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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Brain Tumor - January 2002
National Cancer Institute®
Last Modified: January 1, 2002
Table of Contents
1
UI - 10728683
AU - DiBiase SJ; Zeng ZC; Chen R; Hyslop T; Curran WJ Jr; Iliakis G
TI -
DNA-dependent protein kinase stimulates an independently active,
nonhomologous, end-joining apparatus.
SO - Cancer Res 2000 Mar 1;60(5):1245-53
AD - Department of Radiation Oncology, Kimmel Cancer Center, Philadelphia,
Pennsylvania 19107, USA.
Double-strand breaks (DSBs) can be efficiently removed from the DNA of
higher eukaryotes by nonhomologous end-joining (NHEJ). Genetic studies
implicate the DNA-dependent protein kinase (DNA-PK) in NHEJ, but the
exact function of this protein complex in the rejoining reaction remains
to be elucidated. We compared rejoining of DNA DSBs in a human glioma
cell line, M059-J, lacking the catalytic subunit of DNA-PK (DNA-PKcs),
and their isogenic but DNA-PK-proficient counterpart, M059-K. In both
cell lines, rejoining of DNA DSBs was biphasic, with a fast and a slow
component operating with a half-life of approximately 22 min and 12 h,
respectively. Deficiency in DNA-PK activity did not alter the half-times
of either of these components of rejoining but increased from 17 to 72%
the proportion of DNA DSB rejoining with slow kinetics. DNA DSB
rejoining was nearly complete in both cell lines, and there was only a
small increase in the number of unrejoined breaks in M059-J as compared
with M059-K cells after 30 h of incubation. Wortmannin radiosensitized
to killing M059-K cells and strongly inhibited DNA DSB rejoining.
Wortmannin did not affect the radiosensitivity to killing and produced
only a modest inhibition in DNA DSB rejoining in M059-J cells,
suggesting that, for these end points, DNA-PK is the principal target of
the drug. These observations demonstrate that DNA-PK deficiency
profoundly decreases the proportion of DNA DSB rejoining with fast
kinetics but has only a small effect on the fraction remaining
unrejoined. We propose that in higher eukaryotes, an evolutionarily
conserved, independently active, but inherently slow NHEJ pathway is
stimulated 30-fold by DNA-PKcs to rapidly remove DNA DSBs from the
genome. The stimulation is expected to be of local nature and the
presence of DNA-PKcs in the vicinity of the DNA DSB determines whether
rejoining will follow fast or slow kinetics. Structural and regulatory
functions of DNA-PKcs may mediate this impressive acceleration of DNA
DSB rejoining, and regions of chromatin within a certain range from this
large protein may benefit from these activities. We propose the term
DNA-PK surveillance domains to describe these regions.
2
UI - 11104448
AU - Hardell L; Nasman A; Pahlson A; Hallquist A
TI -
Case-control study on radiology work, medical x-ray investigations, and
use of cellular telephones as risk factors for brain tumors.
SO - MedGenMed 2000 May 4;():E2
AD - Orebro Medical Center, Department of Oncology, Orebro, Sweden.
lennart.hardell@orebroll.se
CONTEXT: Ionizing radiation is a well-established risk factor for brain
tumors. During recent years, microwave exposure from the use of cellular
telephones has been discussed as a potential risk factor. OBJECTIVE: To
determine risk factors for brain tumors. DESIGN: A case-control study,
with exposure assessed by questionnaires. PARTICIPANTS: A total of 233
currently living men and women, aged 20 to 80 years, were included. The
case patients had histopathologically verified brain tumors and lived in
the Uppsala-Orebro region (1994-1996) or the Stockholm region
(1995-1996). Two matched controls to each case were selected from the
Swedish Population Register. MAIN OUTCOME MEASURES: Ionizing radiation
and use of cellular telephones as risk factors for brain tumors.
RESULTS: A total of 209 cases (90%) and 425 controls (91%) answered the
questionnaire. Work as a physician yielded an odds ratio (OR) of 6.00,
with a 95% confidence interval (CI) of 0.62 to 57.7. All three case
patients had worked with fluoroscopy. Radiotherapy of the head and neck
region yielded an OR of 3.61 (95% CI, 0.65-19.9). Medical diagnostic
x-ray examination of the same area yielded an OR of 2.10 (95% CI,
1.25-3.53), with a tumor induction period of 5 years or more. Chemical
industry work yielded an OR of 4.10 (95% CI, 1.25-13.4), and laboratory
work yielded an OR of 3.21 (95% CI, 1.16-8.85). Ipsilateral use of
cellular telephones increased the risk for tumors in the temporal,
temporoparietal, and occipital lobes (OR, 2.42; 95% CI, 0.97-6.05), ie,
the anatomic areas with highest exposure to microwaves from a mobile
telephone. The result was further strengthened (OR, 2.62; 95% CI,
1.02-6.71) in a multivariate analysis that included laboratory work and
medical diagnostic x-ray investigations of the head and neck.
CONCLUSION: Exposure to ionizing radiation, work in laboratories, and
work in the chemical industry increased the risk of brain tumors. Use of
a cellular telephone was associated with an increased risk in the
anatomic area with highest exposure.
3
UI - 11104486
AU - Carlo GL; Jenrow RS
TI -
Scientific progress - wireless phones and brain cancer: current state of
the science.
SO - MedGenMed 2000 Jul 11;():E40
AD - Wireless Technology Research, Washington, DC, USA.
CONTEXT: The current science is not definitive about health risks from
wireless phones; however, the legitimate questions about safety that
have arisen from recent studies make claims of absolute safety no longer
supportable. OBJECTIVE: The objective of this paper is to outline for
primary care providers the results of the most current research on the
possible impact of wireless phone use on human health. Presented are
study results from Wireless Technology Research (WTR) program, the
7-year, $27 million effort funded by the wireless industry in the United
States, that represents the world's most comprehensive research effort
addressing this issue to date. Science-based recommendations for
consumer interventions and future research are presented. DATA SOURCES:
Original studies performed under the WTR program as well as other
relevant research from around the world. STUDY SELECTION: This article
presents a synopsis of the peer-reviewed in vitro and in vivo laboratory
research, and the peer-reviewed epidemiology studies supported by the
WTR, as well as a summary of other relevant work. DATA EXTRACTION: Only
peer-reviewed scientific studies are presented, primarily WTR-sponsored
research. In addition, results of the WTR literature surveillance
program, which identified other relevant toxicology and epidemiology
studies on an ongoing basis, are presented. These studies are presented
in the context of their usefulness in providing intervention
recommendations for consumers. DATA SYNTHESIS: Following a qualitative
synthesis of specific relevant non-WTR research and a critical
assessment of the WTR results, the following represents the current
state of scientific understanding relevant to the public health impact
of wireless phones: laboratory studies appear to have confirmed that
radio frequency radiation from wireless phone antennas is insufficient
to cause DNA breakage; however, this same radiation appears to cause
genetic damage in human blood as measured through the formation of
micronuclei. An increase in the rate of brain cancer mortality among
hand-held cellular phone users as compared to car phone users, though
not statistically significant, was observed in the WTR cohort study. A
statistically significant increase in the risk of neuro-epithelial brain
tumors was observed among cellular phone users in another case-control
study. CONCLUSIONS: As new data emerge, our understanding of this
complex problem will improve; however, at present there is a critical
need for ongoing and open evaluation of the public health impact of new
science, and communication of this science and derivative intervention
options to those who are potentially affected.
4
UI - 11148570
AU - Mena H; Morrison AL; Jones RV; Gyure KA
TI -
Central neurocytomas express photoreceptor differentiation.
SO - Cancer 2001 Jan 1;91(1):136-43
AD - Department of Neuropathology, Armed Forces Institute of Pathology,
Washington, DC 20306-6000, USA.
BACKGROUND: Central neurocytomas are composed of mature neuronal
elements, frequently arranged in rosettes similar to those present in
pineocytomas. This suggests the possibility of similar patterns of
differentiation, including photoreceptor differentiation. The authors
analyzed the immunoreactivity of central neurocytomas for retinal
S-antigen, neuronal, glial, and neuroendocrine markers. METHODS:
Thirty-three central neurocytomas were analyzed with reference to their
clinicopathologic characteristics, immunoreactivity, and the possibility
that anaplastic histologic features correlated with aggressive clinical
behavior. RESULTS: There were 18 male and 15 female patients. The median
age at diagnosis was 30 years (range, 3-69 years). All of the tumors
with specified location were related to the ventricles. Thirty-two
tumors were diagnosed at surgery and 1 at autopsy. Histologic features
included mineralization (20 of 33), foci of necrosis (4 of 33), chronic
inflammation (4 of 33), ganglion cell differentiation (1 of 33), and
lipomatous differentiation (1 of 33). None of the lesions had
significant nuclear pleomorphism, mitotic activity, or vascular
endothelial proliferation. Immunohistochemistry included expression of
synaptophysin (33 of 33), neuron specific enolase (31 of 33), S-100
protein (25 of 33), retinal S-antigen (14 of 24), somatostatin (8 of
27), glial fibrillary acidic protein (4 of 33), neurofilament protein (3
of 22), and leucine enkephalin (1 of 27). At follow-up, 15 of 23
patients were alive an average of 8.1 years (range, 0.91-35.9 years)
after surgery. CONCLUSIONS: Central neurocytomas behave as slowly
growing neoplasms that remain confined within one or several
supratentorial ventricles and are associated with long survival after
surgical excision. Malignant forms with aggressive clinical behavior
were not found. The neoplastic cells can express photoreceptor
differentiation possibly relating central neurocytomas to pineocytomas.
Adipocyte differentiation may be present, and the possibility of a
relation between the central neurocytoma and cerebellar liponeurocytoma
should be entertained.
5
UI - 11332080
AU - Nafe R; Glienke W; Schlote W; Schneider B
TI -
EGFR gene amplification in glioblastomas. Is there a relationship with
morphology of tumor cell nuclei and proliferative activity?
SO - Anal Quant Cytol Histol 2001 Apr;23(2):135-43
AD - Edinger Institute for Neurology and Department of Urology, Clinics of
Johann Wolfgang Goethe University, Frankfurt am Main, Germany.
OBJECTIVE: To confirm a relationship between histomorphology of
glioblastomas and amplification of the gene for the epidermal growth
factor receptor (EGFR) as the most important molecular biologic
alteration in these tumors. STUDY DESIGN: In paraffin sections of
surgical specimens from 71 primary resected glioblastomas, tumor cell
nuclei in the region with the highest proliferative activity (Ki-67
immunostaining) were investigated morphometrically. Shape variables
(roundness factor, Fourier amplitudes) and nuclear area were measured.
Additionally, the numerical density of Ki-67-positive tumor cell nuclei
was estimated. Differential polymerase chain reaction (PCR) was
performed from paraffin sections of the same tumor area. The signals for
the EGFR gene and IFN gamma reference gene were quantified
densitometrically. RESULTS: Cases with distinct EGFR gene amplification
(EGFR/IFN ratios > 5) revealed significantly lower mean values for
several Fourier amplitudes, indicating a more regular nuclear shape when
compared with cases without evidence of EGFR gene amplification
(EGFR/IFN-ratios < or = 1). The Ki-67 index and nuclear area showed no
significant differences between these groups. Although a large variation
in nuclear morphology was observed for cases without evidence of EGFR
gene amplification, discriminant analysis based on morphometric
variables provided a good separation of these cases from cases with
distinct EGFR gene amplification, with a high percentage of
statistically correct reclassified cases. CONCLUSION: Our results
provide evidence of a relationship between genetic alterations and
histomorphology of glioblastomas.
6
UI - 11417411
AU - Szekessy DP; Stoltenburg-Didinger G
TI -
Differentiation, proliferation and apoptosis in primary and recurrent
primitive neuroectodermal tumors of childhood.
SO - Childs Nerv Syst 2001 May;17(6):320-7
AD - Department of Neuropathology, Free University Berlin, Hindenburgdamm 30,
12200 Berlin, Germany. dpszekessy@aol.com
Primitive neuroectodermal tumors (PNETs) of the CNS are a group of
embryonal tumors composed of small undifferentiated or poorly
differentiated cells. Infratentorially located PNETs are a synonym for
medulloblastomas. In this study 31 PNETs, including 5 recurrent tumors,
were examined. All children underwent neurosurgery and chemotherapy
according to the HIT and HIT-SKK protocols. The specimens were
investigated both for their expression of nine immunohistochemical
markers for neuronal, astrocytic, mesenchymal and epithelial
differentiation and for their proliferation. Results regarding cellular
differentiation were confirmed ultrastructurally. Apoptosis was detected
by labeling the 3'OH ends generated by DNA fragmentation and by electron
microscopy. Glial differentiation was shown to have a prognostic
relevance, with an elevated (twofold) risk of recurrence. Neuronal
differentiation also indicated a tendency to poor prognosis. Those
tumors that recurred later showed an increased proliferation rate (69%)
compared with nonrecurrent tumors (58%). Apoptosis was identified in all
tumors examined. The proportion of apoptotic cells could not be related
to the effect of therapy. These results indicate that cellular
differentiation may be a useful predicative factor for the prognosis of
cerebral PNETs.
7
UI - 11419622
AU - Latikka J; Kuurne T; Eskola H
TI -
Conductivity of living intracranial tissues.
SO - Phys Med Biol 2001 Jun;46(6):1611-6
AD - Ragnar Granit Institute, Tampere University of Technology, Finland.
juha.latikka@tut.fi
Resistivity values were measured from living human brain tissue in nine
patients. A monopolar needle electrode was used with a measurement
frequency of 50 kHz. Mean values were 3.51 Ohms m for grey matter and
3.91 Ohms m for white matter. Cerebrospiral fluid had a mean value of
0.80 Ohms m. Values for tumour tissues were dependent on the type of
tumour and ranged from 2.30 to 9.70 Ohms m.
8
UI - 11437285
AU - Zimmermann M; Seifert V; Trantakis C; Raabe A
TI -
Open MRI-guided microsurgery of intracranial tumours in or near eloquent
brain areas.
SO - Acta Neurochir (Wien) 2001;143(4):327-37
AD - Neurosurgical Clinic, Johann Wolfgang Goethe-University Frankfurt am
Main, Germany.
OBJECTIVES: Preservation of brain function while maximizing resection is
the main aim of brain tumour surgery. The purpose of this study was to
evaluate the efficacy of intra-operative magnetic resonance imaging to
preserve brain function in patients with tumours in or near eloquent
fifty-eight craniotomies for intracranial tumours or vascular
malformations have been performed at the University of Leipzig using a
0.5 T superconducting MR system "SIGNA SP" (General Electric Medical
Systems, USA). In 32 of these patients (15 male/17 female) with
intracranial tumours, located in or near eloquent brain areas
(sensorimotor cortex/speech center), 34 craniotomies were performed
using the image guidance of the interventional MRI. RESULTS: Using
intra-operative MRI criteria, complete tumour removal could be achieved
in 28 (82%) of 34 procedures. In 3 patients only subtotal tumour removal
was possible, because the residual tumour was not visible on the
intra-operative MR images, but could be identified on early diagnostic
follow-up MR-scans. In 3 patients, incomplete tumour resection was
performed in order to avoid neurological impairment. In these patients
intra-operative MR-images revealed residual tissue abnormalities
involving or encroaching on deep brain structures or motor/language
cortex. Pre-operative neurological status was unchanged in 24 patients
(70%), worsened in 4 patients (12%) and improved in 6 patients (18%).
CONCLUSIONS: Intra-operative MRI is helpful for navigation as well as to
demonstrate the tumour margins to achieve a complete and safe resection
of intracranial lesions located in or near eloquent brain areas. It
enables an image based functional monitoring of the brain which is
critical for motor, sensory or language function. Complications related
to the surgical procedure are reduced and the risk of neurological
deterioration due to tumour removal and postoperative complications is
minimized.
9
UI - 11444508
AU - Perry A
TI -
Oligodendroglial neoplasms: current concepts, misconceptions, and
folklore.
SO - Adv Anat Pathol 2001 Jul;8(4):183-99
AD - Washington University School of Medicine, St Louis, Missouri 63110-1093,
USA. aperry@pathology.wustl.edu
Given current prognostic and therapeutic implications, the accurate
classification and grading of oligodendroglial neoplasms has become
critical. However, the prevalence of morphologically ambiguous gliomas,
subjective histologic criteria, personal biases, oligodendroglioma
mimics, and the lack of specific oligodendroglioma markers has led to
high interobserver variability and created a contentious problem
encountered daily in active surgical neuropathology practices. Since
histologic assessment is still a powerful prognosticator, it
appropriately remains the diagnostic gold standard. However, recent
efforts have focused on identifying the most reproducible and clinically
relevant criteria, standardizing classification and grading schemes, and
searching for useful ancillary biologic and genetic markers capable of
further stratifying an otherwise heterogeneous patient population. This
paper reviews the morphologic and genetic spectrum of oligodendroglial
neoplasms, recent diagnostic and prognostic developments, and potential
future directions.
10
UI - 11451204
AU - Korshunov A; Golanov A
TI -
Pleomorphic xanthoastrocytomas: immunohistochemistry, grading and
clinico-pathologic correlations. An analysis of 34 cases from a single
Institute.
SO - J Neurooncol 2001 Mar;52(1):63-72
AD - Department of Neuropathology, Neurosurgical NN Burdenko Institute,
Moscow, Russia. akorshunov@nsi.ru
Pleomorphic xanthoastrocytomas (PXAs) are characterized as a
well-delineated tumor entity with clear peculiarities in
clinico-radiological picture, pathological appearance and biological
behavior. Usually the PXAs are associated with relatively good
prognosis. Nevertheless, up to 35% of patients die following one and
more recurrence with or without tumor malignant transformation. Till
now, there is no agreement on what histopathological features constitute
to objective and reliable signs of PXAs malignancy and clinical outcome.
Thirty-four PXAs were subdivided on three subsets: typical (Grade I) -
tumors without mitoses per 20 high power fields, proliferating (Grade
II) tumors with mitoses but without necroses, and malignant (Grade III)
- tumors with elevated mitotic index and necrotic foci. Also,
immunohistochemical investigation with various tumor-associated antigens
was performed. All PXAs subtypes showed differences in clinical
outcomes. There were no recurrences and death among the tumors Grade I.
Five out of 14 (36%) Grade II PXAs have recurred and one of them died.
All 5 patients with PXAs Grade III have rapidly recurred and four of
them died. Immunohistochemical variables, such as Ki-S1, p27/Kip1,
vascular endothelial growth factor expression, p53 immunoreactivity and
apoptotic index also exhibited significant differences among the three
PXAs grades. The progression-free survival was significantly reduced for
PXAs grade and presence of mitoses, whereas overall survival was reduced
for mitotic index >or= 3 and presence of necroses. No one from
immunohistochemical variables reached significant value. In summary, the
three-tiered PXAs subdivision proposed by us is carrying some element of
rationality but, undoubtedly, requires further prospective studies.
11
UI - 11465394
AU - Jukich PJ; McCarthy BJ; Surawicz TS; Freels S; Davis FG
TI -
Trends in incidence of primary brain tumors in the United States,
1985-1994.
SO - Neuro-oncol 2001 Jul;3(3):141-51
AD - Division of Epidemiology and Biostatistics, School of Public Health,
University of Illinois at Chicago, 60612, USA.
Brain tumor incidence has increased over the last 20 years in all age
groups, both overall and for specific histologies. Reasons attributed to
these increases include increase in lymphoma due to HIV/AIDS,
introduction of computed tomography/magnetic resonance imaging, and
changes in coding/classification. The purpose of this study was to
describe overall and histologic-specific incidence trends in a
population-based series of primary benign and malignant brain tumors.
Data from the Central Brain Tumor Registry of the United States from
1985 through 1994 were used to determine incidence trends in the broad
age groups 0-19, 20-64, and > or = 65 years, both overall and for
selected histologies. Poisson regression was used to express trends as
average annual percentage change. Overall, incidence increased modestly
(annual percentage change 0.9%, 95% confidence interval, 0.4, 1.4). When
lymphomas were excluded, this result was not statistically significant
(annual percentage change 0.5%, 95% confidence interval, -0.1, 1.1).
Specific histologies that were increasing were lymphomas in individuals
aged 20 to 64 years and in males aged 65 years or older, ependymomas in
the population aged 20 to 64 years, nerve sheath tumors in males, and
pituitary tumors in females. Increases that were not specific to any
population subgroup were seen for glioblastoma, oligodendrogliomas, and
astrocytomas, excluding not otherwise specified (NOS) tumors.
Corresponding decreases were noted for NOS, astrocytoma NOS, and glioma
NOS. Increasing incidence trends for lymphomas were consistent with
previous literature. Improvements in diagnostic technology in addition
to changes in classification and coding were likely to be responsible
for decreases seen in incidence of NOS subgroups and corresponding
increases in glioma subgroups. In contrast, the increases identified for
ependymomas, nerve sheath tumors, and pituitary tumors were less likely
to be artifacts of improvements in diagnosis, and they warrant further
study.
12
UI - 11465395
AU - Davis FG; Kupelian V; Freels S; McCarthy B; Surawicz T
TI -
Prevalence estimates for primary brain tumors in the United States by
behavior and major histology groups.
SO - Neuro-oncol 2001 Jul;3(3):152-8
AD - Division of Epidemiology and Biostatistics, School of Public Health,
University of Illinois at Chicago, 60612, USA.
Prevalence rates are used to supplement descriptions of disease and are
unavailable for all primary brain tumors in the United States. Data from
two population-based tumor registries were obtained from the Central
Brain Tumor Registry of the United States and used to compute
age-specific incidence rates (1985-1994) and survival curves for further
use in a statistical model to estimate prevalence rates. Prevalence
rates were then used to estimate the number of individuals living with a
brain tumor diagnosis in the U.S. population for the year 2000. The
overall incidence rate in these regions is 13.8 per 100,000 with 2-, 5-,
and 10-year survival rates of 58%, 49%, and 38%, respectively. The
prevalence rate for all primary brain tumors is 130.8 per 100,000 with
approximately 350,000 individuals estimated to be living with this
diagnosis in the United States in 2000. The prevalence rate for
malignant tumors, 29.5 per 100,000, is similar to previous reports. The
prevalence rate for benign tumors, 97.5 per 100,000, is new. Unlike
incidence data, the proportion (and expected number) of existing benign
tumors (75%, 267,000) is considerably greater than that for malignant
tumors (23%, 81,000), reflecting the better prognosis of benign tumors
diagnosed in individuals younger than 60 years old. These data
underscore the impact of primary brain tumors in the U.S. health care
system and emphasize the need for quality-of-life considerations,
particularly for those long-term survivors of benign tumors.
13
UI - 11465400
AU - Jackson RJ; Fuller GN; Abi-Said D; Lang FF; Gokaslan ZL; Shi WM;
TI -
Wildrick DM; Sawaya R
Limitations of stereotactic biopsy in the initial management of gliomas.
SO - Neuro-oncol 2001 Jul;3(3):193-200
AD - Department of Neurosurgery, The University of Texas M.D. Anderson Cancer
Center, Houston 77030, USA.
Stereotactic biopsy is often performed for diagnostic purposes before
treating patients whose imaging studies highly suggest glioma.
Indications cited for biopsy include diagnosis and/or the
"inoperability" of the tumor. This study questions the routine use of
stereotactic biopsy in the initial management of gliomas. At The
University of Texas M. D. Anderson Cancer Center, we retrospectively
reviewed a consecutive series of 81 patients whose imaging studies
suggested glioma and who underwent stereotactic biopsy followed by
craniotomy/resection (within 60 days) between 1993 and 1998. All
relevant clinical and imaging information was reviewed, including
computerized volumetric analysis of the tumors based on pre- and
postoperative MRI. Stereotactic biopsy was performed at institutions
other than M. D. Anderson in 78 (96%) of 81 patients. The majority of
tumors were located either in eloquent brain (36 of 81 = 44%) or
near-eloquent brain (41 of 81 = 51%), and this frequently was the
rationale cited for performing stereotactic biopsy. Gross total
resection (>95%) was achieved in 46 (57%) of 81 patients, with a median
extent of resection of 96% for this series. Diagnoses based on biopsy or
resection in the same patient differed in 40 (49%) of 82 cases. This
discrepancy was reduced to 30 (38%) of 80 cases when the biopsy slides
were reviewed preoperatively by each of three neuropathologists at M. D.
Anderson. Major neurologic complications occurred in 10 (12.3%) of 81
surgical patients and 3 (3.7%) of 81 patients undergoing biopsy.
Surgical morbidity was probably higher in our series than it would be
for glioma patients in general because our patients represent a highly
selected subset of glioma patients whose tumors present a technical
challenge to remove. Stereotactic biopsy is frequently inaccurate in
providing a correct diagnosis and is associated with additional risk and
cost. If stereotactic biopsy is performed, expert neuropathology
consultation should be sought.
14
UI - 11465401
AU - Visted T; Bjerkvig R; Enger PO
TI -
Cell encapsulation technology as a therapeutic strategy for CNS
malignancies.
SO - Neuro-oncol 2001 Jul;3(3):201-10
AD - Department of Anatomy and Cell Biology, University of Bergen, Norway.
Gene therapy using viral vectors has to date failed to reveal its
definitive clinical usefulness. Cell encapsulation technology represents
an alternative, nonviral approach for the delivery of biologically
active compounds to tumors. This strategy involves the use of
genetically engineered producer cells that secrete a protein with
therapeutic potential. The cells are encapsulated in an immunoisolating
material that makes them suitable for transplantation. The capsules, or
bioreactors, permit the release of recombinant proteins that may assert
their effects in the tumor microenvironment. During the last decades,
there has been significant progress in the development of encapsulation
technologies that comprise devices for both macro- and
microencapsulation. The polysaccharide alginate is the most commonly
used material for cell encapsulation and is well tolerated by various
tissues. A wide spectrum of cells and tissues has been encapsulated and
implanted, both in animals and humans, indicating the general
applicability of this approach for both research and medical purposes,
including CNS malignancies. Gliomas most frequently recur at the
resection site. To provide local and sustained drug delivery, the
bioreactors can be implanted in the brain parenchyma or in the
ventricular system. The development of comprehensive analyses of geno-
and phenotypic profiles of a tumor (genomics and proteomics) may provide
new and important guidelines for choosing the optimal combination of
bioreactors and recombinant proteins for therapeutic use.
15
UI - 11459086
AU - Kurosaki M; Saeger W; Ludecke DK
TI -
Immunohistochemical localisation of cytokeratins in craniopharyngioma.
SO - Acta Neurochir (Wien) 2001;143(2):147-51
AD - Division of Neurosurgery, Institute of Neurological Sciences, Tottori
University School of Medicine, Yonago, Japan.
BACKGROUND: Although craniopharyngiomas have been examined in several
microscopical studies to date, immunohistochemical analysis has not been
sufficient. METHOD: In addition to the routine haematoxylin and eosin
staining, 38 cases of intra- and/or supra-sellar craniopharyngioma,
including 34 adamatinomatous and 4 squamous papillary types, were
studied using immunohistochemistry for expression of four types of
cytokeratin. FINDINGS: Histological examination found epithelial cells
in 26 of 38 (68.40%) cases. However, cytokeratins were demonstrated in
35 of 38 (92.1%) cases. The remaining 3 cases without demonstration of
epithelial cell nests were supposed to be adamantinomatous
craniopharyngiomas based on the findings in the stroma. In 31 of 34
adamantinomatous craniopharyngioma cases, the epithelium was detected by
immunostaining for cytokeratins. The epithlieum expressed 56 kDa (KL-1)
and 40 kDa (cytokeratin 19) cytokeratins with similar staining patterns
and intensities. The staining intensity of 54 kDa cytokeratin
(cytokeratin 7) was similar to that of the high molecular weight
cytokeratin (keratin M-903). However, in many cases (15 of 27),
immunoreactivity of cytokeratin 7 was not demonstrated in an outer
palisaded basal layer. In all 4 squamous papillary craniopharyngiomas,
moderate staining with cytokeratin 7 appeared in the superficial layer,
whereas basal or mid-zone epithelial cells were negative for cytokeratin
7. The basal layer stained negatively for KL-1, as well as cytokeratin
7. INTERPRETATION: Immunostaining for cytokeratin is valuable in the
investigation of craniopharyngioma, especially when specimens contain
only a small or questionable part of epithelium. Most notably, KL-1 or
cytokeratin 7 stainings are suitable for analyzing these tumours, with
special reference to histological subtypes.
16
UI - 11485231
AU - Ildan F; Tuna M; Gocer IA; Erman T; Cetinalp E
TI -
Intracerebral ganglioglioma: clinical and radiological study of eleven
surgically treated cases with follow-up.
SO - Neurosurg Rev 2001 Jul;24(2-3):114-8
AD - Cukurova University School of Medicine, Department of Neurosurgery,
Balcali, Adana, Turkey. fildanm@superonline.com
BACKGROUND: Gangliogliomas are rare benign tumors of the CNS consisting
of differentiated neural elements and low-grade glial cells. METHODS: We
reviewed our experience of 11 patients with histologically proven
ganglioglioma who were surgically treated since 1986 at Cukurova
University Medical Center. These patients presented at 18 to 45 years of
age. Five were women and six were men. The most common initial symptom
was seizures (in nine of 11 patients), which had sometimes persisted
over long periods of time. At the time of diagnosis, four patients had
focal neurological deficits and three had signs or symptoms of increased
intracranial pressure. The cystic and well-circumscribed characteristics
of these lesions were detected on computed tomography (CT). Despite
their appearance on CT, all but one of the lesions were found to be
mostly solid at operation. Magnetic resonance imaging (MRI) in six
patients revealed abnormally high signal intensity on T2-imaging. The
temporal lobe was the main tumor location (seven patients). All cases
were diagnosed according to the Russel and Rubinstein histological
criteria for ganglioglioma. RESULTS: Ten patients had radical total
resection and one had subtotal resection. No patient underwent
postoperative radiation or chemotherapy. Except for one, all are still
alive and free of progressive disease 1 to 11 years (mean 6.2) after
operation. Six are seizure-free and three have improved seizure control
under anticonvulsant therapy. CONCLUSIONS: We conclude that
ganglioglioma is a distinct histological phenomenon with mildly
predictable clinical symptoms (seizures), mildly characteristic
radiological features, and long-term survival after surgical resection
without the need of adjuvant treatment such as radiotherapy.
17
UI - 11485247
AU - Rustia A; Wierzbicki V; Marrocco L; Tossini A; Zamponi C; Lista F
TI -
Is exon 5 of the PTEN/MMAC1 gene a prognostic marker in anaplastic
glioma?
SO - Neurosurg Rev 2001 Jul;24(2-3):97-102
AD - r.alexx@tiscalinet.it
Chromosome 10 deletions are among the most common genetic changes in
highly malignant glial tumors. It has been noted that loss of
heterozygosity (LOH) at 10q23 is a frequent alteration in a variety of
human tumors and occurs in approximately 70% of all glioblastomas. By
mapping of homozygous deletions on 10q23, a candidate tumor suppressor
gene has been isolated, called PTEN for "phosphatase and tensin homolog
deleted on chromosome 10" and MMAC1 for "mutated in multiple advanced
cancers-1." Mutations of this tumor suppressor gene PTEN/MMAC1 have been
reported in anaplastic glial tumors. The objective of this paper was to
individuate a prognostic marker in exons 5, 6, 7, and 8 of the
PTEN/MMAC1 gene for the high-grade malignant glioma with the most
aggressive clinical behavior. In this study, we undertook sequence
analysis of these exons in six selected patients with high-grade
malignant gliomas who underwent radical aggressive tumor resection
followed by radiotherapy within 3 weeks after surgery and subsequent
chemotherapy. In them, the exon 5 sequence of the PTEN/MMAC1 gene is
suggestive of a genetic survival marker in gliomas with high-grade
malignancy.
18
UI - 11484819
AU - Weber M; Stockhammer F; Schmitz U; von Deimling A
TI -
Mutational analysis of INI1 in sporadic human brain tumors.
SO - Acta Neuropathol (Berl) 2001 May;101(5):479-82
AD - Institute for Neuropathology, Charite, Humboldt University, Berlin,
Germany.
The INI1/SMARCB1/hSNF5 gene on chromosome 22 is frequently mutated in
rhabdoid tumors. An association of INI1 mutations with allelic losses on
chromosome 22 supports a classical tumor suppressor mechanism. Several
brain tumor entities including astrocytomas, glioblastomas and
ependymomas are characteri
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