Mcm2 and Ki67 labelling indices
(r = 0.76, P < 0.01) but immunohistochemistry for Mcm2 consistently
identified a higher proportion of cells. Mcm2 labelling index was higher
in grade III than grade II tumours (P < 0.001). Cases with a high Mcm2
labelling index showed a poorer prognosis than those with a low index (P
= 0.497) in univariate analysis, but with wide variation in this small
series. Demonstration of Mcm2 expression is of value to demonstrate the
proliferative fraction of tumours and is likely to be of prognostic
value. Its study in a larger series is therefore warranted.
9
UI - 21427676
AU - Peters MA; Janer M; Kolb S; Jarvik GP; Ostrander EA; Stanford JL
TI -
Germline mutations in the p73 gene do not predispose to familial
prostate-brain cancer.
SO - Prostate 2001 Sep 15;48(4):292-6
AD - Division of Clinical Research and Human Biology, Fred Hutchinson Cancer
Research Center, Seattle, Washington 98109-1024, USA. mpeters@fhcrc.org
BACKGROUND: Analysis of high-risk prostate cancer (PC) families with at
least one confirmed case of primary brain cancer (BC) has identified a
region of genetic linkage on chromosome 1p36 termed CAPB. The p36 region
of chromosome one has been reported to have frequent loss of
heterozygosity (LOH) in brain and central nervous system (CNS) tumors
and epidemiological studies have shown an increased relative risk of BC
and tumors of the CNS in PC families. In 1997 a reported tumor
suppressor with high homology to p53, termed p73, was mapped to the p36
region of chromosome one. Here, we examine the p73 gene as a potential
candidate for CAPB. METHODS: Ninety-four members from the 12
prostate-brain cancer families in which linkage was originally found
were examined. The complete coding region and intron-exon boundaries of
the p73 gene were analyzed for germline mutations by Single Stranded
Conformational Polymorphism analysis (SSCP) and direct DNA sequencing.
RESULTS: Silent nucleotide substitutions only were detected within the
coding regions of the gene in affected individuals. Nucleotide changes
were detected in introns 1, 6, 8, 9, and 10, but all were located >or=16
base pairs from the splice site, and are thus unlikely to be deleterious
mutations. CONCLUSIONS: Germline mutations in the p73 gene are unlikely
to be critical for inherited susceptibility to PC in this specified
subset of families. Copyright 2001 Wiley-Liss, Inc.
10
UI - 21439131
AU - Calogero A; Arcella A; De Gregorio G; Porcellini A; Mercola D; Liu C;
TI -
Lombari V; Zani M; Giannini G; Gagliardi FM; Caruso R; Gulino A; Frati
L; Ragona G
The early growth response gene EGR-1 behaves as a suppressor gene that
is down-regulated independent of ARF/Mdm2 but not p53 alterations in
fresh human gliomas.
SO - Clin Cancer Res 2001 Sep;7(9):2788-96
AD - Department of Molecular Pathology, Istituto di Ricovero e Cura a
Carattere Scientifico Neuromed, Pozzilli, 86077 Italy.
calognant@neuromed.it
PURPOSE: EGR-1 is an immediate early gene with diverse functions that
include the suppression of growth. EGR-1 is down-regulated many cancer
cell types, suggesting a tumor suppressor role, and may critically
involve the p53 pathway. The aim of this work was to measure the
expression of EGR-1 and the p16/INK4a/ARF-Mdm2-p53 pathway status in
fresh human gliomas. EXPERIMENTAL DESIGN: Thirty-one human gliomas with
different grades of malignancy were investigated for Egr-1 mRNA and the
protein expression, frequency, and spectrum of p53 gene mutations, mdm2
gene amplification, and p16/INK4a/ARF allele loss. RESULTS: The
amplification of Mdm2 and the deletion of the p16/INK4a gene was found
in 3 and 5 cases, respectively, whereas mutations of p53, including two
novel mutations, were observed in 10 other cases. The three types of
changes occurred strictly mutually exclusively, emphasizing that these
genes operate in a common pathway critical to glioma progression. EGR-1
mRNA was significantly down-regulated in astrocytomas (14.7 +/- 5.1%)
and in glioblastomas (33.6 +/- 10.0%) versus normal brain. Overall,
EGR-1 mRNA was strongly suppressed (average, 15.2 +/- 13.9%) in 27 of 31
cases (87%), independent of changes in p16/INK4a/ARF and Mdm2; whereas 4
of 31 cases with residual EGR-1 expression as well as the highest EGR-1
variance segregated with p53 mutations. Immunohistochemical analyses
confirmed the suppression of EGR-1 protein. CONCLUSIONS: These results
indicate that EGR-1 is commonly suppressed in gliomas independent of
p16/INK4a/ARF and Mdm2 and that suppression is less crucial in tumors
bearing p53 mutations, and these results implicate an EGR-1 growth
regulatory mechanism as a target of inactivation during tumor
progression.
11
UI - 21449534
AU - Couldwell WT; Yong VW
TI -
Glioma invasion.
SO - J Neurosurg 2001 Sep;95(3):379-80
12
UI - 21449546
AU - Duggal N; Iskander S; Hammond RR
TI -
Nestin expression in cortical dysplasia.
SO - J Neurosurg 2001 Sep;95(3):459-65
AD - Department of Clinical Neurological Sciences, London Health Sciences
Centre and The University of Western Ontario, Canada.
OBJECT: It is recognized that cortical dysplasia (CD) is associated with
an increased incidence of glioneuronal neoplasms. Among hypothetical
considerations, there is the possibility that CD and other neuronal
migration abnormalities harbor dysmature cells with the potential to
give rise to glioneuronal neoplasms. Such cells, if present, would be
reasonably expected to display immature features. The goal of the
present study was to characterize the expression of nestin, a
neuroepithelial precursor/stem cell antigen, in CD, along with other
pathological and clinical features of this entity. METHODS: Clinical and
surgical features of 10 recent cases meeting the histological criteria
for CD were reviewed. Expressions of nestin, MAP2, neurofilament, and
glial fibrillary acidic protein (GFAP) were assessed using
immunohistochemical analysis and confocal scanning laser microscopy.
Immunoreactivity for both glial and neuronal antigens as well as nestin
was found in a select group of cells within regions of CD.
Immunohistochemical and confocal microscopic findings demonstrated that
these cells with neuronal or ambiguous features are a mixed population,
some of which are dysmature neurons (positive for nestin and MAP2),
whereas others are astrocytic (positive for nestin and GFAP).
CONCLUSIONS: Further insight into the nature of nestin-positive neurons
may shed light on the cause and pathogenesis of the associated
glioneuronal tumors and the accompanying chronic seizures.
13
UI - 21449549
AU - Kubiatowski T; Jang T; Lachyankar MB; Salmonsen R; Nabi RR; Quesenberry
TI -
PJ; Litofsky NS; Ross AH; Recht LD
Association of increased phosphatidylinositol 3-kinase signaling with
increased invasiveness and gelatinase activity in malignant gliomas.
SO - J Neurosurg 2001 Sep;95(3):480-8
AD - Department of Surgery, University of Massachusetts Medical Center,
Worcester 01655, USA.
OBJECT: Glioblastoma multiforme is the most malignant of the primary
brain tumors and aggressively infiltrates surrounding brain tissue,
resulting in distant foci within the central nervous system, thereby
rendering this tumor surgically incurable. The recent findings that both
phosphatidylinositol 3-kinase (PI 3-K) and the phosphatase and tensin
homolog (PTEN) regulate tumor cell invasiveness have led the authors to
surmise that these lipid signaling molecules might play a role in
regulating matrix metalloproteinases (MMPs), which are essential for
tumor cell invasion. METHODS: Using the C6 glioma cell line, which does
not express measurable amounts of PTEN protein and in which in vitro
invasiveness is MMP dependent, the authors determined that in vitro
glioma cell invasiveness was significantly reduced when cells were
preincubated overnight with LY294002 or wortmannin, two specific
inhibitors of PI 3-K signaling. Next, using gelatin zymography, it was
noted that these compounds significantly inhibited MMP-2 and MMP-9
activities. Moreover, the decrease in MMP activity correlated with the
decrease in PI 3-K activity, as assessed by Akt phosphorylation.
Finally, using semiquantitative reverse transcriptase-polymerase chain
reaction, the authors demonstrated that LY294002 decreased messenger
(m)RNA levels for both MMPs. Thus, these in vitro data indicate that PI
3-K signaling modulates gelatinase activity at the level of mRNA. Using
immunostaining of phosphorylated Akt (p-Akt) as a measure of PI 3-K
activity, the authors next assessed rat brains implanted with C6 cells.
Compared with surrounding brain, there was marked p-Akt staining in C6
glioma cells and in neurons immediately adjacent to the tumor, but not
in normal brain. The p-Akt staining in tumors was especially intense in
perivascular areas. Using double-labeling techniques, colocalization of
p-Akt with MMP-2 and MMP-9 was also noted in perivascular tumor areas.
CONCLUSIONS: The increase in p-Akt staining within these PTEN-deficient
gliomas is consistent with what would be predicted from unchecked PI 3-K
signaling. Furthermore, the immunohistochemically detected
colocalization of p-Akt and MMP-2 and MMP-9 supports the authors' in
vitro studies and the proposed linkage between PI 3-K signaling and MMP
activity in gliomas.
14
UI - 21455949
AU - Aldrich TE; Andrews KW; Liboff AR
TI -
Brain cancer risk and electromagnetic fields (EMFs): assessing the
geomagnetic component.
SO - Arch Environ Health 2001 Jul-Aug;56(4):314-9
AD - Merck Medco Managed Care Franklin, New Jersey, USA.
Cancer cluster studies in North Carolina identified several communities
in which there existed an elevated risk of brain cancer. These findings
prompted a series of case-control studies. The current article, which
originated from the results of the 3rd of such studies, is focused on
inclusion of the earth's own geomagnetic fields that interact with
electromagnetic fields generated from distribution power lines. This
article also contains an assessment of the contribution of confounding
by residential (e.g., urban, rural) and case characteristics (e.g., age,
race, gender). Newly diagnosed brain cancer cases were identified for a
4-county region of central North Carolina, which the authors chose on
the basis of the results of earlier observations. A 3:1 matched series
of cancer cases from the same hospitals in which the cases were
diagnosed served as the comparison group. Extensive geographic
information was collected and was based on an exact place of residence
at the time of cancer diagnosis, thus providing several strategic
geophysical elements for assessment. The model for this assessment was
based on the effects of these two sources of electromagnetic fields for
an ion cyclotron resonance mechanism of disease risk. The authors used
logistic regression models that contained the predicted value for the
parallel component of the earth's magnetic field; these models were
somewhat erratic, and the elements were not merged productively into a
single statistical model. Interpretation of these values was difficult;
therefore, the modeled values for the model elements, at progressive
distances from the nearest power-line segments, are provided. The
results of this study demonstrate the merits of using large,
population-based databases, as well as using rigorous Geographic
Information System techniques, for the assessment of ecologic
environmental risks. The results also suggest promise for exposure
classification that is compatible with the theoretical biological
mechanisms posited for electromagnetic fields.
15
UI - 21423018
AU - Gilbertson R; Wickramasinghe C; Hernan R; Balaji V; Hunt D;
TI -
Jones-Wallace D; Crolla J; Perry R; Lunec J; Pearson A; Ellison D
Clinical and molecular stratification of disease risk in
medulloblastoma.
SO - Br J Cancer 2001 Sep 1;85(5):705-12
AD - Dept. Developmental Neurobiology, St Jude Children's Research Hospital,
Room 2006G, 332 North Lauderdale St, Memphis, TN 38105, USA.
The accurate assessment of disease risk among children with
medulloblastoma remains a major challenge to the field of paediatric
neuro-oncology. In the current study we investigated the capacity of
molecular abnormalities to increase the accuracy of disease risk
stratification above that afforded by clinical staging alone. 41 primary
medulloblastoma tumour samples were analysed for ErbB2 receptor
expression using immunohistochemistry, and for aberrations of chromosome
17 and amplification of the MYC oncogene using fluorescence in situ
hybridisation. The ErbB2 receptor and deletion of 17p were detected in
80% and 49% of tumours, respectively. 17p loss occurred either in
isolation (20%), or in association with gain of 17q (29%), compatible
with an isochromosome of 17q. Amplification of MYC was detected in only
2 tumours. Significant prognostic factors included, 'metastatic disease'
(P = 0.0006), 'sub-total tumour resection' (P = 0.007), 'high ErbB2
receptor expression' (P = 0.003) and 'isolated 17p loss' (P = 0.003).
Combined analysis of clinical and molecular factors enabled greater
resolution of disease risk than clinical factors alone, identifying a
sub-population of patients with particularly favourable disease outcome.
These data support the hypothesis that a combination of clinical and
molecular factors may afford a more reliable means of assigning disease
risk in patients with medulloblastoma, thereby providing a more accurate
basis for targeting therapy in children with this disease. Copyright
2001 Cancer Research Campaign.
16
UI - 21160442
AU - Corrias MV; Occhino M; Croce M; De Ambrosis A; Pistillo MP; Bocca P;
TI -
Pistoia V; Ferrini S
Lack of HLA-class I antigens in human neuroblastoma cells: analysis of
its relationship to TAP and tapasin expression.
SO - Tissue Antigens 2001 Feb;57(2):110-7
AD - Laboratorio di Oncologia, Istituto Scientifico G. Gaslini, Genoa, Italy.
We studied the constitutive and the interferon (IFN)-gamma-induced
expression of HLA class I antigen heavy chain, beta2-microglobulin
(beta2m), TAP-1, TAP-2 and tapasin in a panel of eleven neuroblastoma
cell lines. Surface expression of HLA class I antigens was low in eight
out of eight neuroblastoma cell lines bearing MYC-N amplification and/or
1p deletion, while two out of three neuroblastoma cell lines lacking
these genetic alterations showed normal expression. IFN-gamma treatment
restored HLA class I antigen surface expression in all neuroblastoma
cell lines. Eight out of 11 neuroblastoma cell lines did not express
TAP-1 mRNA and three of them also lacked TAP-2 mRNA. beta2 m mRNA was
barely detectable or absent in five neuroblastoma cell lines, while
tapasin mRNA was always expressed. IFN-gamma upregulated the expression
of HLA class I heavy chain, beta2 m, TAP-1, TAP-2 and tapasin, as
detected at mRNA or protein level. Post-transcriptional events were
involved in altered TAP-1 and beta2 m expression in one peculiar
neuroblastoma cell line. These data indicate that multiple mechanisms
play a role in the HLA class I antigen-deficient phenotype of human
neuroblastoma.
17
UI - 21277034
AU - Anderson RC; Elder JB; Parsa AT; Issacson SR; Sisti MB
TI -
Radiosurgery for the treatment of recurrent central neurocytomas.
SO - Neurosurgery 2001 Jun;48(6):1231-7; discussion 1237-8
AD - Department of Neurosurgery, New York Presbyterian Medical Center, New
York, USA.
OBJECTIVE: Central neurocytomas are benign neoplasms with neuronal
differentiation typically located in the lateral ventricles of young
adults. Although the treatment of choice is complete surgical excision,
patients may experience local recurrence. Adjuvant therapy for patients
with residual or recurrent tumor has included reoperation, radiotherapy,
or chemotherapy. To avoid the side effects of conventional radiotherapy
in young patients, we present a series of patients with clear evidence
of tumor progression who were treated with gamma knife radiosurgery.
METHODS: Four patients (ages 20-49 yr; mean, 28 yr) who presented with
an intraventricular mass on magnetic resonance imaging scans and
underwent craniotomy for tumor resection were reviewed retrospectively.
Histopathological analysis confirmed central neurocytoma in all cases.
Each patient was followed up clinically and radiographically with serial
magnetic resonance imaging. When radiographic signs of tumor progression
were evident, patients were treated with radiosurgery. RESULTS: Complete
radiographic tumor resection was achieved in all patients. There were no
major postoperative complications. Local tumor progression was detected
on magnetic resonance imaging scans 9 to 25 months after surgery
(median, 17.5 mo). All patients achieved complete response to
radiosurgery with reduction in tumor size. There have been no
complications from radiosurgery. Follow-up ranged from 12 to 28 months
(mean, 16.5 mo) after radiosurgery, and from 24 to 84 months (mean, 54.5
mo) after initial presentation. CONCLUSION: Radiosurgery with the gamma
knife unit provides safe and effective adjuvant therapy after surgical
resection of central neurocytomas. Radiosurgery may eliminate the need
for reoperation and avoid the possible long-term side effects from
conventional radiotherapy in young patients.
18
UI - 21277036
AU - Pirouzmand F; Tator CH; Rutka J
TI -
Management of hydrocephalus associated with vestibular schwannoma and
other cerebellopontine angle tumors.
SO - Neurosurgery 2001 Jun;48(6):1246-53; discussion 1253-4
AD - Division of Neurosurgery, Toronto Western Hospital, Ontario, Canada.
OBJECTIVE: Hydrocephalus (HCP) resulting from cerebellopontine angle
(CPA) tumors is not rare. This retrospective study was designed to
investigate the incidence of HCP and the clinical presentations,
management options, and outcomes of HCP in 284 patients with CPA tumors.
METHODS: A retrospective study of 284 consecutive patients with CPA
tumors (mostly vestibular schwannomas) treated from 1985 to 1996 at
Toronto Western Hospital managed by one surgical team consisting of a
neurosurgeon and a neuro-otologist. RESULTS: Thirty-nine patients
(13.7%) had radiographic and/or clinical evidence of HCP, 37
preoperatively and 2 postoperatively. Tumor type distribution was 33
vestibular schwannomas, 5 meningiomas, and 1 cavernous hemangioma. Only
five patients (12%) had obvious obstruction at the fourth ventricular
level. In 36 patients (92%), symptoms were mostly chronic and mild,
consistent with normal pressure hydrocephalus. Multivariate analysis
confirmed the strong association of tumor size and incidence of HCP (P <
.0001). Four patients underwent permanent shunting before microsurgical
tumor excision, mainly because of florid symptoms of HCP. Microsurgical
tumor excision without preoperative shunting was performed in 23
patients, 5 of whom required postoperative shunting in the first 2
months after tumor excision. Eighteen patients (78%) did not need shunts
after tumor resection. With regard to tumor size, the postoperatively
shunted group did not differ from the patients who had surgery but did
not require shunt treatment (P < 0.50). The remaining 10 patients with
preoperative HCP received shunts as the only treatment (3 patients),
stereotactic radiosurgery (3 patients), or expectant management (4
patients). Two other patients without preoperative HCP developed
postoperative HCP and required shunts. Postoperatively, we observed a
significant (P < 0.001) increase in the incidence of pseudomeningocele
and a nonsignificant (P < 0.1) increase in cerebrospinal fluid leaks
(rhinorrhea and/or otorrhea) in patients without shunts as compared with
postoperative patients without HCP. The patients were followed after any
treatment for a mean of 3.2 years (range, 6 mo-10 yr). Follow-up in the
patients who had surgery but did not require a shunt revealed a 61%
decrease in clinical symptoms related to HCP and a 75% decrease in
radiographic signs of HCP. CONCLUSION: In the presence of HCP, operative
resection of CPA tumors can be performed without permanent cerebrospinal
fluid shunting. Precautionary measures to decrease the incidence of
postoperative complications related to cerebrospinal fluid leak in
patients with preoperative HCP include meticulous obliteration of any
exposed air cells, including those around the internal auditory canal,
accurate restoration of the dural barrier, and temporary lowering of
intracranial pressure with a ventricular or lumbar drain. Patients with
persistent symptomatic HCP after tumor excision should be treated with a
ventriculoperitoneal shunt. Delaying this decision until the
postoperative period is safe and avoids unnecessary shunting in the
majority of patients.
19
UI - 21279720
AU - Kaup B; Schindler I; Knupfer H; Schlenzka A; Preiss R; Knupfer MM
TI -
Time-dependent inhibition of glioblastoma cell proliferation by
dexamethasone.
SO - J Neurooncol 2001 Jan;51(2):105-10
AD - University of Leipzig, Childrens' Hospital, Germany.
Because of the outstanding importance of the glucocorticoid
Dexamethasone (DEX) as supportive therapy in the management of brain
tumours, the direct effect of DEX on tumour cell proliferation is of
particular interest. Previous in vitro studies led to contradictory
results. To characterise more precisely the influence of DEX, we
investigated the glioblastoma multiforme (GM) cell lines A172, T98G and
86HG39. Cells were treated with DEX concentrations ranging from 5 x
10(-9) to 5 x 10(-5) M from 24 to 240h under different treatment
conditions. Influence of DEX on glioma cell viability was assessed daily
for 5 days by MTT-assay: (I) with continuous DEX incubation (acute
treatment), (II) in a recultivation period without DEX after 5 days of
DEX pre-incubation (pre-treatment), (III) with continuous DEX incubation
after 5 days of DEX pre-incubation (combination treatment). DEX acute
treatment led to strongly decreased proliferation of A172 cells, whereas
T98G and 86HG39 cells remained uninfluenced. In opposite, a time-delayed
inhibition of cell proliferation was observed in all three cell lines
after DEX pre-treatment. Combination treatment induced a significant
increase of the inhibitory effect in A172 and T98G cells. These data
show a variable, partial time-dependent inhibitory effect of DEX on the
proliferation of GM cells and may open new treatment strategies for
malignant brain tumours.
20
UI - 21279719
AU - Guyotat J; Champier J; Pierre GS; Jouvet A; Bret P; Brisson C; Belin MF;
TI -
Signorelli F; Montange MF
Differential expression of somatostatin receptors in medulloblastoma.
SO - J Neurooncol 2001 Jan;51(2):93-103
AD - Service de Neurochirurgie B, Hjpital Neurologique et Neurochirurgical
Pierre Wertheimer, Lyon, France.
OBJECT: Somatostatin receptors have been found on a variety of tumours
like neuroendocrine breast or brain tumours. Their detection opens new
diagnostic and therapeutic paths. The aim of this work was to
investigate their expression in medulloblastomas. METHODS: Using both
techniques, reverse transcriptase-polymerase chain reaction and
immunohistochemistry, we analysed mRNA of different subtypes of
somatostatin receptors in 15 medulloblastomas and the localisation of
the subtype SSTR2 receptor at the cellular level in 13 medulloblastomas.
All five subtypes mRNA were variably expressed in each medulloblastoma.
The signal obtained after Southern blotting for SSTR2 receptor
amplification was the highest as compared to the signal obtained for the
other receptor subtypes. Immunostaining for SSTR2A receptor was present
in every tumour specimen and was specifically located to the cellular
membrane of neoplastic cells. No staining was identified at the level of
peritumoral veins. CONCLUSION: The evidence of predominant expression of
SSTR2 receptors in medulloblastomas opens interesting prospects for
their diagnosis and therapy.
21
UI - 21369701
AU - Ward S; Harding B; Wilkins P; Harkness W; Hayward R; Darling JL; Thomas
TI -
DG; Warr T
Gain of 1q and loss of 22 are the most common changes detected by
comparative genomic hybridisation in paediatric ependymoma.
SO - Genes Chromosomes Cancer 2001 Sep;32(1):59-66
AD - University Department of Neurosurgery, Institute of Neurology,
University College London, National Hospital for Neurology and
Neurosurgery, London, United Kingdom.
Ependymomas are the third most common brain tumour in the paediatric
population. Although cytogenetic and molecular analyses have pinpointed
deletions of chromosomes 6q, 17, and 22 in a subset of tumours,
definitive patterns of genetic aberrations have not been determined. In
the present study, we analysed 40 ependymomas from paediatric patients
for genomic loss or gain using comparative genomic hybridisation (CGH).
Eighteen of the tumours (45%) had no detectable regions of imbalance. In
the remaining cases, the most common copy number aberrations were loss
of 22 (25% of tumours) and gain of 1q (20%). Three regions of high copy
number amplification were noted at 1q24-31 (three cases), 8q21-23 (two
cases), and 9p (one case). Although there was no association with the
loss or gain of any chromosome arm or with benign versus anaplastic
histologic characteristics, the incidence of gain of 7q and 9p and loss
of 17 and 22 was significantly higher in recurrent versus primary
tumours. This study has identified a number of chromosomal regions that
may contain candidate genes involved in the development of different
subgroups of ependymoma. Copyright 2001 Wiley-Liss, Inc.
22
UI - 21395383
AU - Hlavats'kyi OIa
TI -
[Application of ultrasonic aspiration in surgical treatment of glial
tumors]
SO - Klin Khir 2001;(5):44-6
Results of surgical treatment of 139 patients with cerebral glioma of
supratentorial localization were analyzed. The method of ultrasonic
aspiration of tumor was applied for the surgical intervention radicalism
raising. Application of ultrasonic aspiration had guaranteed the
conditions for the controlled excision of tumoral tissue, the hemostasis
performance, permitted to reduce cerebral traumatization and to preserve
main vessels in the tumor environment, promoted the uncomplicated
postoperative period course, rapid reconvalescence of the patients, the
neurologic functions preservation, reduction of the patient's
invalidization possibility, improvement of his quality of life.
23
UI - 21411325
AU - Karpinski NC; Min KW; Bauserman SC; Cancer Committee, College of
TI -
American Pathologists
Protocol for the examination of specimens from patients with tumors of
the brain/spinal cord: a basis for checklists.
SO - Arch Pathol Lab Med 2001 Sep;125(9):1162-8
AD - Department of Pathology, University of California-San Diego Medical
Center, USA.
24
UI - 21435016
AU - Betlejewski S; Janicka-Beuth L; Beuth W
TI -
Rhinospirography in evaluation of respiratory disorders in patients with
central nervous system tumors.
SO - Med Sci Monit 2000 Jan-Feb;6(1):81-3
AD - Department of Otolaryngology, Medical University, ul. M.
Curie-Sklodowskiej 9, 85-094 Bydgoszcz, Poland.
The aim of the study was to define respiratory disorders caused by
central nervous system tumors. We investigated 51 patients (31 men, 20
women, mean age 58). They were divided into the following groups:
patients with supra-, infratentorial and cranio-vertebral junction
lesions. We analyzed: the localization of tumors based on CT and MRI
examinations and intraoperative observation, the status of consciousness
by GCS scale, neurological status and histological findings. For the
estimation of dynamics of the respiratory changes, rhinospirography
examination was repeated several times in the course of observation. The
alterations of respiration were clearly visible in many cases. We have
confirmed that respiratory disorders found by rhinospirography provide a
source of important clinical information on the effect of the treatment
and prognosis. We have also confirmed that changes in respiration are
observed earlier than changes of consciousness.
25
UI - 21441833
AU - Burger PC; Minn AY; Smith JS; Borell TJ; Jedlicka AE; Huntley BK;
TI -
Goldthwaite PT; Jenkins RB; Feuerstein BG
Losses of chromosomal arms 1p and 19q in the diagnosis of
oligodendroglioma. A study of paraffin-embedded sections.
SO - Mod Pathol 2001 Sep;14(9):842-53
AD - The Department of Pathology, Johns Hopkins University School of
Medicine, Baltimore, Maryland 21287, USA. pburger@jhmi.edu
Comparative genomic hybridization (CGH), fluorescence in situ
hybridization (FISH), polymerase chain reaction-based microsatellite
analysis, and p53 sequencing were performed in paraffin-embedded
material from 18 oligodendrogliomas and histologically similar
astrocytomas. The study was undertaken because of evidence that
concurrent loss of both the 1p and 19q chromosome arms is a specific
marker for oligodendrogliomas. Of the six lesions with a review
diagnosis of oligodendroglioma, all had the predicted loss of 1p and 19q
seen by CGH, FISH, and polymerase chain reaction. Other lesions,
including some considered oligodendroglioma or mixed glioma by the
submitting institution, did not. There were no p53 mutations in any of
the six oligodendrogliomas, whereas 5 of the 10 remaining, successfully
studied cases did have p53 mutations. The results suggest that CGH and
FISH performed on current or archival tissue can aid in classification
of infiltrating gliomas such as oligodendrogliomas and astrocytomas. The
results of the p53 studies are consistent with findings of previous
investigations that such mutations are less common in oligodendrogliomas
than they are in astrocytomas.
26
UI - 21443281
AU - Zlatescu MC; TehraniYazdi A; Sasaki H; Megyesi JF; Betensky RA; Louis
Cancer Types
Bone Cancer
Brain Tumors
Breast Cancer
Carcinoid Tumors
Endocrine System Cancers
Gastrointestinal Cancers
Gynecologic Cancers
Head and Neck Cancers
Leukemia
Lung Cancers
Lymphomas
Myelomas
Pediatric Cancers
Penile Cancer
Prostate Cancer
Sarcomas
Skin Cancers
Testicular Cancer
Thyroid Cancer
Urinary Tract Cancers
OncoLink Vet
Cancer Treatment
Biologic Therapy
Bone Marrow Transplants
Chemotherapy
Clinical Trials
Complementary Medicine
Gene Therapy
General Treatment Concerns
Hormone Therapy
PDT Center
Proton Therapy
Radiation Oncology
Surgical Oncology
Targeted Therapies
Vaccine Therapies
Cancer Support
Caregivers
Hospice Care and Bereavement
Nutrition and Cancer
Sexuality & Fertility
Side Effects
Support
Survivorship
Exercise and Cancer
Cancer Resources
Cancer News
OncoLink University
Nurses' Notes
Conferences
Newly Diagnosed Patients
Causes and Prevention
Legal and Financial Information for Patients
LGBT Resources
NCI Resources
Global Resources
Cancer Resource List
Resources for Young Adults
OncoLink Media Library
OncoLink TV
Book, Music and Video Reviews
Ask the Experts
Brown Bag Chat
Tracy's Corner
About OncoLink
About OncoLink
Giving to OncoLink
Contact Information
Usage Policy
Editorial Board
How to Partner with OncoLink
Link to OncoLink
Mission Statement
