National Cancer Institute®
Last Modified: July 1, 2002
1
UI - 12013686
AU - Lang O; Kondas O; Torok S; Hauser P; Bognar L; Schuler D
TI -
[Incidence of pediatric brain tumors in Hungary between 1989 and 1999]
SO - Orv Hetil 2002 Mar 3;143(9):451-4
AD - Altalanos Orvostudomanyi Kar, II. sz. Gyermekgyogyaszati Klinika,
Semmelweis Egyetem, Budapest.
INTRODUCTION: The incidence of primary brain tumors in childhood has
increased all over the world in the last decades, so it is the second
most frequent tumor after leukaemias. AIMS OF THE STUDY: The aim of this
study was to examine the incidence and relative frequency of central
nervous system tumors diagnosed under 15 years of age in Hungary.
METHODS: The data obtained from the Hungarian Pediatric Oncology Group
and the National Neurosurgical Institute between 1989 and 1998, and the
reports of the head pediatricians of the counties were used. RESULTS:
There were 685 reported cases between 1989 and 1998. The prevalence of
cerebral tumors has increased during the last decade in Hungary like
that in several developed countries. The increase of the incidence of
primary central nervous system tumors in the last ten years was 4.2% per
year. In 1998 the incidence of central nervous system tumors was 42.9
cases per million children. The most frequent histological categories
were: astrocytoma (30%), medulloblastoma/primitive neuroectodermal
tumors (21%), ependymoma (9%) and other tumors (40%). CONCLUSION: The
results suggest an increase in the incidence of primary brain tumors in
Hungary, similar to those reported in several countries.
2
UI - 12015749
AU - Jeuken JW; Sprenger SH; Gilhuis J; Teepen HL; Grotenhuis AJ; Wesseling P
TI -
Correlation between localization, age, and chromosomal imbalances in
ependymal tumours as detected by CGH.
SO - J Pathol 2002 Jun;197(2):238-44
AD - Department of Neurology, University Medical Centre Nijmegen, P.O. Box
9101, 6500 HB, Nijmegen, The Netherlands. j.jeuken@czzorlnm.azn.nl
Ependymal tumours (ETs) are gliomas that arise from the ependymal lining
of the cerebral ventricles and from the remnants of the central canal of
the spinal cord. Both clinical and genetic studies suggest that distinct
genetic subtypes of ETs exist, the subtypes being correlated with
patient age and/or tumour site. In the present study, the tumour genome
of 20 ETs (15 adult and five paediatric cases) was screened for
chromosomal imbalances by comparative genomic hybridization (CGH). The
most frequently detected imbalances were -22q (75%), -10q (65%), -21
(50%), -16p (50%), -1p (45%), +4q (45%), -10p (45%), -2q (40%), -6
(40%), -19 (40%), -2p (35%), -3p (35%), and -16q (35%). Comparison of
the chromosomal imbalances detected in ETs with those previously
reported in oligodendroglial and astrocytic tumours revealed that in
this respect ETs show similarities to these other gliomas. By combining
these results with those of a recent study of Zheng et al. and Hirose et
al., it was found that although ETs from different sites and from adult
and paediatric patients show overlap at the CGH level, some chromosomal
imbalances occur predominantly in a certain category. In adult patients,
spinal ETs relatively often showed +2, +7, +12, and -14q; infratentorial
ETs -22; and supratentorial ETs -9. In addition, in posterior fossa ETs,
-6 and +9 were much more frequent in adults than in children. It is
concluded that the genetic background of ETs is complex and partly
determined by tumour site, histopathological subtype, and age of the
patient. Copyright 2002 John Wiley & Sons, Ltd.
3
UI - 11900859
AU - Zupanska A; Kaminska B
TI -
The diversity of p53 mutations among human brain tumors and their
functional consequences.
SO - Neurochem Int 2002 Jun;40(7):637-45
AD - Laboratory of Transcription Regulation, Department of Cellular
Biochemistry, Nencki Institute of Experimental Biology, 3 Pasteur Str.,
02-093 Warsaw, Poland.
The p53 tumor suppressor is implicated in cell cycle control, DNA
repair, replicative senescence and programmed cell death. Inactivation
of the p53 contributes to the wide range of human tumors, including
glial neoplasms. In this review, we describe the regulation and
biochemical properties of p53 protein that may explain its ability to
activate various genetic programs underlying cellular responses to
stress conditions. The overall spectrum of p53 mutations is rather
shared between tumor types indicating that these mutations are not tumor
type-specific. However, there is one example of germ-line mutation of
p53 gene (the deletion of the codon 236) that is associated with a
familiar brain tumor syndrome. We compare the frequency and type of most
common mutations among various brain tumours (focusing on glioblastomas)
and their consequences on protein functions. Furthermore, we discuss the
most promising approaches of potential brain tumor therapy, including an
adenovirus-mediated p53 gene transfer. Human glioblastomas are highly
sensitive to the effects of p53 activity when the wild-type p53 is
introduced ectopically. It suggests that the genetic or pharmacological
modulation of the p53 pathway is potentially important strategy in the
treatment of human cancers.
4
UI - 12066901
AU - Buatti JM; Friedman WA
TI -
Temporary ventricular drainage and emergency radiotherapy in the
management of hydrocephalus associated with germinoma.
SO - J Neurosurg 2002 Jun;96(6):1020-2
AD - Department of Radiation Oncology, University of Iowa, Iowa City, USA.
OBJECT: The authors used an alternative strategy to avoid shunt
placement for hydrocephalus associated with germinoma, and the ensuing
complications. METHODS: Between 1998 and 2000, five patients presenting
with germinomas of the pineal area and symptomatic obstructive
hydrocephalus were treated with a novel strategy. On arrival, they
underwent ventriculostomy placement and one of several surgical
procedures to obtain tissue for diagnosis. Within several days of the
initial diagnosis, stereotactically guided fractionated radiotherapy was
started. All patients experienced rapid tumor shrinkage and resolution
of hydrocephalus, allowing discontinuation of external ventricular
drainage without the need for permanent shunting of cerebrospinal fluid.
To date, follow up reveals 100% radiographically and clinically
confirmed tumor control. CONCLUSIONS: Prompt resolution of hydrocephalus
and absence of complications make this a potentially valuable therapy
for control of germinomas and their symptoms.
5
UI - 12066902
AU - Tzika AA; Cheng LL; Goumnerova L; Madsen JR; Zurakowski D; Astrakas LG;
TI -
Zarifi MK; Scott RM; Anthony DC; Gonzalez RG; Black PM
Biochemical characterization of pediatric brain tumors by using in vivo
and ex vivo magnetic resonance spectroscopy.
SO - J Neurosurg 2002 Jun;96(6):1023-31
AD - Department of Radiology, Massachusetts General Hospital, Harvard Medical
School, and Shriners Burns Institute, Boston, 02114, USA.
atzika@partners.org
OBJECT: Magnetic resonance (MR) spectroscopy provides biochemical
information about tumors. The authors sought to determine the
relationship between in vivo and ex vivo biochemical characterization of
pediatric brain tumors by using MR spectroscopy. Their hypothesis was
that ex vivo MR spectroscopy provides a link between in vivo MR
spectroscopy and neuropathological analysis. METHODS: In vivo proton MR
spectroscopy was performed before surgery in 11 patients with
neuroepithelial tumors. During resection, a total of 40 tumor biopsy
samples were obtained from within the volume of interest identified on
in vivo MR spectroscopy and were frozen immediately in liquid nitrogen.
High-Resolution Magic Angle Spinning (HRMAS) was used to perform ex vivo
MR spectroscopy in these 40 tumor biopsy samples. Neuropathological
analysis was performed using the same biopsy samples, and the tumors
were classified as ependymoma, choroid plexus carcinoma, pineoblastoma
(one each), and pilocytic astrocytoma, medullobastoma, low-grade glioma,
and glioblastoma multiforme (two each). Ex vivo HRMAS MR spectroscopy
improved line widths and line shapes in the spectra, compared with in
vivo MR spectroscopy. Choline (Cho) detected in vivo corresponded to
three different peaks ex vivo (glycerophosphocholine, phosphocholine
[PCho], and Cho). Metabolite ratios from in vivo spectra correlated with
ratios from ex vivo spectra (Pearson correlation coefficient range r =
0.72-0.91; p < or = 0.01). Metabolite ratios from ex vivo spectra, such
as PCho/ total creatine (tCr) and lipid/tCr, correlated with the
percentage of cancerous tissue and percentage of tumor necrosis,
respectively (r = 0.84; p < 0.001). CONCLUSIONS: Agreement between in
vivo and ex vivo MR spectroscopy indicates that ex vivo HRMAS MR
spectroscopy can improve resolution of this modality and provide a link
between in vivo MR spectroscopy and neuropathological analysis.
6
UI - 11895926
AU - Yamamoto S; Yoshida Y; Aoyagi M; Ohno K; Hirakawa K; Hamada H
TI -
Reduced transduction efficiency of adenoviral vectors expressing human
p53 gene by repeated transduction into glioma cells in vitro.
SO - Clin Cancer Res 2002 Mar;8(3):913-21
AD - Department of Molecular Biotherapy Research, Cancer Chemotherapy Center,
Cancer Institute, Tokyo 170-8455, Japan. yamamoto.nsrg@med.tmd.ac.jp
PURPOSE: Recombinant adenoviral vectors are widely used in clinical and
experimental studies to treat malignant tumors. Recently, host immune
responses have been proposed as a major limitation in using adenoviral
vectors for repeated gene delivery. We demonstrate another limitation
unrelated to host immunity. EXPERIMENTAL DESIGN: We repeatedly
transduced an adenoviral vector expressing the human p53 gene (AxCIhp53)
into U373MG, a p53-susceptible cell line, and established the
AxCIhp53-resistant cell line U373R. Most U373R cells survived even after
AxCIhp53 treatment due to reduced transduction efficiency. Expression
levels of adenovirus receptors were estimated to investigate the cause
of reduced transduction efficiency. The mutant vector was used to
overcome the resistance. RESULTS: The transduction efficiency of an
adenoviral vector possessing the reporter LacZ gene (AxCAZ2-F/wt) for
U373R cells was 25.4-fold less than that for parent cells. The
expression levels of integrins alpha(v)beta(3) and alpha(v)beta(5) were
found to be decreased in U373R cells without affecting the expression
levels of Coxsackievirus and adenovirus receptor. The mutant vector
AxCAZ2-F/K20, with a linker and a stretch of 20 lysine residues at the
COOH-terminal of the fiber protein, improved the transduction efficiency
of U373R cells to 12.6-fold of that of AxCAZ2-F/wt. A mutant vector
carrying the p53 gene, AxCAhp53-F/K20, dramatically induced apoptosis in
U373R cells. CONCLUSIONS: Glioma cells expressing low levels of
adenovirus receptors might survive and proliferate to recur after
repeated adenoviral transduction, even if the adenoviral transduction is
effective at first. Changing the tropism of vectors is a potent method
to overcome resistance.
7
UI - 11955328
AU - Li N; Zhou X; Meng K; Ma H; Wu B; Zheng X; Sun G
TI -
[A clinicopathological and prognostic study of 22 cases central
neurocytoma]
SO - Zhonghua Bing Li Xue Za Zhi 2002 Feb;31(1):12-5
AD - Department of Pathology, Nanjing General Hospital of PLA, Nanjing
210002, China (Email: zjwlnyzl@public1.ptt.js.cn)
OBJECTIVE: To investigate the clinicopathological features and prognosis
of 22 cases of central neurocytoma (CNC), representing 0.48% of a series
of 4 528 patients undergoing biopsy for central nervous system tumors.
METHODS: The histopathological, ultrastructral, immunohistochemical and
clinical features of CNC were studied by electron microscopic
examination and immunohistochemical stain for Synaptophysin (Syn),
neuron special enolase (NSE), Leu-7, glial fibrillary acid protein
(GFAP), MBP and proliferating cell nuclear antigen (PCNA). RESULTS: The
age of the cases ranged from 4 to 44 (average 27.9 years) with all
tumors localized in the ventricles. In the 18 patients followed up, 14
were alive for 8 months to 14 years and 11 months after the operation,
and 4 died. The average survival period was 70.7 months. Histologically,
the tumor in all 22 cases had the oligodendroglioma-like pattern with
honeycomb appearance and cell-free islands of eosinophilic matrix.
Cellular anaplasia, mitosis and necrotic areas were rarely seen in the
tumors. Immunohistochemical study demonstrated strong positivity for
Syn, NSE and Leu-7, and negative for GFAP and MBP. Ultrastructural
features showed presence of round tumor cells with abundant cell
processes containing microtubules, neurosecretory granules, clear
vesicles and lysosome-like structures. CONCLUSIONS: The differential
diagnosis between CNC and oligodendroglioma could not be established by
routine light microscopy. The importance of immunohistochemical and
electron microscopic studies for making a correct diagnosis is
emphasized. The prognosis of patients is usually favorable, even if the
tumor was resected subtotally. The relationship between the presence of
anaplastic histological features in CNC and patient outcome remains
unclear.
8
UI - 11955336
AU - Tian X; Wang J; Zhang J; Du J; Pang CS; Ho-Keung NG
TI -
[The effects of wild-type PTEN transfection on gene expressions of
glioblastomas]
SO - Zhonghua Bing Li Xue Za Zhi 2002 Feb;31(1):46-9
AD - Department of Pathology, Health Science Center, Beijing University,
Beijing 100083, China. tianxinxia@yahoo.com
OBJECTIVE: To study the effects of wild-type PTEN on gene expressions of
glioblastomas. METHODS: Glioblastoma U87MG cells, which express
inactivated PTEN, were transfected with wild-type PTEN constructs and
stable transfected clones were selected. Then, cDNA microarray analyses
were used to identify differentially expressed genes in wild-type PTEN
transfected cells and control cells. RESULTS: Transfected wild-type PTEN
inhibited the proliferation of U87MG. By cDNA microarray analyses, 89
cDNA clones were identified, which were differentially expressed in
wild-type PTEN transfected cells and control cells. Among these genes,
13 genes were unknown and 76 genes were known genes, including glial
fibrillary acidic protein, p21/WAF1, human TGF-beta inducible early
protein, human DNA fragmentation factor 45 etc. CONCLUSION: Wild-type
PTEN can affect the expressions of multiple genes, by which it regulates
the proliferation, differentiation and apoptosis of glioblastomas.
9
UI - 11955327
AU - Fang J; Luo L; Li J; Sun S; Yuan Y
TI -
[Pathological and immunohistochemical study of pineal parenchymal
tumors]
SO - Zhonghua Bing Li Xue Za Zhi 2002 Feb;31(1):8-11
AD - Department of Neuropathology, Beijing Neurosurgical Institute, Beijing
100050, China (Email: fangjingyi@X263.net)
OBJECTIVE: To investigate the histological typing and differentiation as
well as clinical manifestation and prognosis in pineal parenchymal
tumors (PPTs). METHODS: The histological typing of 21 PPTs were made by
using HE staining. Synaptophysin (Syn), neuron special enolase (NSE),
neurofilament (NF), neuroblastoma (NB), glial fibrillary acid protein
(GFAP), cytokeratin (CK), desmin (Des) were detected in 20 cases with SP
immunohistochemical staining methods. Analysis of the clinical data and
follow-up were performed. RESULTS: 9 pineocytomas, 4 pineoblastomas, 8
pineal parenchymal tumors of intermediate differentiation were found in
21 PPTs. Immunoreactivity to Syn, NSE, NF, GFAP, NB were in 20, 20, 14,
15, 2, while Des and CK were negative in all cases. CONCLUSIONS: Pineal
parenchymal tumors of intermediate differentiation were characterized by
a distinctly biphasic pattern, including areas of pineocytoma and
pineoblastoma, or with intermediate differentiation and transitional
feature. PPTs expressed neuronic differentiation. Death rate of PPTs
were higher inside 1 year after the operation.
10
UI - 12048743
AU - Anonymous
TI -
WVU neurosurgeon uses 3-D images to locate brain tumors.
SO - W V Med J 2002 Mar-Apr;98(2):78
11
UI - 12046517
AU - Derenda M
TI -
[Report on the Scientific Conference "On earlier diagnosis of
intracranial tumors." Elblag, October 4, 2001]
SO - Neurol Neurochir Pol 2002 Mar-Apr;36(2):416-9
AD - Oddzialu Neurochirurgii Wojewodzkiego Szpitala Zespolonego w Elblagu.
12
UI - 12015841
AU - Pollack IF; Hamilton RL; Burnham J; Holmes EJ; Finkelstein SD; Sposto R;
TI -
Yates AJ; Boyett JM; Finlay JL
Impact of proliferation index on outcome in childhood malignant gliomas:
results in a multi-institutional cohort.
SO - Neurosurgery 2002 Jun;50(6):1238-44; discussion 1244-5
AD - Departments of Neurosurgery, University of Pittsburgh Medical Center and
the Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Ian.Pollack@chp.edu
OBJECTIVE: Prognoses of pediatric high-grade gliomas are unpredictable,
even when clinical and histological factors are taken into account. In
preliminary studies with an institutional cohort of pediatric high-grade
gliomas, we observed a strong association between outcome and
proliferation index, as assessed by immunolabeling with the MIB-1
antibody. To determine whether this marker could provide prognostically
useful information independent of tumor histology, we examined the
prognostic usefulness of this marker in the multi-institutional cohort
of Children's Cancer Group Study 945, the largest group of childhood
high-grade gliomas analyzed to date. METHODS: The study group consisted
of tumors within this cohort that were classified as high-grade gliomas
on central review according to contemporary World Health Organization
guidelines and that had sufficient histopathological material to permit
proliferation index assessment. Paraffin-embedded sections were cut and
processed, microwave antigen enhancement was used, and MIB-1 indices
were calculated by percent labeling in approximately 2000 cells (5-10
high-power fields) in the areas with greatest labeling. To ensure that
the review diagnostic classification and proliferation labeling index
were assigned independently for each tumor, these analyses were
performed by two different neuropathologists at separate institutions,
and each was blinded to the results of the other. RESULTS: Ninety-eight
tumors met eligibility criteria for this study. Among these high-grade
gliomas, there was a strong association between MIB-1 labeling and
patient outcome: 5-year progression-free survival was 33 +/- 7% in 43
patients whose tumors had MIB-1 indices of less than 18%, 22 +/- 8% in
the 27 patients whose tumors had indices between 18 and 36%, and 11 +/-
6% in the 28 patients whose tumors had indices greater than 36% (P =
0.003). As anticipated, a strong association was also observed between
histology and MIB-1 labeling index in these cases. Mean labeling indices
were 19.4 +/- 2.66 for tumors classified as anaplastic astrocytoma
versus 32.1 +/- 3.08 for those classified as glioblastoma multiforme (P
= 0.0024). Notwithstanding this correlation, a significant association
was noted between labeling index and progression-free survival, even
after the analysis had been stratified by histology (P = 0.001).
Although histology had an independent association with outcome, the
prognostic value of MIB-1 labeling transcended histological subgrouping
and was apparent both in tumors classified as anaplastic astrocytoma (P
= 0.02) and in those classified as glioblastoma multiforme (P = 0.046).
Multivariate regression modeling confirmed the strong independent
association between MIB-1 labeling index and outcome. As a group, tumors
with labeling indices higher than 36% had an almost uniformly poor
outcome, regardless of histology. CONCLUSION: MIB-1 labeling index and
histological categorization are each prognostically relevant in
childhood high-grade gliomas. MIB-1 labeling index can help to refine
the accuracy of histologically based prognostic assessments.
13
UI - 12071633
AU - Prayson RA
TI -
Cell proliferation and tumors of the central nervous system. Part 1:
Evaluation of mitotic activity.
SO - J Neuropathol Exp Neurol 2002 Jun;61(6):501-9
AD - Department of Anatomic Pathology, Cleveland Clinic Foundation, Ohio
44195, USA.
Evaluation of cell proliferation has been long recognized in pathology
as a mainstay of diagnosis and important in the prognostication of a
variety of neoplasms. Routine light microscopic evaluation of mitotic
activity has long served as a reasonable assessment of cell
proliferation. Counting mitotic figures has the advantage of being
inexpensive and relatively quick. The main objections leveled against
utilization of mitosis counts in diagnostic decision making are related
to the instability of mitotic figures due to prefixation and fixation
issues and problems with interobserver reproducibility of counts. This
paper reviews factors that affect the identification of mitotic figures
and the determination of mitosis counts. The role mitosis evaluation
plays in the evaluation of certain neoplasms of the central nervous
system is discussed.
14
UI - 12071636
AU - Okada Y; Nishikawa R; Matsutani M; Louis DN
TI -
Hypomethylated X chromosome gain and rare isochromosome 12p in diverse
intracranial germ cell tumors.
SO - J Neuropathol Exp Neurol 2002 Jun;61(6):531-8
AD - Department of Pathology and Neurosurgical Service, Massachusetts General
Hospital, Harvard Medical School, Boston, USA.
Twenty-five primary intracranial germ cell tumors (11 germinomas, 5
teratomas, 5 mixed teratomas-germinomas. 1 mixed
choriocarcinoma-teratoma, 1 yolk sac tumor, 1 mixed yolk sac
tumor-teratoma, and 1embryonal carcinoma; from 24 males and 1 female)
were studied by fluorescence in situ hybridization with probes to the X
and Y chromosomes, chromosome 12p, the CDKN2A/p16 gene, and chromosome
13q-loci previously noted to be altered in either intracranial or
systemic germ cell tumors. An increased number of X chromosomes,
typically 1 extra copy, was observed in 23 of 25 cases (92%), with
methylation-sensitive PCR demonstrating that the additional X
chromosomes were hypomethylated in 13 of 16 (81%) studied tumors. Five
cases (20%) had increased copy numbers of 12p (including tumors with
isochromosome 12p), and 3 (12%) had 13q loss. No tumors had CDKN2A/p16
deletion or mutation, and 16 of 25 (64%) were positive for p16
expression by immunohistochemistry. Genetic alterations such as
isochromosome 12p, 13q loss and CDKN2A/p16 are therefore not common in
intracranial germ cell tumors. However, gains of hypomethylated, active
X chromosomes occur in nearly all intracranial germ cell tumors,
regardless of histological subtype. Along with the observed male
predominance of intracranial germ cell tumors and the predisposition in
Klinefelter syndrome patients for these lesions, the data argue strongly
that sex chromosome aberrations, rather than isochromosome 12p, are
integral to intracranial germ cell tumorigenesis
15
UI - 11912479
AU - Zingale A; Albanese V
TI -
Thallium-201 SPECT and equivocal neuroradiological supratentorial
lesions.
SO - J Neurosurg Sci 2001 Dec;45(4):241-2
16
UI - 11937896
AU - Trobe JD
TI -
Photophobia in anterior visual pathway disease.
SO - J Neuroophthalmol 2002 Mar;22(1):1-2
17
UI - 12019170
AU - Fulci G; Ishii N; Maurici D; Gernert KM; Hainaut P; Kaur B; Van Meir EG
TI -
Initiation of human astrocytoma by clonal evolution of cells with
progressive loss of p53 functions in a patient with a 283H TP53
germ-line mutation: evidence for a precursor lesion.
SO - Cancer Res 2002 May 15;62(10):2897-905
AD - Laboratory of Molecular Neuro-Oncology, Department of Neurosurgery and
Winship Cancer Institute, Emory University School of Medicine, 1365B
Clifton Road, Atlanta, GA 30322, USA.
Little is known about the genetic and molecular events leading to the
early stages of human astrocytoma formation. To examine this issue, we
analyzed the significance of sequential accumulation of two somatic
point mutations (R267W and E258D) in the TP53 gene during the initiation
of astrocytoma in a patient born with a single germ-line p53 point
mutation (R283H). We adapted a p53 transcriptional assay in yeast to
establish the temporal occurrence and allelic distribution of the p53
mutations present in the patient and characterized these mutations
through functional assays and structural modeling. Our results show that
the first somatic mutation occurred at codon 267 on the p53 allele
harboring the germ-line mutation R283H, whereas the second somatic
mutation occurred in the remaining wild-type (wt) allele at codon 258.
These two mutations induced the formation of tumor cells with the
genotype p53(267W+283H/258D), which comprised 70% of the cells in the
primary WHO grade II astrocytoma. Another 8% of cells within the tumor
had the partially mutated genotype p53(267W+283H/WT) and represented the
remnants of a clinically undetectable intermediate stage of astrocytic
neoplastic transformation. The remaining 22% of cells had the
constitutive p53(283H/WT) genotype and likely consisted of nontumor
cells. Functional analysis of the p53 alleles present in the patient's
tumor indicated that the germ-line p53(R283H) could transactivate the
CDKN1A((p21, WAF1, cip1, SDI1)) but not the BAX gene and retained the
ability to induce growth arrest of human glioblastoma cells. The
p53(R267W+R283H) and p53(E258D) were incapable of transactivating either
promoter or inducing growth arrest. Modeling of p53 interaction with DNA
suggests that R283H mutation may weaken the sequence-specific
interaction of p53 lysine 120 with the BAX gene but not the CDKN1A
p53-responsive elements. Taken together, these results have
characterized, for the first time, the genetic events defining a
clinically undetectable precursor lesion leading to a grade II
astrocytoma. They also suggest that astrocytoma initiation in this
patient resulted from monoclonal evolution driven by a sequential loss
of proapoptotic and growth arrest functions of p53.
18
UI - 12077919
AU - Novak L; Emri M; Balkay L; Galuska L; Esik O; Molnar P; Csecsei G; Tron
TI -
L
[The PET scan in neuro-oncology--indications, differential diagnosis and
clinical application]
SO - Orv Hetil 2002 May 26;143(21 Suppl 3):1289-94
AD - Debreceni Egyetem, Orvos- es Egeszsegtudomanyi Centrum, Idegsebeszeti
Klinika, Debrecen. lnovak@jaguar.dote.hu
Results of 157 PET (positron emission tomography) studies in 102
patients with known or presumed intracranial (ic.) tumors are reviewed.
In 106 studies [18F]-2-fluoro-2-deoxy-D-glucose (FDG) and in 51 cases
[11C]-methionine (MET) was used as the PET tracer. CT and MRI imaging
accompanied the PET studies in each case. Results of pre- and/or
postoperative studies are compared. PET was concluded to have a
fundamental role in the precise differential diagnosis in case of ic.
space-occupying pathologies since it is capable of providing information
that is not obtainable or may be equivocal based solely on CT and/or MRI
investigations. However, it is also mandatory to be aware of the limits
of PET.
19
UI - 12065727
AU - Pannequin J; Oiry C; Morel C; Kucharczak J; Camby I; Kiss R; Gagne D;
TI -
Galleyrand JC; Martinez J
C-terminal heptapeptide of gastrin inhibits astrocytomas motility by
interacting with a new gastrin binding site.
SO - J Pharmacol Exp Ther 2002 Jul;302(1):274-82
AD - Laboratory of Amino Acids, Peptides and Proteins, Free University of
Brussels, Brussels, Belgium.
It is well known that the amidated C-terminal part of gastrin is crucial
for its interaction with the classical seven transmembrane domain
receptors CCK-1 or CCK-2. Nevertheless, over the past 10 years, several
groups have characterized new binding sites using peptides related to
gastrin (particularly glycine-extended forms of gastrin) on various
tumoral and nontumoral cell lines. In the present study, we focused on
the human astrocytic tumoral cell line U373. Although it has been
described that gastrin was able to inhibit the motility of these cells,
we were unable to detect any classical CCK/gastrin receptor. On the
other hand, by using the radiolabeled C-terminal heptapeptide of gastrin
((125)I-G-7), we evidenced a new binding site that possessed a
pharmacological profile different from the classical CCK/gastrin
receptors. This new gastrin binding site seemed to be coupled to G
proteins and be implicated in c-Fos transcription gene. Moreover, we
showed that G-7 was able to induce a strong inhibition of U373 cell
migration, a crucial biological effect when we know that astrocytoma
cells' migration in brain parenchyma constitutes a major feature of
malignancy in astrocytic tumors.
20
UI - 12076945
AU - Barboriak DP; Provenzale JM
TI -
Evaluation of software for registration of contrast-enhanced brain MR
images in patients with glioblastoma multiforme.
SO - AJR Am J Roentgenol 2002 Jul;179(1):245-50
AD - Department of Radiology, Box 3808, Duke University Medical Center,
Durham, NC 27710, USA.
OBJECTIVE: We evaluated commercially available software that rapidly and
automatically registers brain MR images on a clinical workstation, and
we studied the accuracy of these registrations. SUBJECTS AND METHODS:
Ten patients with a diagnosis of glioblastoma multiforme underwent
contrast-enhanced inversion recovery prepared three-dimensional (3D)
volumetric spoiled gradient-recalled acquisition in the steady state
(SPGR) MR imaging (contiguous 1.5-mm slice thickness, 96-104 slices).
After this imaging sequence, each patient was brought out of the head
coil into a sitting position and then repositioned in the coil. The
inversion recovery prepared 3D SPGR sequence was then repeated. A
commercially available software program operating on a clinical
workstation was used to automatically register the second inversion
recovery prepared SPGR series to the first. The speed of registration
was recorded. The accuracy of each registration was estimated by
recording the coordinates of eight anatomic landmarks on the registered
and reference series and by calculating the mean error among matching
landmarks. RESULTS: In nine of 10 patients, the registration software
produced a visually satisfactory registration. In one patient, a second
registration was necessary to produce a satisfactory registration. The
processing time for each iteration was 48.3 +/- 3.8 sec (mean +/- SD).
The mean error in aligning matching anatomic landmarks ranged from 0.67
to 1.41 mm, with an overall mean of 1.18 mm. The largest error among
matching landmarks was 2.3 mm. CONCLUSION: Commercially available
registration software can automatically register 3D imaging volumes in
less than 1 min. The mean error in registration was approximately
equivalent to the dimensions of a single voxel.
21
UI - 12076946
AU - Bourekas EC; Varakis K; Bruns D; Christoforidis GA; Baujan M; Slone HW;
TI -
Kehagias D
Lesions of the corpus callosum: MR imaging and differential
considerations in adults and children.
SO - AJR Am J Roentgenol 2002 Jul;179(1):251-7
AD - Department of Radiology, Section of Neuroradiology, The Ohio State
University, 160 Means Hall, 1654 Upham Dr., Columbus, OH 43210-1250,
USA.
22
UI - 11702135
AU - Essig M; Metzner R; Bonsanto M; Hawighorst H; Debus J; Tronnier V; Knopp
TI -
MV; van Kaick G
Postoperative fluid-attenuated inversion recovery MR imaging of cerebral
gliomas: initial results.
SO - Eur Radiol 2001;11(10):2004-10
AD - Department of Radiology, German Cancer Research Center, University
Hospitals, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
m.essig@dkfz-heidelberg.de
Fluid-attenuated inversion-recovery (FLAIR) imaging has shown to be a
valuable imaging modality in the assessment of intra-axial brain tumors;
however, no data are available about the role of this technique in the
clinically important postoperative stage. The purpose of this study was
to evaluate the diagnostic potential of FLAIR MR imaging in residual
tumor after surgical resection of cerebral gliomas. Fifteen patients
with residual cerebral gliomas were examined within the first 18 days
after partial surgical resection of cerebral gliomas. The imaging
protocol included T1-weighted spin echo, T2- and proton-density-weighted
fast spin echo, and FLAIR imaging with identical slice parameters. T1
and FLAIR were repeated after contrast media application. Detection and
delineation of residual tumor were the primary parameters of the image
analysis. Additionally, the influence of image artifacts on the image
interpretation was assessed. On FLAIR images residual signal
abnormalities at the border of the resection cavities were observed in
all patients, whereas T2- and T1-weighted images present residual
abnormalities in 13 of 15 and 10 of 15 patients, respectively. The FLAIR
imaging was found to be superior to conventional imaging sequences in
the delineation of these changes and comparable to contrast enhanced
T1-weighted imaging in the delineation of residual enhancing lesions.
Because of protein cell components and blood byproducts within the
resection cavity, FLAIR imaging was unable to suppress the cerebrospinal
fluid (CSF) in 4 patients. After the decomposition of proteins and
blood, CSF could again be completely suppressed and residual or
recurrent tumors were clearly identified. Our preliminary study has
shown that FLAIR may be a valuable diagnostic modality in the early
postoperative MR imaging after resection of cerebral gliomas due to its
better delineation of residual pathologic signal at the border of the
resection cavity. It should therefore be integrated into the early
and/or intraoperative MR imaging protocol.
23
UI - 11706434
AU - Pesudo Martinez JV; Gonzalez-Darder JM; Feliu Tatay R; Belloch Ugarte V;
TI -
Vera Roman J; Gil Salu JL
[Assessment of the degree of resection of high grade supratentorial
gliomas with early postoperative magnetic resonance]
SO - Neurocirugia (Astur) 2001;12(1):43-50
AD - Servicio de Neurocirugia, Hospital General de Castellon, ERESA.
In this paper we report the results of a prospective study in which we
evaluate the degree of tumor removal of 25 supratentorial high grade
gliomas by means of an MRI performed in the early postoperative period.
In all cases, there was preoperative enhancement 8 patients had been
previously operated on while the others had their first operation. In
all cases the postoperative early MRI was performed within the first
week and in 15 within the first 3 days. In order to evaluate the degree
of tumor removal the presence or not of enhancement was considered and
if it existed, classified as linear or nodular. RESULTS: To avoid
postsurgical artifacts it is important to perform the MRI as soon as
possible after surgery, especially within the first 3 days. Generally,
linear enhancement disappeared on subsequent follow-up examinations,
showing that it probably does no represent residual, tumor while nodular
enhancement usually does. Survival with the high-grade tumors was
slightly higher in the group without postoperative enhancement or linear
one than in the group with nodular enhancement but the difference was
not significant.
24
UI - 11813879
AU - Zagzag D; Capo V
TI -
Angiogenesis in the central nervous system: a role for vascular
endothelial growth factor/vascular permeability factor and tenascin-C.
Common molecular effectors in cerebral neoplastic and non-neoplastic
"angiogenic diseases".
SO - Histol Histopathol 2002 Jan;17(1):301-21
AD - Department of Pathology, New York University Medical Center, NY, USA.
dz4@nyu.edu
Human pathological conditions of the central nervous system (CNS)
associated with angiogenesis (i.e. neovascularization) include
neoplastic, as well as infectious, ischemic, and traumatic processes.
Upregulation of vascular endothelial growth factor/vascular permeability
factor (VEGF/VPF) and tenascin-C (TN-C) is spatially and temporally
related to neovascularization. Spatially, VEGF/VPF and TN-C are both
found at the site of neovascularization, but they are not detected in
areas of normal brain or in areas without neovascularization.
Temporally, VEGF/VPF and TN-C are found at the peak of angiogenesis and
are not detected when angiogenesis had ceased.
25
UI - 11813884
AU - Hasegawa M; Muramatsu N; Tohma Y; Fukaya K; Fujisawa H; Hayashi Y;
TI -
Tachibana O; Kida S; Yamashita J; Saito K
Expression of E-cadherin-catenin complex in human benign schwannomas.
SO - Histol Histopathol 2002 Jan;17(1):39-44
AD - Department of Neurosurgery, Graduate School of Medical Science, Kanazawa
University, Japan. hasegawa@ns.m.kanazawa-u.ac.jp
The Ca2+-dependent cell adhesion molecule E-cadherin has been known to
express in normal and reactive Schwann cells in rodents, and to play an
important role in Schwann cell-Schwann cell adhesion and maintenance of
peripheral nervous tissue architecture. However, little is known about
expression of E-cadherin in schwannomas. The aim of the present study
was to investigate the cellular expression and localization of
E-cadherin, and its associated protein, alpha E-, alpha N- and
beta-catenins in human schwannomas, which are supposed to derive from
Schwann cells. We tested the hypothesis that these proteins might show
an altered expression/distribution in schwannoma cells which correlates
with their neoplastic behavior, including sparse cell-cell contact, as
seen those in meningiomas and various carcinomas. In human schwannomas,
however, E-cadherin, alpha E-catenin, and beta-catenin were detected by
western blotting and immunohistochemistry, whereas alpha N-catenin was
not. Immunoprecipitation using anti-E-cadherin antibody resulted in
alpha E-catenin forming a complex with E-cadherin. SSCP analysis
revealed no mutations in the transmembrane domain or in intracellular
catenin-binding site of E-cadherin. These data suggest that the
E-cadherin-alpha E-catenin complex is well preserved in human schwannoma
cells, which is compatible with its benign behavior, and these molecules
might be used as additional cell markers of Schwann cell-derived tumors.
26
UI - 11837741
AU - Carlotti CG Jr; Salhia B; Weitzman S; Greenberg M; Dirks PB; Mason W;
TI -
Becker LE; Rutka JT
Evaluation of proliferative index and cell cycle protein expression in
choroid plexus tumors in children.
SO - Acta Neuropathol (Berl) 2002 Jan;103(1):1-10
AD - Division of Neurosurgery, The Hospital for Sick Children, Toronto,
Ontario, Canada.
Choroid plexus tumors are papillary neoplasms originating from the
epithelium of the choroid plexus within the cerebral ventricles. They
may be highly proliferative tumors, but detailed studies confirming
their proliferative potential are lacking. Accordingly, we performed a
clinicopathological correlation study of neoplasms arising from the
choroid plexus in children using immunohistochemistry to characterize
both their proliferative potential and their degree of cell cycle
dysregulation when compared to non-neoplastic choroid epithelium. Twelve
children with choroid plexus papillomas (CPPs) and 11 with choroid
plexus carcinomas (CPCs) were identified from the time period 1982-1997.
The outcome and survival of these children following treatment was
determined from the medical record. Immunohistochemical studies were
performed on CPPs and CPCs in this patient population and on
non-neoplastic choroid epithelium using antibodies to MIB-1, p53, cyclin
E, retinoblastoma protein (pRB), p107, and E2F-1. In 5 children with
CPCs, tumor tissue was available for immunohistochemistry at a second
surgery after cycles of chemotherapy had been given. The mean survival
for patients with CPPs was 8.5 years, and with CPCs 5.2 years with a
minimum follow-up of 4 years for the group. The expression of cell cycle
markers and MIB-1 was greater in CPCs than in CPPs or normal choroid
plexus. The expression of MIB-1, p53, pRB, and E2F-1 was significantly
lower in patients with CPCs after chemotherapy than before. The MIB-1
labeling index for CPC patients who are alive and well after treatments
was 15.19+/-3.2 compared to 22.63+/-3.04 for patients who have died from
their disease (P<0.05). We conclude that CPCs in children are
characterized by a higher MIB-1 labeling index and greater cell cycle
dysregulation than are CPPs. Chemotherapy may work in part on CPCs to
decrease their proliferative potential and expression of cell cycle
regulatory proteins.
27
UI - 11938773
AU - Hu S; Huang C; Chen B
TI -
[Enhanced cytotoxicity of VM-26 in human malignant glioma cells by
calcium channel blocker nicardipine in vitro]
SO - Hunan Yi Ke Da Xue Xue Bao 1999;24(2):143-6
AD - Department of Neurosurgery, Second Affiliated Hospital, Hunan Medical
University, Changsha 410011.
Using the monolay tumor cell culture system and the method or MTT
colorimetric analysis, the cytotoxicity of the anticancer drug VM-26 and
Nicardipine(NCDP) in human malignant glioma cell line U251 was studied.
The results showed that the cytotoxicity of VM-26 in U251 was enhanced
by NCDP at a low dose which did not show direct cytotoxicity. The
authors considered that VM-26 combined with NCDP can heighten the
intracellular anticancer drug concentration, reverse the drug resistance
and heterogeneity in human malignant glioma cells. The mechanism of the
enhanced effect was also discussed. These findings will provide an
alternative chemotherapeutic clue to treat the postoperative malignant
gliomas.
28
UI - 12057111
AU - DeAngelis LM
TI -
Primary central nervous system lymphomas.
SO - Curr Treat Options Oncol 2001 Aug;2(4):309-18
AD - Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY
10021-6700, USA. deangell@mskcc.org
Primary central nervous system lymphoma (PCNSL) is widely regarded as
one of the primary brain tumors most amenable to treatment. Although
whole brain radiotherapy was the cornerstone of therapy for decades,
recent work clearly indicates that chemotherapy has become the primary
focus of treatment for this disease. The initial treatment of PCNSL for
all patients, including the elderly, should be chemotherapy using a
high-dose methotrexate-based regimen. Although cranial irradiation has
often been combined with methotrexate, the unacceptably high incidence
of late neurotoxicity, particularly in older patients, has caused many
to eliminate radiotherapy, especially in those older than age 60 years.
Emerging data support the validity of this approach, and the development
of more efficacious chemotherapeutic regimens has been the focus of
recent research.
29
UI - 12057095
AU - Stieber VW
TI -
Low-grade gliomas.
SO - Curr Treat Options Oncol 2001 Dec;2(6):495-506
AD - Department of Radiation Oncology, Wake Forest University Baptist Medical
Center, Medical Center Boulevard, Winston-Salem, NC 27157-1030, USA.
vstieber@wfubmc.edu
Low-grade gliomas are uncommon primary brain tumors classified as
histologic grades I or II in the World Health Organization (WHO)
classification. The most common variants are pilocytic and low-grade
astrocytomas, oligodendrogliomas, and mixed oligo-astrocytomas located
in the cerebral hemispheres. Prognostic factors that predict
progression-free and overall survival include young age, pilocytic
histology, good Karnofsky performance status, gross total resection,
lack of enhancement on imaging, and small preoperative tumor volumes.
Edema and vasogenic effects are typically managed with corticosteroids.
Dexamethasone is given at an initial dosage of 4 mg given four times
daily. Anticonvulsants are given prophylactically after resection and
for patients who present with seizures. The rationale for open
craniotomy depends on the need for immediate palliation of symptoms by
reduction of intracranial pressure or focal mass effect, and/or improved
oncologic control. Gross total resection of tumor is generally defined
as the absence of residual enhancement on contrast-enhanced
postoperative MRI scan. Most retrospective studies suggest that patients
who have undergone a gross total resection of tumor have improved
survival. Depending upon the proximity of the tumor to eloquent brain,
gross total resection may or may not be possible. In these cases a
stereotactic biopsy is required to provide the histologic diagnosis.
Adjuvant radiotherapy is recommended for patients with incompletely
resected grade II tumors or for patients older than age 40 regardless of
extent of resection. It may be considered for any pilocytic astrocytoma
from which a biopsy has been performed. Phase III randomized prospective
trials have shown statistically significantly improved progression-free
survival at 5 years with the addition of radiotherapy, though overall
survival does not appear different. Based on prospective randomized
phase III trials, 50.4 Gy to 54 Gy of conventionally fractionated
radiotherapy appears to be a safe and effective regimen with minimal
neurotoxicity; 45 Gy may be adequate for biopsied pilocytic
astrocytomas. Currently, RTOG trial 98-02 is investigating the efficacy
of postradiation PCV chemotherapy (procarbazine, CCNU, and vincristine)
in the treatment of newly diagnosed unfavorable low-grade gliomas. Other
areas of investigation include Temozolomide chemotherapy and the
association of 1p and 19q chromosomal deletions with prolonged survival
in oligodendrogliomas and sensitivity to PCV chemotherapy. Radiosurgery