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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Brain Tumor - March 2002
National Cancer Institute®
Last Modified: March 1, 2002
Table of Contents
1
UI - 11840333
AU - Shou J; Ali-Osman F; Multani AS; Pathak S; Fedi P; Srivenugopal KS
TI -
Human Dkk-1, a gene encoding a Wnt antagonist, responds to DNA damage
and its overexpression sensitizes brain tumor cells to apoptosis
following alkylation damage of DNA.
SO - Oncogene 2002 Jan 31;21(6):878-89
AD - Department of Neurosurgery, The University of Texas M.D. Anderson Cancer
Center, 1515 Holcombe Road, Houston, TX 77030, USA.
The human Dkk-1 (hDkk-1) gene, a transcriptional target of the p53 tumor
suppressor, encodes a powerful inhibitor of the Wnt signaling pathway
and regulates the spatial patterning/morphogenesis of the mammalian
central nervous system. We investigated the p53-related functions of the
hDkk-1 gene by studying its response to DNA damage and its modulation of
apoptosis in human glioma cells. Various chemotherapeutic and other
agents that induce DNA adducts and compromise its integrity
(1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) and UV
rays) enhanced the expression of hDkk-1 significantly. The
damage-induced increase in hDkk-1 mRNA levels occurred in many human
tumor cell lines, irrespective of their p53 gene status. The human
glioblastoma cell line, U87MG, which had undetectable hDkk-1 expression,
was engineered to express moderate levels of the hDkk protein by stable
transfection. The engineered cells did not show any morphological
changes, but underwent marked apoptosis after ceramide treatment.
Further, the DNA cross-linking drugs BCNU and cisplatin, but not the
microtubule poison vincristine, induced significant cell death in
U87MG/hDkk cells, and this was accompanied by altered Bcl-2/Bax
expression and a reduction in the amount of telomere DNA as visualized
by fluorescence in situ hybridization. These results show that hDkk-1 is
a pro-apoptotic gene and suggest that it may play important roles in
linking the oncogenic Wnt and p53 tumor suppressor pathways.
2
UI - 11840337
AU - Konduri SD; Osman FA; Rao CN; Srinivas H; Yanamandra N; Tasiou A; Dinh
TI -
DH; Olivero WC; Gujrati M; Foster DC; Kisiel W; Kouraklis G; Rao JS
Minimal and inducible regulation of tissue factor pathway inhibitor-2 in
human gliomas.
SO - Oncogene 2002 Jan 31;21(6):921-8
AD - Division of Cancer Biology, Department of Biomedical and Therapeutic
Sciences, University of Illinois School of Medicine, One Illini Drive,
Peoria, IL 61656, USA.
Tissue factor pathway inhibitor-2 (TFPI-2), a serine protease inhibitor
abundant in the extra cellular matrix, is highly expressed in
non-invasive cells but undetectable levels in highly invasive human
glioma cells. The mechanisms responsible for its transcriptional
regulation are not well elucidated. In this study, we made several
deletion constructs from a 3.6 kb genomic fragment from Hs683 cells
containing the 5'-flanking region of the TFPI-2 gene, transiently
transfected with these constructs into non-invasive (Hs683) and highly
invasive (SNB19) human glioma cells, and assessed their expression by
using a luciferase reporter gene. Three constructs showed high promoter
activity (pTF5, -670 to +1; pTF6, -312 to +1; pTF2, -1511 to +1).
Another construct, pTF8 (-81 to +1), showed no activity. PTF9, a variant
of pTF5 in which a further 231 bp fragment (-312 to -81) was deleted,
from the [-670 to +1] pTF5 region, also showed no promoter activity.
Hence, (-312 to -81) this region is essential for the transcription of
TFPI-2 in glioma cells. Sequencing of this promoter region revealed that
it has a high G+C content, contains potential SP1 and AP1 binding
motifs, and lacks canonical TATA and CAAT boxes immediately upstream of
the major transcriptional initiation site, although CAAT boxes were
found about -3000 bp upstream of the transcription start site. We also
found a strong repressor in the region between -927 to -1181, upstream
of the major transcriptional initiation site, followed by positive
elements or enhancers between -1511 to -1181. These positive elements
masked the silencer effect. Finally TFPI-2 was induced in Hs683 cells
transfected with the pTF6 construct (-312 to +1) and stimulated with
phorbol-12-myristate-13-acetate (PMA). We conclude that the -312 to +1
region is critical for the minimal and inducible regulation of TFPI-2 in
non-invasive (Hs683) and highly invasive (SNB19) human glioma cell
lines.
3
UI - 11858377
AU - Yaris N; Akyuz C; Coskun T; Kutluk T; Buyukpamukcu M
TI -
Nutritional status of children with cancer and its effects on survival.
SO - Turk J Pediatr 2002 Jan-Mar;44(1):35-9
AD - Department of Pediatrics, Hacettepe University Faculty of Medicine,
Ankara, Turkey.
In the present study we aimed to determine the nutritional status of our
patients and to assess its relationship with survival. The nutritional
status of 47 patients with cancer was evaluated at diagnosis, three
months after initiation of the treatment and at the end of therapy.
Weight for height, height for age, and weight for age of children were
expressed as percent of standard. Values for each nutritional index were
converted into standard deviation (Z) scores. Three-year overall
survival (OS) and event-free survival (EFS) rates of patients were
determined according to their nutritional status. The overall prevalence
of malnutrition at diagnosis was 29.8%. Three months later the
malnutrition ratio reached 38.3% and then decreased again to 18.5% at
the end of the therapy. Although the prevalence of malnutrition at the
third month of treatment was significantly higher from the prevalence at
diagnosis (p: 0.001) and at the end of the therapy (p: 0.009), the mean
Z scores of the nutritional indexes before and during the treatment were
not significantly different. The survival rates of malnourished patients
were not different from those of well nourished patients. In conclusion,
malnutrition is one of the main problems in children with cancer;
hovewer, nutritional status has no effect on survival.
4
UI - 11778821
AU - Sano K
TI -
Intracranial dysembryogenetic tumors: pathogenesis and their order of
malignancy.
SO - Neurosurg Rev 2001 Dec;24(4):162-7; discussion 168-70
AD - Department of Neurosurgery, Teikyo University School of Medicine, Tokyo,
Japan. neurosur@med.teikyo-u.ac.jp
Dysembryogenetic tumors can be classified into three main categories:
(1) tumors derived from embryonal cell rests in situ such as
craniopharyngioma, Rathke's cleft cyst, chordoma, etc., (2) tumors
derived from embryonal cells straying into the tissue ("verirrte Keime")
such as so-called germ cell tumors, epidermoid, dermoid, lipoma,
hamartoma, etc., and (3) included twin (fetus-in-fetu) tumors. The
pathogenesis of the second one may be that the embryonic cells of
various stages of embryogenesis are misplaced in the bilaminar embryonic
disc at the time of the primitive streak formation, becoming involved in
the stream of lateral mesoderm and carried to the neural plate area to
become incorrectly enfolded into the brain at the time of neural tube
formation. The third category of tumor may be related to sequestration
of cells of the blastocyst before differential blocking of the genome
has occurred. The author propounds the following hypothesis:
intracranial dysembryogenetic tumors composed of cells resembling the
cells that appear in the earlier stages of embryogenesis are more
malignant than those composed of cells resembling those appearing in the
later stages of embryogenesis.
5
UI - 11778828
AU - Csokay A; Nagy L; Novoth B
TI -
Avoidance of vascular compression in decompressive surgery for brain
edema caused by trauma and tumor ablation.
SO - Neurosurg Rev 2001 Dec;24(4):209-13
AD - Department of Neurosurgery, National Institute of Traumatology,
Budapest, Hungary. parkdros@elender.hu
BACKGROUND: In case of severe brain swelling especially caused by trauma
or other operative manipulation (tumor ablation), decompressive
craniectomy with durotomy has not resulted in significant chances of
recovery. Decompressive craniectomy has been defined only as an option
within guidelines. METHOD: A new operative technique was developed to
improve the efficacy of decompressive surgery. With an increase in
intracranial pressure (ICP) threatening with brainstem herniation, wide
bilateral craniectomy was carried out, followed by dura opening and
subsequent formation of a vascular tunnel in a simple way--using
hemostatic sponge cushions--around the main cortical veins at the
entering points of the herniated area. The maintenance of vessel patency
prevents the herniated brain segment from venous congestion, i.e., from
further swelling and necrosis. RESULTS: Twenty operations with traumatic
brain edema were performed using this vascular tunnel method. All
patients were exposed to surgery in the state of coma. One operation was
performed after tumor removal. The results were promising in comparison
with the well-known surgical or conservative treatment. DISCUSSION:
Applying very strict selection criteria (Glasgow coma scale < 6, signs
of severe edema on CT, or intracranial pressure permanently > or = 30
mmHg) in this small series of patients with severe brain injury, good
results were achieved using the new operative technique. In case of
postoperative edema after tumor ablation, it also showed promising
results.
6
UI - 11838818
AU - Strowitzki M
TI -
Interactive magnetic resonance imaging.
SO - J Neurosurg 2002 Feb;96(2):383-5
7
UI - 11857005
AU - Swanson KR; Alvord EC Jr; Murray JD
TI -
Virtual brain tumours (gliomas) enhance the reality of medical imaging
and highlight inadequacies of current therapy.
SO - Br J Cancer 2002 Jan 7;86(1):14-8
AD - Department of Applied Mathematics, Box 352420, University of Washington,
Seattle, Washington WA 98195, USA. swanson@amath.washington.edu
Gliomas are brain tumours that differ from most other cancers by their
diffuse invasion of the surrounding normal tissue and their notorious
recurrence following all forms of therapy. We have developed a
mathematical model to quantify the spatio-temporal growth and invasion
of gliomas in three dimensions throughout a virtual human brain. The
model quantifies the extent of tumorous invasion of individual gliomas
in three-dimensions to a degree beyond the limits of present medical
imaging, including even microscopy, and makes clear why current
therapies based on existing imaging techniques are inadequate and cannot
be otherwise without other methods for detecting tumour cells in the
brain. The model's estimate of the extent of tumourous invasion beyond
that defined by standard medical imaging can be useful in more
accurately planning therapy regimes as well as predicting sites of
potential recurrence without waiting for reemergence on follow-up
imaging.
8
UI - 11857311
AU - Perret AG; Duthel R; Fotso MJ; Brunon J; Mosnier JF
TI -
Stromelysin-3 is expressed by aggressive meningiomas.
SO - Cancer 2002 Feb 1;94(3):765-72
AD - Department of Pathology, Hopital de Bellevue, Centre Hospitalier
Universitaire de Saint-Etienne, Saint-Etienne, France.
BACKGROUND: Stromelysin-3 (ST3) that belongs to the metalloproteinase
family is proposed to play a role in tumor invasion. The purpose of this
work was to study the variation of ST3 expression in meningiomas.
METHODS: Twenty atypical meningiomas were retrieved from the Pathology
Department's files at Hopital de Bellevue, Saint-Etienne, France. They
were compared with 20 benign meningiomas randomly selected from the same
file. The tumors were classified using standard histologic criteria.
Frozen sections of the tumors were immunostained for ST3 and MIB-1 to
evaluate the proliferative activity of tumor cells. RESULTS: The study
included 5 fibrous meningiomas, 10 transitional meningiomas, 20
syncitial meningiomas, 2 secretory meningiomas, 2 microcystic
meningiomas, and 1 angiomatous meningioma. Stromelysin-3 was expressed
within the stromal and neoplastic cells of only 1 benign meningioma and
13 atypical meningiomas. The MIB-1 proliferation index was significantly
higher in the meningiomas expressing ST3 (Student t test: P < 0.001).
The invasion of bone, muscle, and brain by meningiomas as well the
recurrence were statistically correlated with their ST3 expression
(Kruskal-Wallis nonparametric correlation test, P = 0.001 and P = 0.008,
respectively). CONCLUSIONS: Stromelysin-3 might play an important role
in the invasiveness of meningiomas. Therefore, considering, ST3 in
association with evaluation of the MIB-1 proliferating index may be an
useful tool to assess the behavior of meningiomas. Copyright 2002
American Cancer Society. DOI 10.1002/cncr.10270
9
UI - 11808129
AU - Kazumoto K
TI -
[Brain tumor]
SO - Nippon Rinsho 2001 Nov;59 Suppl 7():257-66
AD - Neurosurgery Clinic, Saitama Cancer Center.
10
UI - 11850836
AU - Vortmeyer AO; Huang SC; Pack SD; Koch CA; Lubensky IA; Oldfield EH;
TI -
Zhuang Z
Somatic point mutation of the wild-type allele detected in tumors of
patients with VHL germline deletion.
SO - Oncogene 2002 Feb 14;21(8):1167-70
AD - Molecular Pathogenesis Unit, Surgical Neurology Branch, National
Institute of Neurological Disorders and Stroke, Building 10, Room 5D37,
Bethesda, MD 20892, USA.
The majority of patients with Von Hippel-Lindau (VHL) disease are
affected by a VHL germline mutation involving one copy of the VHL gene.
Loss of heterozygosity of the second VHL allele can be consistently
demonstrated in tumor tissue from these patients, suggesting that
allelic deletion is a very early or even initiating event for
tumorigenesis. Approximately 20% of VHL disease patients, however,
exhibit germline deletion of one entire copy or at least a substantial
part of the VHL gene. To investigate the nature of the "second genetic
hit" in this patient population, we analysed two renal cell carcinomas
and one CNS hemangioblastoma from three unrelated patients for genetic
changes of the second copy of the VHL gene. All three tumors showed
retention of one VHL allele by FISH. Single-strand conformation
polymorphism and mutation analysis of microdissected tumor DNA revealed
somatic point mutations of the wild-type VHL copies in each of the three
tumors. The results indicate that the "two hit model" is equally
applicable to patients with VHL germline mutation and VHL germline
deletion. In contrast to tumors from patients with VHL germline
mutation, however, point mutations of the wild-type allele can be
detected in tumors from patients with VHL germline deletion.
11
UI - 11054516
AU - Do V; Gebski V; Barton MB
TI -
The effect of waiting for radiotherapy for grade III/IV gliomas.
SO - Radiother Oncol 2000 Nov;57(2):131-6
AD - Division of Radiation Oncology, Westmead Hospital, Westmead, NSW 2145,
Australia.
AIM: To determine the effect of waiting time for radiotherapy on the
overall survival of patients with high-grade gliomas. METHODS: We
examined records of patients with grade III/IV gliomas who were referred
to radiotherapy after surgery or biopsy - ECOG <3, any age, radical
intent or palliative intent with dose >50 Gy, no interstitial or
radiosurgery boost. Waiting time was defined in two ways, time from
biopsy to radiotherapy and time from presentation to radiotherapy
department to start of radiotherapy. RESULTS: There were 182 patients in
the study having a median survival of 8.5 months, with a median follow
up of 10.5 months. The group comprised of 63 (35%) grade III and 119
(65%) grade IV gliomas. Median times and ranges from biopsy and
presentation to treatment were 26 days (4-78 days) and 15 days (1-62
days), respectively. The median dose was 60 Gy in a median of 30
fractions over a median of 46 days. Tumour progression before and during
radiotherapy occurred in seven patients (4%) and 19 patients (11%),
respectively. One hundred and seventy-nine patients died of disease. The
seven patients whose tumour progressed before radiotherapy were excluded
from the analysis of prognostic variables. In a multivariate analysis
the variables that were significantly associated with worse survival
were older age, reduced dose and prolonged waiting time from
presentation. The risk of death increased by 2% for each day of waiting
for radiotherapy. CONCLUSION: The study showed longer waiting time from
presentation at radiotherapy department to treatment to be a significant
predictor of overall survival for patients with high-grade glioma.
12
UI - 11603814
AU - Przkora R; Meyer-Puttlitz B; Schmitt O; Berthold F; Nothen M; Krauss J;
TI -
Tonn JC; von Deimling A; Wiestler OD; Pietsch T
Analysis of the TSC2 gene in human medulloblastoma.
SO - Acta Neuropathol (Berl) 2001 Oct;102(4):380-4
AD - Department of Neuropathology, University of Bonn Medical Center,
Germany.
Medulloblastoma (MB) represents the most frequent malignant brain tumor
of childhood. Recent studies have shown that deregulation of
developmental control genes may play an important role in its
pathogenesis. Tuberous sclerosis is associated with hamartomas and
cortical tubers, consisting of both glial and neuronal cellular
components. MBs can also show markers of these lineages, raising the
question of the potential involvement of TSC genes in these malignant
tumors. Here we investigated tuberous sclerosis 2 (TSC2), one of the two
genes responsible for tuberous sclerosis, in sporadic MBs. We analyzed
MBs for allelic losses at the TSC2 locus and for the frequency of a
polymorphism first described in gangliogliomas. Sixty-eight MBs were
examined for this polymorphism located in intron 4, 3 base pairs 5' to
the first coding nucleotide of exon 5. The distribution of the alleles
was significantly different in MBs as compared to 208 control samples,
(P=0.0017, Chi-square test). In MBs the frequency of the rare allele
(A2) was 0.184 (18.4%), whereas in the control group it occurred in a
frequency of 8.7%. Microsatellite analysis of the TSC2 region in 50
tumors did not identify allelic losses. TSC2 mRNA transcript was
detectable via reverse transcription-PCR in all tumors as well as in
normal cerebellum. Northern blot analysis of an MB cell line homozygous
for the rare allele of the polymorphism and two other cell lines
homozygous for the frequent allele revealed normal splicing patterns and
normal expression levels of the TSC2 transcript. These findings may
indicate that the presence of the rare TSC2 allele is associated with a
predisposition for the development of MBs.
13
UI - 11760795
AU - Erdem E; Zimmerman RA; Haselgrove JC; Bilaniuk LT; Hunter JV
TI -
Diffusion-weighted imaging and fluid attenuated inversion recovery
imaging in the evaluation of primitive neuroectodermal tumors.
SO - Neuroradiology 2001 Nov;43(11):927-33
AD - Department of Radiology, The Children's Hospital of Philadelphia, PA
19104, USA.
The aim of our study was to determine whether fluid-attenuated inversion
recovery (FLAIR) imaging and diffusion-weighted imaging (DWI) would be
helpful in characterizing primitive neuroectodermal tumors (PNET) from
other pediatric brain tumors. We expected that the compact cellular
nature and the relatively small extracellular space of this tumor would
affect the signal intensity on both pulse sequences relative to the more
sparsely cellular glial tumors that have larger extracellular spaces.
Eighteen pediatric patients with PNET were examined on a 1.5 T MRI with
routine imaging plus FLAIR and compared with 28 patients with nonPNET.
DWI was also performed in 7 PNET and 18 non-PNET. Seventyeight percent
of PNET were isointense to gray matter on FLAIR while 82% of non-PNET
were hyperintense and only one was isointense (3%). Diffusion was
abnormally restricted in all 7 PNET examined (100%) but was restricted
in non-PNET in only 1 out of 18 (6%) patients who had DWI. The
differences in the histologic architecture between PNET and non-PNET are
reflected in both FLAIR imaging and in DWI.
14
UI - 11760804
AU - Brunereau L; Leveque C; Bertrand P; Tranquart E; Cordoliani Y; Rouleau
TI -
P; Labauge P
Familial form of cerebral cavernous malformations: evaluation of
gradient-spin-echo (GRASE) imaging in lesion detection and
characterization at 1.5 T.
SO - Neuroradiology 2001 Nov;43(11):973-9
AD - Service de Radiologie Adultes Bretonneau, CHRU Tours, France.
l.brunereau@bretonneau.chu-tours.fr
The purpose of this study was to evaluate the turbo gradient-spin-echo
sequence (GRASE) in the MR assessment of the familial form of cerebral
cavernous malformations (CCM). Twenty-one patients (15 male, six female)
aged from 21 to 68 years (mean = 42.2 years) were prospectively examined
with cerebral MR imaging, including T2-weighted turbo gradient-spin-echo
(TGSE), turbo spin-echo (TSE) and gradient-echo (GRE) sequences. All
sequences were performed in the same plane, the same matrix and the same
field of view and were analyzed for signal-to-noise ratio (SNR),
contrast-to-noise ratio (CNR), susceptibility effects, number of CCM,
size of CCM and signal of CCM. It was found that SNR and CNR in the TGSE
sequence were significantly inferior to those in both TSE and GRE
sequences. TGSE and TSE sequences were significantly less prone to
susceptibility effects than the GRE sequence. The sensitivity of TGSE
and TSE sequences in detecting CCM was significantly lower than that of
the GRE sequence. TGSE and TSE sequences provided comparable information
about CCM size and signal. It was concluded that GRASE imaging was less
sensitive than the GRE sequence in the detection of CCM and provided
information similar to that yielded by the TSE sequence in the
characterization of lesions, but with a higher number of artifacts.
GRASE imaging cannot therefore replace TSE or GRE sequences in the MR
evaluation of the familial form of CCM.
15
UI - 11826027
AU - Shinar Y; Ben-Zeev B; Brand N; Lahat H; Gross-Zur V; MacGregor D; Bahan
TI -
T; Kastner DL; Pras E
A common ancestral haplotype in carrier chromosomes from different
ethnic backgrounds in vacuolating megalencephalic leucoencephalopathy
with subcortical cysts.
SO - J Med Genet 2002 Jan;39(1):54-7
16
UI - 11830784
AU - Eisner W; Steude U; Burtscher J; Bise K
TI -
Surgery of lesions in the motor strip combining a
stereotactically-guided mini-craniotomy with electrophysiological
mapping of the motor cortex.
SO - Minim Invasive Neurosurg 2001 Dec;44(4):230-3
AD - Department of Neurosurgery, Leopold Franzens University, Innsbruck,
Austria. wilhelm.eisner@uklibk.ac.at
The removal of space-occupying lesions in the sensori-motor cortex
carries a considerable risk of postoperative palsy. Therefore
subcortical lesions located in the sensori-motor strip are often
considered to be inoperable. Treatment options are stereotactic biopsy
and radiosurgery beside radiological control examinations without
surgery or surgery with a higher risk of postoperative deficits. The
following article focusses on a combined approach involving a
stereotactically guided and electrophysiologically controlled surgery.
The instruments used (stereotactical system and electric stimulator) are
available in almost every neurosurgical department in the Western and
Eastern world and had been the first navigation systems in the human
brain.
17
UI - 11788993
AU - Hanash SM; Bobek MP; Rickman DS; Williams T; Rouillard JM; Kuick R;
TI -
Puravs E
Integrating cancer genomics and proteomics in the post-genome era.
SO - Proteomics 2002 Jan;2(1):69-75
AD - University of Michigan Medical Center, Ann Arbor, MI 48109-0656, USA.
shanash@umich.edu
The dawn of the post-genome era is leading to extraordinary
opportunities in biomedicine. Our group has embarked on a major effort
to integrate genomics, transcriptomics and proteomics for the profiling
of tumor tissues, an approach we refer to as operomics. Our major goals
are the molecular classification of tumors and the identification of
markers for the early detection of cancer. Molecular analyses of tumors
rely on microdissected tissues, which are simultaneously investigated
for genomic, transcriptomic and proteomic changes. Genomic alterations
in tumor cells being investigated include deletions, amplifications and
methylation changes across the entire genome as well as point mutations
in specific genes. Expression analysis at the RNA level is being
undertaken using oligonucleotide and cDNA based microarrays. An
important aspect of our approach is the large-scale identification and
quantitative analysis of tumor proteins in whole cell lysates as well as
in protein compartments. Protein separation strategies include
two-dimensional polyacrylamide gel electrophoresis and liquid
chromatography. Specific protein subsets, of interest include membrane
proteins, secreted proteins and antigenic proteins as sources of
biomarkers for early detection of cancer. Our current approach is
illustrated with findings stemming from our studies of human gliomas.
18
UI - 11721860
AU - Pitzalis S; Di Russo F
TI -
Spatial anisotropy of saccadic latency in normal subjects and
brain-damaged patients.
SO - Cortex 2001 Sep;37(4):475-92
AD - Department of Psychology, University of Rome La Sapienza, Italy.
In the present study, reaction time of oblique and orthogonal saccades
was investigated in normal subjects and in two groups of patients with
right (RBD) and left (LBD) vascular cerebral lesions and no signs of
spatial neglect. Clear altitudinal effects were present in each group of
subjects: saccadic latencies were longer in the lower than in the upper
part of the visual field for both orthogonal and oblique saccades.
Asymmetry along the horizontal meridian was present only in case of
right hemisphere damage. This supports the view that a lesion in the
right hemisphere causes a greater deficit of visual-spatial processing
than a left hemisphere lesion. A cerebral lesion in the right and/or
left hemisphere produces a general slowing in the saccadic latency and a
general reduction in the accuracy of saccades with respect to normal
subjects performance. Further, it seems that making saccades in oblique
direction reduces the general saccade efficiency.
19
UI - 11807556
AU - Pomeroy SL; Tamayo P; Gaasenbeek M; Sturla LM; Angelo M; McLaughlin ME;
TI -
Kim JY; Goumnerova LC; Black PM; Lau C; Allen JC; Zagzag D; Olson JM;
Curran T; Wetmore C; Biegel JA; Poggio T; Mukherjee S; Rifkin R;
Califano A; Stolovitzky G; Louis DN; Mesirov JP; Lander ES; Golub TR
Prediction of central nervous system embryonal tumour outcome based on
gene expression.
SO - Nature 2002 Jan 24;415(6870):436-42
AD - Division of Neuroscience, Department of Neurology, Massachusetts General
Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
scott.pomeroy@tch.harvard.edu
Embryonal tumours of the central nervous system (CNS) represent a
heterogeneous group of tumours about which little is known biologically,
and whose diagnosis, on the basis of morphologic appearance alone, is
controversial. Medulloblastomas, for example, are the most common
malignant brain tumour of childhood, but their pathogenesis is unknown,
their relationship to other embryonal CNS tumours is debated, and
patients' response to therapy is difficult to predict. We approached
these problems by developing a classification system based on DNA
microarray gene expression data derived from 99 patient samples. Here we
demonstrate that medulloblastomas are molecularly distinct from other
brain tumours including primitive neuroectodermal tumours (PNETs),
atypical teratoid/rhabdoid tumours (AT/RTs) and malignant gliomas.
Previously unrecognized evidence supporting the derivation of
medulloblastomas from cerebellar granule cells through activation of the
Sonic Hedgehog (SHH) pathway was also revealed. We show further that the
clinical outcome of children with medulloblastomas is highly predictable
on the basis of the gene expression profiles of their tumours at
diagnosis.
20
UI - 11857353
AU - Castino R; Pace D; Demoz M; Gargiulo M; Ariatta C; Raiteri E; Isidoro C
TI -
Lysosomal proteases as potential targets for the induction of apoptotic
cell death in human neuroblastomas.
SO - Int J Cancer 2002 Feb 20;97(6):775-9
AD - Dipartimento di Scienze Mediche, Laboratorio di Patologia Molecolare,
Universita A. Avogadro, Novara, Italy.
Neuroblastoma is the most common type of cancer in infants. In children
this tumor is particularly aggressive; despite various new therapeutic
approaches, it is associated with poor prognosis. Given the importance
of endosomal-lysosomal proteolysis in cellular metabolism, we
hypothesized that inhibition of lysosomal protease would impact
negatively on neuroblastoma cell survival. Treatment with E-64 or
CA074Me (2 specific inhibitors of cathepsin B) or with pepstatin A (a
specific inhibitor of cathepsin D) was cytotoxic for 2 neuroblastoma
cell lines having different degrees of malignancy. Cell death was
associated with condensation and fragmentation of chromatin and
externalization of plasma membrane phosphatidylserine, 2 hallmarks of
apoptosis. Concomitant inhibition of the caspase cascade protected
neuroblastoma cells from cathepsin inhibitor-induced cytotoxicity. These
data indicate that prolonged inhibition of the lysosomal proteolytic
pathway is incompatible with cell survival, leading to apoptosis of
neuroblastoma cells, and that the cathepsin-mediated and
caspase-mediated proteolytic systems are connected and cooperate in the
regulation of such an event. Since modern antitumor chemotherapy is
aimed at restoring the normal rate of apoptosis in neoplastic tissues,
the demonstration that endosomal-lysosomal cathepsins are involved in
this process may constitute a basis for novel strategies that include
cathepsin inhibitors in the therapeutic regimen. Copyright 2001
Wiley-Liss, Inc.
21
UI - 11857361
AU - Paunu N; Pukkala E; Laippala P; Sankila R; Isola J; Miettinen H; Simola
TI -
KO; Helen P; Helin H; Haapasalo H
Cancer incidence in families with multiple glioma patients.
SO - Int J Cancer 2002 Feb 20;97(6):819-22
AD - Department of Pathology, Tampere University Hospital, Tampere, Finland.
Twenty-four Finnish families with 2 or more glioma patients were
identified through questionnaires sent to 369 consecutive glioma
patients receiving surgery at Tampere University Hospital during
1983-94. To explore whether unusual cancer susceptibility is involved,
the cancer risk of 2,664 family members was estimated using
population-based data from the Finnish Cancer Registry. Among the total
cohort of relatives, 88 cancers were observed during 1953-97. The
overall cancer risk among 12 families with juvenile onset gliomas was
significantly decreased (standardized incidence ratio [SIR] 0.6, 95%
confidence interval [CI]: 0.4-0.9). Among 12 families with adult onset
gliomas, the overall cancer risk was equal to that of the reference
population (SIR 1.1, 95% CI: 0.8-1.4) whereas the risk of skin melanoma
(SIR 4.0, 95% CI: 1.5-8.8) and meningioma (SIR 5.5, 95% CI: 1.1-16) were
significantly increased. Several other tumors, including those
associated with neurofibromatosis 1 and 2, tuberous sclerosis and
Li-Fraumeni and Turcot syndromes were surveyed, but no elevated risks
were observed. In conclusion, the presence of meningiomas and skin
melanomas in glioma families may indicate a novel association as a
cancer susceptibility trait. Copyright 2001 Wiley-Liss, Inc.
22
UI - 11784893
AU - Pereira RA; Koifman S
TI -
[Association between dietary factors and brain tumors in adults: a
review]
SO - Cad Saude Publica 2001 Nov-Dec;17(6):1313-34
AD - Instituto de Nutricao Josue de Castro, Centro de Ciencias da Saude,
Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-590,
Brasil. rpereira@nitnet.com.br
This paper reviews the scientific literature published from 1986 to 1999
assessing the relationship between dietary factors and brain tumors in
adults. The work aimed to describe the estimated associations and to
discuss methodological aspects that might influence the results. The
studies generally appear to show a moderate association between dietary
factors and brain tumors. There is evidence that N-nitroso compounds
enhance the risk of developing such tumors and that consumption of
fruits and vegetables can inhibit them. Use of proxies in most of the
studies may have introduced bias, thereby contributing to some
inconsistent observations. Epidemiological research on diet and brain
tumors should consider other components of food besides N-nitroso
compounds. It is important to carefully assess exposure periods and to
prevent bias related to control selection and recall.
23
UI - 11678426
AU - Izumoto S; Ohnishi T; Kanemura H; Arita N; Maruno M; Moriuchi T; Suzuki
TI -
S; Yoshimine T
PTEN mutations in malignant gliomas and their relation with meningeal
gliomatosis.
SO - J Neurooncol 2001 May;53(1):21-6
AD - Department of Neurosurgery, Osaka University Graduate School of
Medicine, Suita, Japan. sizumoto@nsurg.med.osaka-u.ac.jp
A putative tumor suppressor, the PTEN gene at chromosome 10q23. was
identified and found to be mutated in many different human tumors. PTEN
was recently found to be also involved in focal cell adhesion and cell
migration. To identify the role of PTEN gene in malignant gliomas. we
used PCR-SSCP and direct sequencing methods to examine 44 malignant
gliomas comprising 29 cases without and 15 cases with meningeal
gliomatosis. In malignant gliomas without meningeal gliomatosis, 2/29
(7%) of the cases showed alteration of the PTEN gene. In contrast, 5/15
(33%) of malignant gliomas with meningeal gliomatosis cases showed this
alteration. These findings indicate that PTEN gene mutation contributes
not only to the neoplastic evolution in gliomas but also to the
meningeal dissemination of glioma cells.
24
UI - 11678428
AU - Korones DN; Butterfield R; Meyers SP; Constine LS
TI -
The role of surveillance magnetic resonance imaging (MRI) scanning in
detecting recurrent brain tumors in asymptomatic children.
SO - J Neurooncol 2001 May;53(1):33-8
AD - Department of Pediatrics, University of Rochester School of Medicine and
Dentistry, New York, USA. david_korones@urmc.rochester.edu
BACKGROUND: There is controversy regarding the utility of routine
surveillance scanning for asymptomatic children with brain tumors.
Although the role of CT or magnetic resonance imaging (MRI) scanning in
this setting has been examined in several studies, none have focused on
children followed exclusively by MRI. The purpose of this study was to
determine how often recurrent brain tumors are detected by routine MRI
surveillance in asymptomatic children. METHODS: The medical records of
all children with brain tumors treated at Children's Hospital at Strong
from 1990-1999 were reviewed. Recurrence was defined as an increase in
size of the tumor on MRI scan. Astrocytomas and gangliogliomas were
classified as low-grade tumors; high-grade astrocytomas,
medulloblastomas, and ependymomas were classified as high-grade tumors.
RESULTS: Of the 112 evaluable children with brain tumors during this
time period, 46 (41%) suffered an MRI-documented recurrence. Of these 46
patients, 13 (28%) had low-grade tumors and 33 (72%) had high-grade
tumors. Twenty-seven of the 46 recurrences (59%) occurred in
asymptomatic children. Ten of the 13 children (77%) with recurrent
low-grade tumors were asymptomatic compared to 17 of 33 children (52%)
with recurrent high-grade tumors (p = 0.18). The median survival from
time of recurrence for the symptomatic children was seven months, while
the median survival from time of recurrence for the asymptomatic
children has not yet been reached (p = 0.025). When the analysis was
confined to children with high-grade tumors, there was no difference in
median survival from the time of recurrence for symptomatic versus
asymptomatic children (5 mo. versus 7 mo.) (p = 0.25). The frequency of
detection of recurrences by surveillance scanning in asymptomatic
children was 4.2% (one recurrence detected per 24 surveillence MRI
scans). CONCLUSION: The majority of recurrent brain tumors are detected
by MRI surveillence in asymptomatic children. However, asymptomatic
recurrences were detected in only a small proportion of surveillance
scans and had no impact on survival in children with high-grade tumors.
25
UI - 11678430
AU - Diete S; Treuheit T; Dietzmann K; Schmidt U; Wallesch CW
TI -
Sex differences in length of survival with malignant astrocytoma, but
not with glioblastoma.
SO - J Neurooncol 2001 May;53(1):47-9
AD - Department of Neurology, Otto-von-Guericke-University, Magdeburg,
Germany.
In a retrospective analysis based on a malignant glioma databank, we
describe effects of age, sex and diagnosis upon survival in patients
with malignant cerebral glioma with a pre-treatment Karnofsky-index of
60 or more. All patients had been treated with 55-60Gy radiotherapy and
nitrosurea-based adjuvant chemotherapy. We found an age-dependent sex
effect upon survival in grade III astrocytoma patients, but not with
glioblastoma.
26
UI - 11786566
AU - Samnick S; Bader JB; Hellwig D; Moringlane JR; Alexander C; Romeike BF;
TI -
Feiden W; Kirsch CM
Clinical value of iodine-123-alpha-methyl-L-tyrosine single-photon
emission tomography in the differential diagnosis of recurrent brain
tumor in patients pretreated for glioma at follow-up.
SO - J Clin Oncol 2002 Jan 15;20(2):396-404
AD - Department of Nuclear Medicine, Saarland University Medical Center,
Homburg/Saar, Germany. rassam@med-rz.uni-saarland.de
PURPOSE: To assess the clinical potential of
iodine-123-alpha-methyl-L-tyrosine (IMT) and single-photon emission
tomography (SPET) in the differential diagnosis of recurrences in
patients pretreated for gliomas at follow-up. PATIENTS AND METHODS:
Seventy-eight patients were examined after primary therapy over 36
months. Histopathologic diagnoses of all patients was known at first
treatment; magnetic resonance and/or computed tomography examination was
performed in addition to IMT-SPET. Cerebral SPET images were acquired 20
minutes after intravenous application of 190 +/- 10 MBq of IMT. SPET
images were classified as positive or negative for recurrent tumor
visually and by calculating the ratios between tracer accumulation in
the lesion and the unaffected contralateral regions of reference using
region of interest. Final diagnoses were based on prospective
clinicopathologic findings obtained independently of IMT-SPET. RESULTS:
IMT-SPET detected all high-grade recurrent gliomas (grade 4;
sensitivity, 100%). A difference could be demonstrated in grade 2 and 3
recurrences (sensitivity, 84% and 92%, respectively). Moreover, benign
posttherapeutic lesions (postoperative scars, radiation necrosis) were
correctly diagnosed as negative for tumor recurrence. In general, IMT
uptake in grade 2 (1.45 +/- 0.24) was significantly lower than that in
grades 3 (1.70 +/- 0.41) and 4 (1.88 +/- 0.32). However, it was
difficult to evaluate tumor grade only from the IMT accumulation in
individual cases. CONCLUSION: IMT-SPET seems highly useful for detecting
and delineating recurrent gliomas and differentiating between benign
posttherapeutic lesions and malignant tumor tissue. It may be a valuable
clinical tool to diagnose recurrences in patients pretreated for gliomas
at follow-up. However, it showed limitations in determining histologic
tumor grade.
27
UI - 11844831
AU - Chakravarti A; Noll E; Black PM; Finkelstein DF; Finkelstein DM; Dyson
TI -
NJ; Loeffler JS
Quantitatively determined survivin expression levels are of prognostic
value in human gliomas.
SO - J Clin Oncol 2002 Feb 15;20(4):1063-8
AD - Department of Radiation Oncology, Massachusetts General Hospital Cancer
Center, Boston, MA 02129, USA. achakravarti@partners.org
PURPOSE: Survivin is a novel antiapoptotic gene that has been recently
cloned and characterized. Its expression has been found to be of
prognostic significance in several tumor types. This is the first study
on the prognostic significance of survivin expression in human gliomas.
MATERIALS AND METHODS: We used quantitative Western blot analysis with
densitometry to determine survivin protein expression levels in 92
glioma cases for which frozen tissue was available for analysis.
Survivin positivity and expression levels were correlated with
histopathologic features of the tumors, apoptosis (as measured by
cleaved, or activated, caspase 3 levels), and clinical outcome. RESULTS:
Survivin expression has clear prognostic value in human gliomas.
Patients with detectable survivin expression had significantly shorter
overall survival times (P <.0001) compared with those without detectable
expression when all glioma patients were considered. Although
glioblastoma multiforme (GBM) patients had significantly higher rates of
survivin positivity and higher levels of survivin expression (P <.0001)
than their non-GBM counterparts, the prognostic value of survivin
expression seemed to be independent of histology alone.
Survivin-positive GBM patients had significantly shorter overall
survival times compared with survivin-negative GBM patients (P <.0001).
Likewise, survivin-positive non-GBM patients had shorter survival times
compared with survivin-negative non-GBM patients (P =.029). Furthermore,
increasing levels of survivin expression significantly correlated with
reduced survival times when all glioma patients were considered, and
markedly so for GBM patients (P <.0001). Increasing survivin levels
significantly correlated with reduced expression of cleaved caspase 3,
indicating its association with antiapoptotic activity. CONCLUSION:
Survivin positivity and protein expression levels, as determined
quantitatively, are of significant prognostic value in human gliomas and
seem to be associated with reduced apoptotic capacity of these tumors.
28
UI - 11878577
AU - Stavrou T; Bromley C M; Nicholson H S; Byrne J; Packer R J; Goldstein A
TI -
M; Reaman G H
Prognostic factors and secondary malignancies in childhood
medulloblastoma.
SO - J Pediatr Hematol Oncol 2001 Oct;23(7):431-6
AD - Department of Hematology-Oncology, Children's National Medical Center,
Washington, DC, USA.
PURPOSE: Little is known of the outcome of long-term survivors of
childhood medulloblastoma, one of the most common pediatric
malignancies. To determine the potential for secondary malignancies, a
retrospective outcome evaluation in 88 consecutive cases of childhood
medulloblastoma was performed. PATIENTS AND METHODS: The records of all
patients with childhood medulloblastoma diagnosed at Children's National
Medical Center in Washington, DC from 1969 through 1997 were reviewed.
RESULTS: The median follow-up time was 92 months (range 6-257 months).
Overall survival was 59% at 5 years and 52% at 10 years. Univariate
analysis showed that age at diagnosis, extent of surgical resection,
presence of metastatic disease (M stage), ventriculoperitoneal shunt
placement within 30 days from diagnosis, posterior fossa radiation
therapy dose, and adjuvant chemotherapy significantly affected survival.
Although based on small numbers, the risk of second neoplasms was
significantly increased in this cohort. Multiple basal cell carcinomas
developed in the areas of radiation therapy in two patients; these
patients also had nevoid basal cell carcinoma syndrome (NBCCS)
diagnosed. One other patient died of glioblastoma multiforme 8 years
after treatment of medulloblastoma. A meningioma developed in another
patient 10 years after radiation therapy. CONCLUSION: As survival of
medulloblastoma patients improves, increased surveillance regarding
secondary malignancies is required, especially because radiation-induced
tumors may occur many years after treatment. These two cases of NBCCS
also illustrate the importance of considering the concomitant diagnosis
of NBCCS in young patients with medulloblastoma. In those patients,
alternative therapy should be considered to minimize radiation
therapy-related sequelae.
29
UI - 11826360
AU - Wyatt-Ashmead J; Kleinschmidt-DeMasters B; Mierau GW; Malkin D; Orsini
TI -
E; McGavran L; Foreman NK
Choroid plexus carcinomas and rhabdoid tumors: phenotypic and genotypic
overlap.
SO - Pediatr Dev Pathol 2001 Nov-Dec;4(6):545-9
AD - Pathology Department, The Children's Hospital, 1056 East 19th Avenue
B120, Denver, CO 80218, USA.
Five of six poorly differentiated choroid plexus carcinomas identified
at our institution contained cells displaying a rhabdoid phenotype.
Immunoperoxidase stains showed focal positivity for cytokeratin,
epithelial membrane antigen, glial fibrillary acidic protein, S100, and
vimentin. The MIB-1 proliferative index ranged from 7.0% to 27.1%. All
six tumors were p53 positive. Only the one child with Li-Fraumeni
syndrome had a p53 germline mutation. Electron microscopy verified
choroid plexus differentiation and the co-existence of rhabdoid cells.
Of the five studied, four had deletions of chromosome 22 [three with
monosomy 22 and one with del(22)(q12)]. Thus, there was a phenotypic and
genotypic overlap between choroid plexus carcinomas and rhabdoid tumors.
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