| 1: Br J Cancer.
2005 Jul 11;93(1):152-8. |
|
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mRNA quantification and clinical evaluation of telomerase
reverse transcriptase subunit (hTERT) in intracranial tumours of patients in
the island of Crete.
Yannopoulos
A, Dimitriadis
E, Scorilas
A, Trangas
T, Markakis
E, Talieri
M.
Department of Neurosurgery, University Hospital of Heraclio, Heraclio,
Crete, Greece.
Telomerase is a reverse transcriptase that maintains telomeres by adding
telomeric TTAGGG repeats to the ends of human chromosomes. The aim of this
study was to evaluate quantitatively the mRNA expression of telomerase
catalytic subunit (hTERT) in different types of intracranial tumours in
relation to their histologic pattern and grade and correlate it with
progression-free (PFS) and overall survival (OS) of patients. Human
telomerase reverse transcriptase mRNA levels were estimated by the use of
real time RT-PCR in 68 samples of intracranial tumours. It revealed
statistical correlation between hTERT mRNA expression levels and the grade
of the tumours (P<0.001). Patients having negative expression of hTERT
mRNA had statistically longer PFS (P=0.031) and OS (P=0.047). Cox univariate
regression analysis revealed that hTERT mRNA-positive patients had a high
and statistically significant risk of relapse (hazard ratio (HR) of 2.24 and
P=0.038). In the Cox multivariate regression model, the levels of hTERT mRNA
were adjusted for tumour grade and patients age, and since there was
statistically significant relationship between the levels of hTERT mRNA and
the grade of the tumours (P=0.003 or P=0.006, respectively), hTERT mRNA
levels could not be considered as an independent prognostic factor for PFS
or OS.
PMID: 15986035 [PubMed - indexed for MEDLINE]
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| 2: Br J Cancer.
2005 Jul 11;93(1):124-30. |
|
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Mutations in Rb1 pathway-related genes are associated
with poor prognosis in anaplastic astrocytomas.
Backlund
LM, Nilsson
BR, Liu
L, Ichimura
K, Collins
VP.
Department of Oncology-Pathology, Karolinska Institutet, Karolinska
University Hospital, SE-171 76 Stockholm, Sweden.
Magnus.Backlund@onkpat.ki.se
Anaplastic astrocytoma (AA, WHO grade III) is, second to Glioblastoma, the
most common and most malignant type of adult CNS tumour. Since survival for
patients with AA varies markedly and there are no known useful prognostic or
therapy response indicators, the primary purpose of this study was to
examine whether knowledge of the known genetic abnormalities found in AA had
any clinical value. The survival data on 37 carefully sampled AA was
correlated with the results of a detailed analysis of the status of nine
genes known to be involved in the development of astrocytic tumours. These
included three genes coding for proteins in the p53 pathway (TP53,
p14(ARF)and MDM2), four in the Rb1 pathway (CDKN2A, CDKN2B, RB1 and CDK4)
and PTEN and EGFR. We found that loss of both wild-type copies of any of the
three tumour suppressor genes CDKN2A, CDKN2B and RB1 or gene amplification
of CDK4, disrupting the Rb1 pathway, were associated with shorter survival
(P=0.009). This association was consistent in multivariate analysis,
including adjustment for age (P=0.013). The findings suggest that analysis
of the genes coding for Rb1 pathway components provides additional
prognostic information in AA patients receiving conventional therapy.
PMID: 15970925 [PubMed - indexed for MEDLINE]
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| 3: J
Clin Oncol. 2005 Oct 1;23(28):7178-87. |
|
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Phase I trial of temozolomide plus o6-benzylguanine for
patients with recurrent or progressive malignant glioma.
Quinn
JA, Desjardins
A, Weingart
J, Brem
H, Dolan
ME, Delaney
SM, Vredenburgh
J, Rich
J, Friedman
AH, Reardon
DA, Sampson
JH, Pegg
AE, Moschel
RC, Birch
R, McLendon
RE, Provenzale
JM, Gururangan
S, Dancey
JE, Maxwell
J, Tourt-Uhlig
S, Herndon
JE 2nd, Bigner
DD, Friedman
HS.
Brain Tumor Center at Duke, Room 047 Baker House, Trent Dr, S Hospital,
Durham, NC 27710; e-mail: quinn008@mc.duke.edu.
PURPOSE We conducted a two-phase clinical trial in patients with progressive
malignant glioma (MG). The first phase of this trial was designed to
determine the dose of O(6)-BG effective in producing complete depletion of
tumor AGT activity for 48 hours. The second phase of the trial was designed
to define the maximum tolerated dose (MTD) of a single dose of temozolomide
when combined with O(6)-BG. In addition, plasma concentrations of O(6)-BG
and O(6)-benzyl-8-oxoguanine were evaluated after O(6)-BG. PATIENTS AND
METHODS For our first phase of the clinical trial, patients were scheduled
to undergo craniotomy for AGT determination after receiving a 1-hour O(6)-BG
infusion at 120 mg/m(2) followed by a continuous infusion at an initial dose
of 30 mg/m(2)/d for 48 hours. The dose of the continuous infusion of O(6)-BG
escalated until tumor AGT was depleted. Once the O(6)-BG dose was
established a separate group of patients was enrolled in the second phase of
clinical trial, in which temozolomide, administered as a single dose at the
end of the 1-hour O(6)-BG infusion, was escalated until the MTD was
determined. Results The O(6)-BG dose found to be effective in depleting
tumor AGT activity at 48 hours was an IV bolus of 120 mg/m(2) over 1 hour
followed by a continuous infusion of 30 mg/m(2)/d for 48 hours. On enrolling
38 patients in six dose levels of temozolomide, the MTD was established at
472 mg/m(2) with dose-limiting toxicities limited to myelosuppression.
CONCLUSION This study provides the foundation for a phase II trial of
O(6)-BG plus temozolomide in temozolomide-resistant MG.
PMID: 16192602 [PubMed - in process]
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| 4: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
|
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Journal of Neuro-Oncology: Childhood Brain Tumors.
Packer
RJ.
Center for Neuroscience and Behavioral Medicine Chair, Department of
Neurology Children's National Medical Center, Professor of Neurology and
Pediatrics,, The George Washington University, Professor of Neurology,
Georgetown University, Professor in Neurosurgery, University of Virginia,
Charlottesville, VA, USA, rpacker@cnmc.org.
PMID: 16195808 [PubMed - as supplied by publisher]
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| 5: J Neurooncol.
2005 Sep 9; [Epub ahead of print] |
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Progress and challenges in childhood brain tumors.
Packer
RJ.
Center for Neuroscience and Behavioral Medicine, USA.
Although many challenges lie ahead, there has been definite progress made in
the management of childhood brain tumors. Some of these advances have
increased progression-free and overall survival. Other advances, while not
improving survival, have resulted in a better quality of life for long-term
survivors. Probably the best example of progress is manifest in the outcome
of children with medulloblastoma. Seventy percent, and in some subsets as
high as 80% of children with this disease can be expected to be cured,
compared to approximately 50% three decades ago. This improvement in disease
control has been associated with a reduction in the dose of radiotherapy for
many patients and possibly an improved quality of survival. For other tumor
types, especially brain stem gliomas, there has been little progress made. A
primary challenge in the years ahead will be how to integrate biologic
discoveries into the care of children for brain tumors, with the hope that
molecular biologically based therapy will be more effective and improve the
quality of life for survivors.
PMID: 16195807 [PubMed - as supplied by publisher]
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| 6: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
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Neuroradiology of childhood brain tumors: new challenges.
Vezina
LG.
Children's National Medical Center, Radialogy and Pediatrics, 111 Nichigan
Avenue NW, Washington, DC, 20010-2970, USA, mbadejo@yahoo.com.
PMID: 16195806 [PubMed - as supplied by publisher]
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| 7: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
|
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The treatment of high grade gliomas and diffuse intrinsic
pontine tumors of childhood and adolescence: a historical - and futuristic -
perspective.
Finlay
JL, Zacharoulis
S.
The Neural Tumors Program, Childrens Center for Cancer and Blood Diseases,
Childrens Hospital Los Angeles, USA.
Pediatric high grade gliomas represent a heterogeneous group of tumors with
poor prognoses despite the use of multimodal treatment. Very little progress
has been made over the past decades in identifying efficacious therapeutic
modalities against both high grade gliomas and diffuse brainstem gliomas in
children. The degree of surgical resection is the most important clinical
prognostic factor for children with high grade gliomas, and a complete
resection should be attempted whenever feasible. The role of radiation
therapy in the treatment of older children with high grade gliomas and
diffuse brain stem gliomas is undisputed; however the benefit of using
radiation for patients less than 6 years of age (with high grade gliomas)
might be questionable. Despite the absence of solid evidence to support its
use, chemotherapy is routinely used against these tumors. Currently
temozolomide is being investigated due to its activity in adult trials and
based on preliminary data regarding recurrent disease. A small subgroup of
patients can be successfully treated with high dose chemotherapy followed by
autologous stem cell rescue. Early trials using this modality in the past
had been associated with high morbidity and mortality. High dose
chemotherapy with autologous stem cell rescue in selected patients with
minimal residual disease, angiogenesis inhibitors, radiosensitizers and
other biological modifiers are being currently investigated in phase I/II
trials.
PMID: 16195805 [PubMed - as supplied by publisher]
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| 8: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
|
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Pediatric high-grade glioma: molecular genetic clues for
innovative therapeutic approaches.
Rood
BR, Macdonald
TJ.
Division of Hematology/Oncology, Center for Cancer and Immunology Research,
Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC,
20010, USA, Brood@cnmc.org.
High grade glioma remains the most intractable childhood tumor of the
central nervous system. The molecular genetics of childhood high grade
glioma remain largely unknown in comparison to that of their adult
counterparts. In an era of molecularly targeted therapies, this dearth of
knowledge will present particular challenges to those who must design and
implement the next generation of therapeutic trials with these new agents.
In this review, we discuss the current understanding of the molecular
genetics of childhood high grade glioma and compare/contrast it to that of
the adult tumors bearing the same classification for the purpose of
beginning to identify the most promising therapeutic targets.
PMID: 16195804 [PubMed - as supplied by publisher]
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| 9: J Neurooncol.
2005 Sep 12; [Epub ahead of print] |
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Molecular biology of medulloblastoma: will it ever make a
difference to clinical management?
Gilbertson
RJ, Gajjar
A.
Departments of Developmental Neurobiology, St. Jude Children's Research
Hospital, 332 North Lauderdale St., Memphis, TN, 38105, USA.
Over the last 10 years approximately 750 children with medulloblastoma have
been treated on consortia based clinical trials at an estimated cost of over
$150 million. Despite this enormous effort, no meaningful molecular data has
been generated that will inform the next generation of clinical studies. It
is imperative that the neuro-oncology community give greater priority to
studies of medulloblastoma molecular biology: unless we do this our patients
will face a bleak future in which there is no accurate disease-risk
stratification tool and no effective new treatments. We review some of the
reasons we have failed to translate knowledge of medulloblastoma disease
biology to the clinic and look forward to the next generation of clinical
and molecular studies that are seeking to correct this.
PMID: 16195803 [PubMed - as supplied by publisher]
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| 10: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
|
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The therapy of infantile malignant brain tumors: current
status?
Kalifa
C, Grill
J.
Pediatric Department, Institut Gustave Roussy, 39 rue Camille Desmoulins,
94805, Villejuif cedex, France, kalifa@igr.fr.
PMID: 16195802 [PubMed - as supplied by publisher]
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| 11: J Neurooncol.
2005 Sep 20; [Epub ahead of print] |
|
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Considerations on the Role of Chemotherapy and Modern
Radiotherapy in the Treatment of Childhood Low Grade Glioma.
Perilongo
G.
Neuro-oncology Program, Division of Haematology-Oncology, Department of
Pediatrics - University Hospital of Padua, Via Giustiniani 3, 35128, Padua,
Italy, perilongo@pediatria.unipd.it.
The treatment of childhood low grade glioma (LGG), if not amenable to
complete resection, quite often is a relevant clinical challenge. LGG in
many instances are indeed slow growing tumors, which, if not controlled, can
cause severe morbidity and ultimately jeopardize life. Most of the time
children bearing an unresectable LGG can be considered affected by a chronic
disease, deserving protracted cures. The treatment philosophy, which has
dictated the treatment of malignant cancers, has also inspired the
therapeutic concepts for managing childhood LGG. However, it is getting more
and more evident that different strategies are needed for them. LGG
represent a highly heterogeneous group of neoplasm and comprehensive
treatment concepts rarely meet the individual patient's needs. After more
than 20 years of clinical research it can be stated with confidence that for
unresectable, progressive LGG, chemotherapy (CT) represents an effective
treatment modality. It delays tumor growth and postpones the use of
radiotherapy (RT), thus sparing the deleterious effects of irradiation on a
developing brain. However, CT rarely cures LGG and definitively obviates the
need of RT or aggressive surgery. Furthermore, little is known on the actual
impact of CT on patients' overall health status. Recent progresses in RT
delivering techniques, which allow reducing the safety margins, are
tempering the concerns related to the use of this treatment modality in
children. This manuscript reviews and expands these data, trying to combine
them in a coherent picture that it is hoped can help in directing future
research in this field.
PMID: 16195800 [PubMed - as supplied by publisher]
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| 12: J Neurooncol.
2005 Sep 20; [Epub ahead of print] |
|
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New delivery approaches for pediatric brain tumors.
Pollack
IF, Keating
R.
Department of Neurosurgery, Children's Hospital of Pittsburgh, University of
Pittsburgh Brain Tumor Center, University of Pittsburgh School of Medicine,
3705 Fifth Avenue, Pittsburgh, PA, 15213, USA, ian.pollack@chp.edu.
For many types of childhood brain tumors, including malignant gliomas,
disease progression at the primary site is the predominant mode of treatment
failure. Accordingly, interest has been directed during the last decade on
exploring strategies to enhance the delivery of therapeutically active
agents into the tumor microenvironment. Two approaches that have been the
focus of considerable attention in the treatment of adult malignant brain
tumors include interstitial administration of chemotherapeutic agents using
time-release polymers and convection-enhanced delivery of immunotoxin
conjugates targeted to receptors overexpressed in brain tumors relative to
normal brain cells. Although it remains to be determined whether these
approaches will lead to meaningful improvements in disease control and
long-term prognosis in children with brain tumors, the encouraging results
from studies in adults support the rationale for further exploring these
strategies in the pediatric setting.
PMID: 16195798 [PubMed - as supplied by publisher]
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| 13: J Neurooncol.
2005 Sep 10; [Epub ahead of print] |
|
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Molecularly Targeted Therapy for Pediatric Brain Tumors.
Warren
KE.
National Cancer Institute, Neuro-Oncology Branch, Bloch Bldg 82, Rm 224,
9030 Old Georgetown Road, 20892-8200, Bethesda, Maryland, USA,
warrenk@mail.nih.gov.
Treatment of pediatric brain tumors remains a challenge because of the
toxicity associated with conventional treatment and the relative resistance
of tumors at the time of recurrence. The traditional approach of
administering cytotoxic agents at the maximum tolerated dose is being
supplanted by the development of molecularly targeted agents aimed at
critical cellular changes that are responsible for the growth and spread of
cancer cells. These agents theoretically should be more specific for tumor
cells and less toxic to normal cells. While the idea of targeted therapy has
generated much excitement in the oncology community, the degree of benefit
to patients with central nervous system (CNS) tumors remains unclear.
Numerous challenges remain in the development of these agents, including
identification of meaningful targets, delivery of agents in sufficient
quantity at the target site, and determination of any biologic response to
these agents. This article discusses the rationale behind several of these
agents and their use in pediatric patients with brain tumors.
PMID: 16195796 [PubMed - as supplied by publisher]...
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| 14: J Neurooncol.
2005 Sep;74(2):219-20. |
|
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Left temporal glioblastoma presenting with the
involvement of selective memory: a case report.
Raffaele
R, Vecchio
I, Alvano
A, Rampello
L.
Department of Neuroscience, University of Catania, Azienda
Policlinico-Neurologia, via S. Sofia, 78, 95125, Catania, Italy,
rampello@unict.it.
PMID: 16193397 [PubMed - in process]
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| 15: J Neurooncol.
2005 Sep;74(2):211-5. |
|
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Results of a Survey of Neurosurgical Practice Patterns
Regarding the Prophylactic use of Anti-Epilepsy Drugs in Patients with Brain
Tumors.
Siomin
V, Angelov
L, Li
L, Vogelbaum
MA.
Department of Neurosurgery, The Cleveland Clinic Brain Tumor Institute, 9500
Euclid Ave, ND-40, Cleveland, OH, 44195, USA, vogelbm@neus.ccf.org.
Introduction: The American Association of Neurology issued guidelines
discouraging the prophylactic use of anti-epilepsy drugs (AEDs) in patients
with brain tumors. We surveyed neurosurgeons to evaluate practice patterns
with regard to using AEDs in neurosurgical patients with brain tumors.
Methods: The survey consisted of 18 questions. Two group email blasts
containing an internet link to the survey were sent to members of the
American Association of Neurological Surgeons with email addresses. Uni- and
multi-variate analysis of the responses was performed using t-test, Fisher's
exact test, or chi-squared test, where appropriate. Results: The response
rate was 15.5% (386/2491). The majority of respondents (270/386; 70.0%) had
more than 5 years of experience in neurosurgery. Most respondents described
their practices as general (224/379; 59.1%); about one-third were members of
the Joint Section on Tumors (136/381; 35.7%). More than 70% of respondents
reported routine use of AED prophylaxis for patients with intra-axial
gliomas or brain metastases. AED prophylaxis was also routinely used for
extra-axial benign tumors or stereotactic biopsies by 53.8% and 21.4%,
respectively. On multivariate analysis, the number of years in practice of
ABNS certified neurosurgeons was the strongest predictor for the use of AED
prophylaxis. Conclusions: Routine use of AED prophylaxis in patients with
brain tumors undergoing neurosurgical procedures remains the prevailing
practice pattern among members of the AANS. Additional larger prospective
studies with appropriate patient stratification culminating in development
of neurosurgical guidelines on AED prophylaxis in brain tumor patients is
warranted.
PMID: 16193395 [PubMed - in process]
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| 16: J Neurooncol.
2005 Sep;74(2):195-9. |
|
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Growth retardation and bilateral cataracts followed by
anaplastic meningioma 23 years after high-dose cranial and whole-body
irradiation for acute lymphoblastic leukemia: case report and review of the
literature.
Korenkov
AI, Imhof
HG, Brandner
S, Taub
E, Huguenin
PU, Gaab
MR, Yonekawa
Y.
Department of Neurosurgery, University Greifswald, Sauerbruchstrasse, 17487,
Greifswald, Germany, alexeikorenkov@aol.com.
We report a case of meningioma diagnozed 23 years after high-dose cranial
and whole-body irradiation for the treatment of acute lymphocytic leukemia
(ALL). Radiotherapy in this case also caused early radiation injury to the
lenses and the pituitary gland, with growth retardation and mineralizing
angiopathy. Radiation-induced meningiomas are more commonly malignant, more
commonly multiple, and more likely to recur after resection than
non-radiation-induced meningiomas. Survivors of childhood ALL treated with
high-dose cranial irradiation are at risk both for early radiation injury in
radiosensitive organs, such as the lens and pituitary gland, and for the
later development of a radiation-induced meningioma.
PMID: 16193392 [PubMed - in process]
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| 17: J Neurooncol.
2005 Sep;74(2):179-181. |
|
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Huge Bilateral Pulmonary and Pleural Metastasis from
Intracranial Meningioma: A Case Report and Review of the Literature.
Erman
T, Hanta
I, Haciyakupoglu
S, Zorludemir
S, Zeren
H, Gocer
AI.
Department of Neurosurgery, Cukurova University School of Medicine, Balcali,
01330, Adana, Turkey, ermant@cu.edu.tr.
A case of recurrent meningioma with atypical features and extracranial
metastases is reported. A 34-year-old female was operated in 1996, 2000, and
2002, and frontal parasagital meningioma was extirpated. Histological
diagnoses of all the resected tumors were meningotheliomatous meningioma,
WHO Grade I. However, 2 years later, the tumor recurred in the frontal scalp
and was removed again totally. Histological diagnosis was reported as an
atypical meningioma; meningotheliomatous type; WHO Grade II. She received
radiation therapy. But the tumor had metastasized to the lung and pleura.
Transthoracic tru-cut biopsy was performed from large mass of the left lung.
Cytopathology was consistent with malignant meningioma, metastasis from the
patient's known intracranial meningioma. Ki-67 staining index at the primary
and metastatic sites of the present cases were 7 and 5%, respectively. We
reviewed and discussed the histopathological features and mechanisms of
metastasizing meningioma.
PMID: 16193389 [PubMed - as supplied by publisher]
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| 18: J Neurooncol.
2005 Sep;74(2):167-71. |
|
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Stereotactically Guided Fractionated Re-irradiation in
Recurrent Glioblastoma Multiforme.
Combs
SE, Gutwein
S, Thilmann
Ch, Huber
P, Debus
J, Schulz-Ertner
D.
Department of Radiation Oncology, German Cancer Research Center (DKFZ), INF
280, Heidelberg, Germany.
Purpose. To assess the feasibility, efficacy and toxicity of fractionated
stereotactic radiotherapy in the treatment of recurrent glioblastoma
multiforme.Patients and Methods. From January 1995 to July 2003, 53 patients
with histologically proven glioblastoma multiforme were treated at
recurrence with fractionated stereotactic radiation therapy. A median dose
of 36 Gy using a median fractionation of 5 x 2 Gy/week was applied.Results.
Median overall survival was 21 months, and median overall survival from the
time point of re-irradiation was 8 months. The median time interval between
primary and secondary radiation therapy was 10 months. In this patient
population, no variables predicting longer overall survival could be
determined. However, neurosurgical resection at relapse was associated with
increased survival after re-irradiation (p=0.04), but left progression-free
survival unaltered. Treatment was well-tolerated and no severe toxicities
developed.Conclusion. Stereotactically guided fractionated re-irradiation is
a safe and effective treatment modality in selected cases of recurring
glioblastoma multiforme. Since this is not a randomized study, further
evaluation in larger patient collectives is warranted. Also, based on recent
results of radiochemotherapy in the treatment of primary glioblastoma
multiforme, concomitant chemotherapy at relapse might be considered in the
future.
PMID: 16193388 [PubMed - in process]
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| 19: J Neurooncol.
2005 Sep;74(2):157-65. |
|
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Prolonged oral hydroxyurea and concurrent 3d-conformal
radiation in patients with progressive or recurrent meningioma: results of a
pilot study.
Hahn
BM, Schrell
UM, Sauer
R, Fahlbusch
R, Ganslandt
O, Grabenbauer
GG.
Department of Radiation Oncology and NOVALIS Shaped Beam Surgery Center,
University of Erlangen, 91054, Erlangen, Germany.
Purpose: Treatment of recurrent and progressive meningiomas remains a
challenge in clinical neurooncology. This study was designed to evaluate the
efficacy of the simultaneous application of 3d-conformal radiotherapy and
chemotherapy with hydroxyurea (HU).Patients and methods: Twenty-one patients
with recurrent or progressive meningiomas (13 benign, 4 atypical and
malignant, 4 with unproven histology) received treatment by fractionated
3d-conformal radiation (55.8-59.4 Gy) and concurrent HU, administered for a
median time of three months with a daily dosage of 20 mg/kg. Response was
evaluated using clinical and neuro-imaging data.Results: Disease
stabilization was achieved in 14/21 patients (pts). Three pts had
significant improvement of tumor associated neurological symptoms with
imaging criteria of minor response. Progression free survival rates 1 year
and 2 years after the initiation of radio-chemotherapy were 84% and 77%,
respectively. At the time of analysis a total of 6/21 pts presented with
progressive disease with a median time to progression of 59 weeks.
Documented radio- and chemotherapy associated toxicity was minimal; only one
patient discontinued HU treatment due to gastrointestinal symptoms such as
anorexia and weight loss.Conclusion: Results obtained in this study indicate
that treatment with HU and simultaneous radiotherapy is safe and effective
with disease stabilization in the majority of patients. Randomized trials
comparing radiosurgery versus radiochemotherapy versus fractionated
radiotherapy are warranted.
PMID: 16193387 [PubMed - in process]
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| 20: J Neurooncol.
2005 Sep;74(2):141-9. |
|
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Inactivation of p53 Sensitizes Astrocytic Glioma Cells to
BCNU and Temozolomide, but not Cisplatin.
Xu
GW, Mymryk
JS, Cairncross
JG.
Departments of Oncology, University of Western, Ontario, Canada.
p53 inactivation sensitizes U87MG astrocytic glioma cells to
1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs
used clinically to treat high-grade astrocytomas. In this report, we
examined the effect of p53 inactivation on the chemosensitivity of two
additional human astrocytic glioma cell lines, D54 and A172, in order to
assess whether sensitization is a general property of astrocytic tumor
cells. Compared to control cells with intact p53 function, derived lines in
which p53 was inactivated displayed significantly reduced clonogenic
survival after exposure to BCNU and TMZ. Sensitization to both BCNU and TMZ
was associated with failure of p21(WAF1) induction, lack of a sustained G2
cell cycle arrest and significant tumor cell death. These findings suggest
that enhanced sensitivity to BCNU and TMZ is a general property of human
astrocytic glioma cells in which p53 was disrupted. In contrast, p53
inactivation rendered D54 and U87MG cells significantly more resistant to
cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which
high-grade astrocytomas sometimes respond. These results indicate that p53
status influences the chemosensitivity of astrocytic glioma cells in a
drug-type specific manner, a finding that may have implications for the
selection of drug treatments for patients with astrocytic gliomas.
PMID: 16193384 [PubMed - in process]
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| 21: J Neurooncol.
2005 Sep;74(2):135-40. |
|
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Local Delivery of Interleukin-2 and Adriamycin is
Synergistic in the Treatment of Experimental Malignant Glioma.
Hsu
W, Lesniak
MS, Tyler
B, Brem
H.
Departments of Neurosurgery and Oncology, The Johns Hopkins University
School of Medicine, Baltimore, MD.
Introduction: Local delivery of adriamycin (ADR) via biodegradable polymers
has been shown to improve survival in rats challenged intracranially with 9L
gliosarcoma. Likewise, local delivery of interleukin-2 (IL-2) has been shown
to extend survival in experimental brain tumor models. In the current study,
we hypothesized that local delivery of ADR and IL-2 might act
synergistically against experimental intracranial glioma.Methods:
Polyanhydride polymers (PCPP-SA) containing 5% ADR by weight were prepared
using the mix-melt method. IL-2 polymer microspheres (IL-2 MS) were produced
via the complex coacervation of gelatin and chondroitin sulfate in the
presence of IL-2. Sixty male Fisher 344 rats received an intracranial
challenge with a lethal dose of 9L gliosarcoma cells. In addition, a group
of rats were injected with either IL-2 MS or empty microspheres. Five days
later they received ADR or blank polymer. There were a total of four
treatment groups: (1) empty microspheres, blank polymer; (2) empty
microspheres, ADR polymer; (3) IL-2 MS, blank polymer; and (4) IL-2 MS, ADR
polymer.Results: Compared to control animals treated with empty microspheres
and blank polymer, animals receiving empty microspheres and ADR polymer (P
< 0.0004), IL-2 MS and blank polymer (P < 0.0005), and IL-2 MS
combined with ADR polymer (P < 0.0000002) all showed statistically
significant improvement in survival. In addition, animals receiving the
IL-2/ADR combination had significantly extended survival compared to either
ADR or IL-2 alone (P < 0.000003 and P < 0.0004,
respectively).Conclusions: Both ADR and IL-2, when delivered locally, are
effective monotherapeutic agents against experimental intracranial
gliosarcoma. The combination ADR and IL-2 therapy is more effective than
either agent alone.
PMID: 16193383 [PubMed - in process]
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| 22: J Neurooncol.
2005 Sep;74(2):123-33. |
|
-
Glucose metabolism heterogeneity in human and mouse
malignant glioma cell lines.
Griguer
CE, Oliva
CR, Gillespie
GY.
Department of Surgery, University of Alabama at Birmingham, 1918 University
Blvd., THT 1046, Birmingham, AL, 35294-0005, USA, cgriguer@uab.edu.
The current study examined specific bioenergetic markers associated with the
metabolic phenotype of several human and mouse glioma cell lines. Based on
preliminary studies, we hypothesized that glioma cells would express one of
at least two different metabolic phenotypes, possibly acquired through
progression. The D-54MG and GL261 glioma cell lines displayed an oxidative
phosphorylation (OXPHOS)-dependent phenotype, characterized by extremely
long survival under glucose starvation, and low tolerance to poisoning of
the electron transport chain (ETC). Alternatively, U-251MG and U-87MG glioma
cells exhibited a glycolytic-dependent phenotype with functional OXPHOS.
These cells displayed low tolerance to glucose starvation and were resistant
to a ETC blocker. Moreover, these cells could be rescued in low glucose
conditions by oxidative substrates (e.g., lactate, pyruvate). Finally, these
two phenotypes could be distinguished by the differential expression of LDH
isoforms. OXPHOS-dependent cells expressed both LDH-A and -B isoforms
whereas glycolytic-dependent glioma cells expressed only LDH-B. In the
latter case, LDH-B would be expected to be essential for the use of
extracellular lactate to fuel cell activities. These observations raise the
possibility that the heterogeneity in glucose metabolism and, in particular,
the sole expression of LDH-B, might identify an important biological marker
of glioma cells that is critical for their progression and that might afford
a new target for anticancer drugs.
PMID: 16193382 [PubMed - in process]
-
| 23: J Neurooncol.
2005 Sep;74(2):113-121. |
|
-
Expression of Drug Resistance Proteins Pgp, MRP1, MRP3,
MRP5 AND GST-pi in Human Glioma.
Calatozzolo
C, Gelati
M, Ciusani
E, Sciacca
FL, Pollo
B, Cajola
L, Marras
C, Silvani
A, Vitellaro-Zuccarello
L, Croci
D, Boiardi
A, Salmaggi
A.
Istituto Nazionale Neurologico 'C.Besta', Via Celoria 11, 20133, Milano,
Italy, salmaggi@istituto-besta.it.
Chemotherapy in glioma is poorly effective: the blood-brain barrier and
intrinsic and/or acquired drug resistance of tumor cells could partly
explain this lack of major effect. We investigated expression of
P-glycoprotein (Pgp), multidrug resistance protein (MRP) 1, MRP3, MRP5 and
glutathione-S-transferase pi (GST-pi) in malignant glioma patients.
Cytofluorimetric analysis of 48 glioma specimens and 21 primary cultures
showed high levels of MRP1, moderate levels of MRP5 and low levels of Pgp,
GST-pi and MRP3. Immunohistochemistry (25 glioma specimens) showed
expression of GST-pi (66.7% of cases), MRP1 (51.3%), MRP5 (45.8%), Pgp
(34.8%) and MRP3 (29.9%) in tumor cells. Moreover, analysis of tumor samples
by real time quantitative PCR showed mRNA expression of all investigated
genes. Tumor vasculature, analyzed in glioma specimens and in tumor derived
endothelial cells, showed expression of all investigated proteins. Non-tumor
brain samples (from a patient with arteriovenous malformation and from one
with epilepsy), normal human astrocytes and cultured endothelial cells were
also analyzed: astrocytes and endothelial cells expressed the highest levels
of the investigated proteins, mainly MRP1 and MRP5. No significant
differences in proteins expression were detected between primary or
recurrent gliomas, suggesting that glioma chemoresistance is mostly
intrinsic. Therefore, we detected, for the first time, the presence of MRP3
and MRP5 on glioma specimens - both in tumor and endothelial cells - and we
delineated an expression profile of chemoresistance proteins in glioma. The
possible association of inhibitors of drug efflux pumps with chemotherapy
could be investigated to improve drugs delivery into the tumor and their
cytotoxic effects.
PMID: 16193381 [PubMed - as supplied by publisher]
-
| 24: J Neurooncol.
2005 Sep;74(2):99-103. |
|
-
Radiation-enhanced vascular endothelial growth factor
(VEGF) secretion in glioblastoma multiforme cell lines - a clue to
radioresistance?
Hovinga
KE, Stalpers
LJ, van
Bree C, Donker
M, Verhoeff
JJ, Rodermond
HM, Bosch
DA, van
Furth WR.
Department of Radiotherapy, University of Amsterdam, Amsterdam, The
Netherlands.
Objective: Postoperative radiotherapy is standard treatment for patients
with a glioblastoma multiforme (GBM). However, a GBM is radioresistant and
almost always recurs, even after a high dose of radiation. A GBM is
characterized by its extensive neo-angiogenesis, which can be attributed to
the high levels of vascular endothelial growth factor (VEGF). The scope of
this study is to investigate the VEGF secretion by GBM cells with different
radiosensitivity after irradiation. Methods:Three human GBM cell lines
(U251, U251-NG2 and U87) were irradiated with single doses of 0, 5, 10 and
20 Gy of gamma-rays from a (137)Cs source. VEGF levels in medium were
measured by ELISA at 24, 48 and 72 h after radiation. Cell survival was
measured by the XTT assay 7 days after irradiation. Results:Following single
dose radiation, the VEGF levels showed a dose dependent increase in U251,
U251-NG2 and U87 glioma cells. Both base-line and radiation-enhanced VEGF
levels were about 10-fold higher in U87 compared to U251 and U251-NG2 cells.
In addition, in the XTT assay, the U87 was more radioresistant than both
U251 and U251-NG2 cell lines (dose modifying factor (DMF) = 1.6 and 1.7
resp). Conclusion:Irradiation enhanced VEGF secretion in all three tested
glioma cell lines (up to eight times basal levels). It is tempting to
associate the radiation-enhanced VEGF secretion with an increased angiogenic
potential of the tumor, which may be a factor in radioresistance.
PMID: 16193379 [PubMed - in process]
-
| 25: J Neurooncol.
2005 Sep;74(3):283-6. |
|
-
Irinotecan Therapy in a 12-year-old Girl with Recurrent
Brain Stem Glioma and without Functional Polymorphisms in UGT1A1 Activity:
Case Report.
Ishikawa
K, Kajita
Y, Hasegawa
Y, Noda
Y, Yoshida
J, Nabeshima
T.
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya
University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya,
466-8560, Japan, kaz-ishi@med.nagoya-u.ac.jp.
A 10-year-old girl was diagnosed with astrocytoma grade 2.
Immuno-chemo-radiotherapy (interferon, ranimustine, and radiation),
second-line chemotherapy (carboplatin and etoposide, 7 cycles) and
third-line chemotherapy (ifosfamide, carboplatin, and etoposide) was given
to treat progressive disease. Finally, irinotecan therapy was initiated and
led to dramatic clinical improvement. Irinotecan is metabolized by
carboxylesterase to form an active SN-38, which is further conjugated and
detoxified by UDP-glucuronosyltransferase (UGT) to yield its
beta-glucuronide. The polymorphic UGT isoenzyme, UGT1A1 has genetic variants
which decrease in SN-38 glucuronidating capacity and could help predict
irinotecan-associated toxicity. The patient suffered excessive toxicity with
low-dose irinotecan although no functional polymorphism in UGT1A1 was
identified. We suggest that irinotecan offers an effective treatment option
for children with recurrent brain stem glioma and other genetic variants
except UGT1A1 may be a risk factor for irinotecan-induced toxicity.
PMID: 16187025 [PubMed - in process]
-
| 26: J Neurooncol.
2005 Sep;74(3):281-2. |
|
-
Panventricular medulloblastoma.
Bhatoe
HS, Dutta
V, Chaturvedi
A.
Department of Neurosurgery, Army Hospital (Research & referral), Delhi
Cantt, 110010, New Delhi, India, hsbhatoe@indiatimes.com.
PMID: 16187024 [PubMed - in process]
-
| 27: J Neurooncol.
2005 Sep;74(3):249-60. |
|
-
Therapeutic Implications of Interferon Regulatory Factor
(IRF)-1 and IRF-2 in Diffusely Infiltrating Astrocytomas (DIA): Response to
Interferon (IFN)-beta in Glioblastoma Cells and Prognostic Value for DIA.
Yoshino
A, Katayama
Y, Yokoyama
T, Watanabe
T, Ogino
A, Ota
T, Komine
C, Fukushima
T, Kusama
K.
Department of Neurological Surgery, Nihon University School of Medicine,
30-1 Oyaguchi- Kamimachi, Itabashi-ku, Tokyo, 173-8610, Japan,
ayoshino@med.nihon-u.ac.jp.
The precise mechanisms governing the direct effect of IFN-beta, including
apoptosis induction, are not yet fully understood. To gain a better insight
into these mechanisms, we investigated the signaling pathways focusing
particularly on interferon regulatory factor 1 (IRF-1) and IRF-2 in
glioblastoma cell lines. Furthermore, we attempted to determine whether or
not IRF-1 and IRF-2 act as additional prognostic indicators in diffusely
infiltrating astrocytomas (DIA). We first assessed the cytotoxic effects of
IFN-beta based on a cell growth study and modified MTT assay, and then
quantified the apoptosis using a sandwich enzyme immunoassay following
IFN-beta treatment in the cell lines, U-87MG, T98G, and A-172. Subsequently,
we carried out an analysis of apoptosis-related molecules as evaluated by
densitometric analysis of Western blots, focusing on IRF-1 and IRF-2, and
two major initiator caspases, caspase-8 and caspase-9. Furthermore, we
assessed the expression of type I IFN receptor, IRF-1, and IRF-2 using
immunohistochemical techniques in 63 DIA (15 of WHO grade II, 18 of grade
III, and 30 of grade IV), and analyzed their impact on prognosis. An
increase in apoptosis was apparent after 48 h of IFN-beta treatment (1 x
10(4) IU/ml) in T98G but not in U-87MG or A-172. IFN-beta treatment for 6 h
significantly enhanced the expression of IRF-1 in all three cell lines.
However, an enhanced expression of IRF-2 was observed only in the
not-most-sensitive, non-apoptosis-induced U-87MG and A-172. While minimal
processing of caspase-8 was noted in the three cell lines throughout the
experiment, caspase-9 activation was observed in the apoptosis-detected T98G
after 48 h of treatment, as indicated by a 1.33-fold increase (P=0.037). On
the other hand, the IRF-1 LI and IRF-1/IRF-2 LI ratio were greater in
low-grade DAI, and were negatively correlated with the histopathological
grade in DIA (P=0.017 and P=0.001, respectively). Furthermore, the
IRF-1/IRF-2 LI ratio was negatively correlated with the MIB-1 LI in DIA
(P=0.004), and represented an independent and most powerful determinant of
overall survival compared to other conventional prognostic factors
(P=0.018). However, the relation was not statistically significant when only
patients with high-grade DIA were assessed. Our findings suggest that
up-regulation of IRF-1 and IRF-2 might be an important determinant of
susceptibility to IFN-beta mediated cytotoxicity including apoptosis.
Furthermore, the IRF-1/IRF-2 LI ratio may reflect the proliferative state of
DIA and constitute an important prognostic marker in DIA. Thus, IRF-1 and
IRF-2 could represent one of the therapeutic target sites for the regulation
of cell growth in DIA.
PMID: 16187022 [PubMed - in process]
-
| 28: J Neurooncol.
2005 Sep;74(3):233-9. |
|
-
Inhibition of glioma cell proliferation by neural stem
cell factor.
Suzuki
T, Izumoto
S, Wada
K, Fujimoto
Y, Maruno
M, Yamasaki
M, Kanemura
Y, Shimazaki
T, Okano
H, Yoshimine
T.
Department of Neurosurgery, Osaka University Medical School, 2-2 Yamadaoka,
Suita, Osaka, 565-0871, Japan, sizumoto@nsurg.med.osaka-u.ac.jp.
Neural stem cells (NSC) have unique differentiation-, proliferation-, and
motility properties. To investigate whether they secrete factors that
interfere with the proliferation of glioma cells, we grew glioma cells in
conditioned medium (CM) obtained from cultures of neurospheres including
neural stem / progenitor cells (NSPC) isolated from embryonic (E14)- or
adult mouse brain or fetal human brain.
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and
BrdU-labeling assays showed that CM from NSPC (NSPC/CM) contained factor(s)
that inhibited the proliferation of glioma cells by 28-87%.
Filter-fractionation of NSPC/CM revealed that the 50,000-100,000 nominal
molecular weight limit (NMWL) fraction contained the inhibitory activity. On
the basis of these observations we transplanted 203G glioma cells and/or
NSPC into the intrathecal space of the cisterna magna of mice to investigate
whether NSPC interfere with the proliferation of glioma cells in vivo. Mice
transplanted with both 203G and NSPC survived significantly longer than did
mice transplanted only with 203G. We concluded that NSPC secrete factor(s)
that may control glioma cell proliferation.
PMID: 16187020 [PubMed - in process]
-
| 29: J Neurooncol.
2005 Sep;74(3):225-32. |
|
-
Retinamide-Induced Apoptosis in Glioblastomas is
Associated with Down-Regulation of Bcl-xL and Bcl-2 Proteins.
Lytle
RA, Jiang
Z, Zheng
X, Higashikubo
R, Rich
KM.
Department of Neurological Surgery, Washington University School of
Medicine, 660 South Euclid Avenue, 8057, St. Louis, 63110, Missouri, United
States.
Glioblastomas are among the most difficult neoplasms to treat with continued
poor prognosis for long-term survival. Glioblastomas have developed
effective mechanisms to resist chemotherapy including levels anti-apoptotic
proteins, Bcl-xL and Bcl-2. Chemotherapy agents that promote down-regulation
of Bcl-xL and Bcl-2 may enhance sensitivity to chemotherapy in
glioblastomas. The ability of the synthetic retinoid N-(4-hydroxyphenyl)
retinamide to modulate these anti-apoptotic proteins and to enhance
apoptosis and chemotherapy was examined in glioblastoma cells. Expression of
Bcl-2 family member proteins Bcl-xL and Bcl-2 were assessed in glioblastomas
from three cell lines including U87, U251, and U138. Cells were treated with
either retinamide alone or in combination with the chemotherapy agent, BCNU.
The incidence of apoptosis was determined with flow cytometry analysis
(FACS). Based on Western blots the levels of Bcl-2 and Bcl-xL were decreased
in glioblastoma cells after treatment with retinamide. Retinamide treatment
resulted in increased ratios of deamidated verses transamidated levels of
Bcl-xL in U87 cells. BCNU chemotherapy combined with retinamide markedly
down-regulated levels of both Bcl-xL and Bcl-2 proteins in glioblastoma and
enhanced the incidence of apoptosis in U87 cells. These studies demonstrate
that modulation of levels of the anti-apoptotic proteins, Bcl-xL and Bcl-2,
may enhance the sensitivity of glioblastoma toward chemotherapy.
PMID: 16187019 [PubMed - in process]
-
| 30: Neurology. 2005 Jan
11;64(1):69-74. |
|
-
Chemoradiotherapy for primary CNS lymphoma: an
intent-to-treat analysis with complete follow-up.
Omuro
AM, DeAngelis
LM, Yahalom
J, Abrey
LE.
Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
OBJECTIVE: To assess the efficacy and safety of a preradiation chemotherapy
regimen in patients with primary CNS lymphoma (PCNSL), with emphasis on
long-term outcomes. METHODS: In this prospective phase II trial, patients
with a new diagnosis of PCNSL received two cycles of intrathecal (12 mg) and
IV (1 g/m2) methotrexate (MTX), thiotepa (30 mg/m2), and procarbazine (75
mg/m2), prior to whole-brain radiotherapy (RT). RESULTS: Seventeen patients
were enrolled (ages 26 to 71, median 53). Median Karnofsky performance scale
score was 70. After chemotherapy, 7 patients (41%) had a complete response
(CR) and 7 (41%) a partial response (PR). After RT, 13 (76%) patients
achieved a CR, 2 (12%) a PR, and 2 (12%) had disease progression. Relapse
occurred in 7 (41%) patients; median disease-free survival was 18 months.
Fifteen (88%) patients have died: 8 (47%) from PCNSL, 5 (29%) from
neurotoxicity, and 2 (12%) from unknown causes. Median overall survival was
32 months. Two patients (12%) are alive and disease free at 12 years
follow-up. Nephrotoxicity was a minor complication, but grades 3 and 4
myelosuppression were found in 5 (29%) patients. CONCLUSIONS: This regimen
resulted in an efficacy and toxicity profile comparable to other combined
modality treatments, despite the relatively low dose of methotrexate. It may
be a useful option in patients unable to tolerate higher doses. Procarbazine
and thiotepa are potential candidates for incorporation into chemotherapy
regimens aiming to decrease the incidence of neurotoxicity. First relapse
and neurotoxicity within 2 years of diagnosis seem to be critical for
predicting long-term outcomes.
Publication Types:
- Clinical Trial
- Clinical Trial, Phase II
PMID: 15642906 [PubMed - indexed for MEDLINE]
-
| 31: Neuroradiology. 2004
Dec;46(12):1039-43. Epub 2004 Nov 18. |
|
-
Desmoplastic infantile ganglioglioma: MRI and
histological findings case report.
Nikas
I, Anagnostara
A, Theophanopoulou
M, Stefanaki
K, Michail
A, Hadjigeorgi
Ch.
Department of Radiological Imaging, Children's Hospital Agia Sophia,
Epaminonda 14, 16674, Glyfada, Athens, Greece.
Desmoplastic infantile gangliogliomas (DIG) are rare intracranial tumors
occurring during the 1st year of life. They arise invariably in the
supratentorial region and have a great size at presentation, commonly
involving more than one lobe. They are composed of a solid peripheral
component of variable size, which involves the superficial cerebral cortex
and the leptomeninges, and a large cystic part. Despite the great size at
presentation and occasional mitotic activity in the variable
undifferentiated component, this entity constitutes a distinct
clinicopathological entity with benign prognosis. We hereby present the MRI
and histological findings of two cases of DIG in infants aged 9 and 10
months, respectively.
Publication Types:
PMID: 15551129 [PubMed - indexed for MEDLINE]
-
| 32: Pediatr
Hematol Oncol. 2005 Apr-May;22(3):235-46. |
|
Central nervous system lymphoma in children.
Porto
L, Kieslich
M, Schwabe
D, Yan
B, Zanella
FE, Lanfermann
H.
Neuroradiology Department, Klinikum der Johann Wolfgang Goethe-Universitat,
Frankfurt am Main, Germany. luciana.porto@kgu.de
This paper describes the rare MR and CT features of central nervous system
(CNS) lymphoma in immunocompetent children and in survivors of childhood
acute lymphoblastic leukemia (ALL) and discusses the causative role of
cranial irradiation and/or leukoencephalopathy preceding central nervous
system (CNS) lymphoma in survivors of childhood leukemia. The authors
reviewed MR and CT scans of 3 children with biopsy-proved CNS lymphoma. One
child had tumor infiltration within the optic nerve sheaths and optic chiasm
by previously known non-Hodgkin lymphoma. In 2 patients, CNS lymphoma
developed 8 and 10 years after initial ALL treatment. In both cases CNS
lymphoma was preceded by cranial irradiation and leukoencephalopathy. A
single lesion was present in 3 out of 4 patients. All lesions were
isointense or hypointense on the T1-weighted images relative to gray matter
and showed homogeneous enhancement. One lesion was centered in the central
gray matter, one lesion was centered within a cerebral hemisphere, one
lesion was in optic nerve, and there were 2 parasellar lesions. CNS lymphoma
has a variable appearance in children. Knowledge of risk factors in children
may help in the early recognition of disease, allowing for timely
intervention. This may prompt early biopsy or a conservative management in
the appropriate clinical setting.
Publication Types:
PMID: 16020108 [PubMed - indexed for MEDLINE]
-
| 33: Surg Neurol.
2005 Oct;64(4):285. |
|
An introduction to molecular analysis and
characterization of gliomas.
Ausman
JI.
Publication Types:
PMID: 16181992 [PubMed - in process]
-
| 34: Surg Neurol.
2005 Sep;64(3):272-5. |
|
-
Application of multichannel near-infrared spectroscopic
topography to physiological monitoring of the cortex during cortical
mapping: technical case report.
Hoshino
T, Sakatani
K, Katayama
Y, Fujiwara
N, Murata
Y, Kobayashi
K, Fukaya
C, Yamamoto
T.
Department of Neurological Surgery, Nihon University School of Medicine,
Tokyo 173-8610, Japan.
BACKGROUND: Cortical stimulation via a subdural grid electrode (SGE) is one
of the most reliable methods for identifying eloquent areas before surgery.
However, the physiological conditions of the cortex during stimulation
cannot be monitored electrophysiologically because of electrical artifacts.
In the present case, we tested whether or not multichannel near-infrared
spectroscopy (NIRS) topography, a noninvasive optical imaging technique, is
applicable for monitoring the physiological conditions of the stimulated
cortex. CASE DESCRIPTION: The patient (a 27-year-old right-handed man)
suffered from glioma in the left frontal lobe. For preoperative cortical
mapping, SGEs were implanted over the left motor cortex before tumor
resection. Employing NIRS topography, we undertook 2 dimensional imaging of
the changes in oxyhemoglobin (Oxy-Hb) and deoxyhemoglobin (Deoxy-Hb)
concentration during electrical stimulation. Five-hertz stimulation with 5
mA at the left-hand area produced a localized increase in Oxy-Hb and a
decrease in Deoxy-Hb, associated with slight twitching of the right hand. In
contrast, 50-Hz stimulation produced significant increases in both Oxy-Hb
and Deoxy-Hb at the stimulation site, and the area with such cerebral blood
oxygenation (CBO) changes propagated beyond the hand area associated with
prominent muscle contractions of the right upper extremity, suggesting that
50-Hz stimulation caused epileptic discharge. CONCLUSION: Near-infrared
spectroscopy topography may represent a useful tool for imaging the degree
and extent of the physiological effects of electrical stimulation on the
cortex, and permits safe and accurate cortical mapping.
Publication Types:
PMID: 16099265 [PubMed - indexed for MEDLINE]
-
| 35: Surg Neurol.
2005 Sep;64(3):207-12. |
|
-
Role of stereotactic radiosurgery as a primary treatment
option in the management of newly diagnosed multiple (3-6) intracranial
metastases.
Jawahar
A, Shaya
M, Campbell
P, Ampil
F, Willis
BK, Smith
D, Nanda
A.
Department of Neurosurgery, Louisiana State University Health Sciences
Center in Shreveport, Shreveport, LA 71130, USA. ajawah@lsuhsc.edu
OBJECTIVE: The objective of this study was to assess the role of
stereotactic radiosurgery in the management of newly diagnosed multiple
intracranial metastases from known primary cancer locations. METHODS: Fifty
(29 women and 21 men) patients received radiosurgery for newly diagnosed 3
or more metastatic brain tumors. Their mean age was 53 years. Lung cancer
was the most common primary cancer (66%). RESULTS: Arrest in the growth of
irradiated tumors was achieved in 41 (82%) patients. Eight patients (16%)
required further intervention for tumors in other brain locations. Mean
survival after diagnosis of brain disease was 12 months and the brain
disease-controlled period was 19 months. The period of brain disease control
prolonged (P=.03) with decreasing tumor volumes (<10 mL). Control of
treated tumors positively affected survival after diagnosis of brain disease
(P=.0001). CONCLUSION: Radiosurgery as an adjuvant improves survival in
patients with cancer who have newly diagnosed multiple intracranial
metastases by arresting the growth of tumors.
PMID: 16099246 [PubMed - indexed for MEDLINE]
-
| 36: Pediatr Neurosurg.
2005 Sep-Oct;41(5):258-63. |
|
-
Asymptomatic syringomyelia in the course of
medulloblastoma.
Hamlat
A, Le
Strat A, Boisselier
P, Brassier
G, Carsin-Nicol
B.
Department of Neurosurgery, CHRU Pontchaillou, Rennes, France.
Syringomyelia is frequently associated with Chiari malformation or one of
many otherpathological conditions. Its co-occurrence with medulloblastoma is
rare, and to our knowledge, only 4 patients have been reported, although
some reports have documented on syringomyelia associated with intracranial
processes or intramedullary tumor. The authors describe an unusual case of
asymptomatic thoracic syringomyelia complicated by an intrasyringal
hemorrhage in a child with medulloblastoma. This report illustrates that,
although unusual, syringomyelia is a potential complication in the natural
history of medulloblastoma, and the authors consider the possible
pathogenesis of syrinx enlargement. Copyright (c) 2005 S. Karger AG, Basel.
PMID: 16195679 [PubMed - in process]
-
| 37: Pediatr Neurosurg.
2005 Jul-Aug;41(4):224-5. |
|
-
Posterior fossa tumor presenting as a giant macrocranium
in an infant.
Muzumdar
DP.
Department of Neurosurgery, Seth Gordhandas Sunderdas Medical College, King
Edward VII Memorial Hospital, Mumbai, India. dmuzumdar@hotmail.com
Publication Types:
PMID: 16088261 [PubMed - indexed for MEDLINE]
-
| 38: Pediatr Neurosurg.
2005 Jul-Aug;41(4):206-11. |
|
-
Supratentorial arterial ischemic stroke following
cerebellar tumor resection in two children.
Catsman-Berrevoets
CE, van
Breemen M, van
Veelen ML, Appel
IM, Lequin
MH.
Department of Child Neurology, Erasmus MC/Sophia Children Hospital,
Rotterdam, The Netherlands. c.catsman@erasmusmc.nl
We describe two children who developed ischemic strokes in the territory of
the middle cerebral artery, one 7 days and one 11 days after resection of a
cerebellar tumor. In the first child, another infarction occurred in the
territory of the contralateral middle cerebral artery 5 days after the first
stroke. No specific cause or underlying risk factor other than the surgical
procedure was found. The subacute clinical course at stroke onset resembled
that of the 'posterior fossa syndrome', suggesting a common underlying
mechanism.
Publication Types:
PMID: 16088257 [PubMed - indexed for MEDLINE]
-
|
Volume 4, Number
41 - 4 October 2005