| 1: Arch Pathol Lab Med. 2004 Jun;128(6):707-8. |
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Pathologic quiz case: a 15-year-old girl with an
intracranial midline mass. Pineoblastoma, World Health Organization Grade
IV.
Song K, Nasim M, Agarwal R, Benardete E.
Department of Pathology, Kings County Hospital Center, Brooklyn, NY, USA.
sjw0422@yahoo.com
Publication Types:
PMID: 15163221 [PubMed - indexed for MEDLINE]
 http://arpa.allenpress.com/pdfserv/10.1043/1543-2165(2004)128<707:PQCAYG>2.0.CO;2
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| 2: Br J Cancer. 2004 Oct 12 [Epub ahead of print] |
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Surgery and adjuvant dendritic cell-based tumour
vaccination for patients with relapsed malignant glioma, a feasibility
study.
Rutkowski S, De Vleeschouwer S, Kaempgen E, Wolff JE, Kuhl J, Demaerel P,
Warmuth-Metz M, Flamen P, Van Calenbergh F, Plets C, Sorensen N, Opitz A,
Van Gool SW.
1Department of Pediatric Oncology, Children's Hospital, University of
Wuerzburg, Josef-Schneider-Str. 2, D-97080 Wuerzburg, Germany.
Patients with relapsed malignant glioma have a poor prognosis. We developed
a strategy of vaccination using autologous mature dendritic cells loaded
with autologous tumour homogenate. In total, 12 patients with a median age
of 36 years (range: 11-78) were treated. All had relapsing malignant glioma.
After surgery, vaccines were given at weeks 1 and 3, and later every 4
weeks. A median of 5 (range: 2-7) vaccines was given. There were no serious
adverse events except in one patient with gross residual tumour prior to
vaccination, who repetitively developed vaccine-related peritumoral oedema.
Minor toxicities were recorded in four out of 12 patients. In six patients
with postoperative residual tumour, vaccination induced one stable disease
during 8 weeks, and one partial response. Two of six patients with complete
resection are in CCR for 3 years. Tumour vaccination for patients with
relapsed malignant glioma is feasible and likely beneficial for patients
with minimal residual tumour burden.British Journal of Cancer advance online
publication, 12 October 2004; doi:10.1038/sj.bjc.6602195 www.bjcancer.com.
PMID: 15477864 [PubMed - as supplied by publisher]
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| 3: Cancer. 2004 Oct 8 [Epub ahead of print] |
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Adult glioma incidence trends in the United States,
1977-2000.
Hess KR, Broglio KR, Bondy ML.
Department of Biostatistics and Applied Mathematics, The University of Texas
M. D. Anderson Cancer Center, Houston, Texas.
BACKGROUND: Several authors have reported an increase in the incidence of
brain tumors, especially among the elderly. A more complete understanding of
adult glioma incidence trends might provide indications of risk factors for
gliomas and contribute to the search for improved therapies. METHODS: The
authors used the Surveillance, Epidemiology, and End Results (SEER) registry
public use data tapes, which included data on patients with cancer diagnosed
between 1973 and 2000. For 3 histologies as well as for 12 histology
categories combined, the authors used Poisson regression to model incidence
as a function of year of diagnosis, age at diagnosis, race (white or African
American), and gender. They used cubic splines to fit age at diagnosis and
year of diagnosis and tested for all pair-wise interactions. RESULTS: The
interaction between year of diagnosis and age at diagnosis was significant
in all four groups modeled. In glioblastoma, there was also a significant
interaction between gender and age at diagnosis. In anaplastic astrocytoma,
there was a significant interaction between gender and year of diagnosis. In
oligodendroglioma, there was a significant interaction between race and
gender. In the 12 histology categories combined, there was a significant
interaction between gender and age at diagnosis. CONCLUSIONS: The results in
the current study were consistent with other published reports that showed
an increase in the incidence of brain tumors using SEER data. Although
others have observed increasing incidence trends among the elderly, the
authors formally tested and found a statistically significant interaction
between age at diagnosis and year of diagnosis. Cancer 2004. (c) 2004
American Cancer Society.
PMID: 15476282 [PubMed - as supplied by publisher]
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| 4: Cancer Genet Cytogenet. 2004 Oct 15;154(2):119-23. |
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Evidence for gains at 15q and 20q in brain metastases of
prostate cancer.
Wullich B, Riedinger S, Brinck U, Stoeckle M, Kamradt J, Ketter R, Jung
V.
Department of Urology and Pediatric Urology, University of the Saarland,
66421 Homburg/Saar, Germany.
Many detailed genetic studies have been reported on prostate carcinogenesis.
A major shortcoming of these studies, however, is the fact that most data
have been gained from investigations that were performed at a single point
of time during tumor development. Only little is known on the dynamic
process of genetic changes during the course of the disease. We performed
comparative genomic hybridization in two cases of prostate cancer brain
metastases. Tissue samples from the primary tumors, the locally recurrent
tumor in one case, and the brain metastases from both cases were available
for analysis. The number of chromosome abnormalities was found to be
increased in the metastases. This contrasts to a remarkably stable
chromosome composition of the primary tumor over several years, even in an
androgen-depleted environment. When focusing on these changes, which either
emerged as new common aberrations in both brain metastases, or which were
commonly present in the primary and metastatic tumors, we were able to
delineate five chromosomal sites that are assumed to be related to prostate
cancer metastasis: 8q21 approximately q22, 8q24, 15q24 approximately q26,
20q12 approximately q13.1, and Xq12 approximately q21. These findings
provide new evidence for a putative role of genes at 15q and 20q in the
metastatic process of prostate cancer.
PMID: 15474146 [PubMed - in process]
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| 5: Clin Cancer Res. 2004 Oct 1;10(19):6732-43. |
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Inhibition of the Type III Epidermal Growth Factor
Receptor Variant Mutant Receptor by Dominant-Negative EGFR-CD533 Enhances
Malignant Glioma Cell Radiosensitivity.
Lammering G, Hewit TH, Holmes M, Valerie K, Hawkins W, Lin PS, Mikkelsen
RB, Schmidt-Ullrich RK.
Department of Radiation Oncology, Medical College of Virginia, Virginia
Commonwealth University, Richmond, Virginia.
PURPOSE: The commonly expressed variant epidermal growth factor receptor
(EGFR), the type III EGFR variant (EGFRvIII), functions as an oncoprotein
promoting neoplastic transformation and tumorigenicity. The role of EGFRvIII
in cellular responses to genotoxic stress, such as ionizing radiation, is
only minimally defined. Thus, we have investigated EGFRvIII as a potential
modulator of cellular radiation responses and explored the feasibility of
adenovirus (Ad)-mediated expression of dominant-negative EGFR-CD533 as a
gene therapeutic approach for inhibiting EGFRvIII function in vitro and in
vivo. Experimental Design and RESULTS: EGFR-CD533 and EGFRvIII were
expressed in vitro and in vivo in malignant U-373 MG glioma cells through
transduction with an Ad vector, Ad-EGFR-CD533 and Ad-EGFRvIII, respectively.
In vivo studies defined the importance of EGFRvIII as a modulator of
radiation responses, demonstrating a 2.6-fold activation of EGFRvIII in
U-373 malignant glioma tumors. Concomitant expression of EGFR-CD533
inhibited the radiation-induced activation of EGFRvIII in vitro and
completely abolished the enhanced clonogenic survival conferred by EGFRvIII.
The ability of EGFR-CD533 to inhibit EGFRvIII function was further confirmed
in vivo through complete inhibition of EGFRvIII-mediated increased
tumorigenicity and radiation-induced activation of EGFRvIII. Growth delay
assays with U-373 xenograft tumors demonstrated that the expression of
EGFR-CD533 significantly enhanced radiosensitivity of tumor cells under
conditions of intrinsic and Ad-mediated EGFRvIII expression. CONCLUSIONS: We
conclude that EGFRvIII confers significant radioresistance to tumor cells
through enhanced cytoprotective responses, and we have demonstrated that
dominant-negative EGFR-CD533 effectively inhibits EGFRvIII function. These
data affirm the broad potential of EGFR-CD533 to radiosensitize human
malignant glioma cells.
PMID: 15475464 [PubMed - in process]
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| 6: J Clin Oncol. 2004 Oct 15;22(20):4228-30. |
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Unusual Sites of Hodgkin's Lymphoma: CASE 2. Hodgkin's
Lymphoma of the CNS Masquerading As Meningioma.
Figueroa BE, Brown JR, Nascimento A, Fisher DC, Tuli S.
PMID: 15483035 [PubMed - in process]
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| 7: J Neurosurg. 2004 Oct;101(4):700-3. |
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Perfusion imaging of high-grade gliomas: a comparison
between contrast harmonic and magnetic resonance imaging. Technical note.
Harrer JU, Moller-Hartmann W, Oertel MF, Klotzsch C.
Departments of Neurology, Neuroradiology, and Neurosurgery, Aachen
University Hospital, Aachen, Germany. Judith.Harrer@web.de
Transcranial contrast harmonic (CH) imaging is emerging as a promising tool
for the evaluation of brain perfusion. The authors report on two cases of
histologically proven high-grade gliomas evaluated using CH imaging in
comparison to perfusion magnetic resonance (pMR) imaging. In both cases, pMR
imaging results demonstrated a massive decrease in signal intensity and an
elevated regional cerebral blood volume (rCBV) in the tumor region; however,
signal decrease was less prominent and rCBV was lower in healthy brain
tissue. In one patient, the rCBV ratio of tumor/brain was 5.0 and the
maximal signal decay occurred 3.1 times deeper in the tumor than in the
healthy brain tissue. Results of an ultrasonography examination using CH
imaging revealed similar data: the tumor/brain ratio for the area under the
curve, a parameter corresponding to rCBV, was 4.1. The maximal signal
intensity in the tumor was 3.3 times greater than in adjacent healthy brain.
Comparable data were obtained in a second patient. Taken together, these
findings indicate that CH imaging may be a valuable alternative to pMR
imaging. This new, cost-effective bedside ultrasonic technique could be
helpful not only as a means of noninvasive staging of gliomas but also as a
follow-up imaging modality to evaluate postoperative tumor recurrence or
response to antiangiogenic therapy.
PMID: 15481731 [PubMed - in process]
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| 8: J Neurosurg. 2004 Oct;101(4):659-63. |
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Induction of the DNA repair gene O6-methylguanine-DNA
methyltransferase by dexamethasone in glioblastomas.
Ueda S, Mineta T, Nakahara Y, Okamoto H, Shiraishi T, Tabuchi K.
Department of Neurosurgery, Faculty of Medicine, Saga University, Saga,
Japan. uedas@post.saga-med.ac.jp
OBJECT: The DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT)
inhibits the cytotoxic effect of alkylating agents on tumor cells. The
presence of two nonconsensus glucocorticoid-responsive elements in the human
MGMT promoter region indicates the potential regulation of MGMT expression
by glucocorticoid agents. This study was performed to elucidate whether
dexamethasone affects the expression of MGMT in glioblastoma multiforme
(GBM) cells, thereby limiting the benefit of chemotherapeutic alkylating
agents. METHODS: Four GBM cell lines (A172, T98G, U138MG, and U87MG) were
exposed to the alkylating agent 1-(4-amino-2-methyl-5-pyrimidinyl)
methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) with or without
dexamethasone. The expression levels of MGMT were correlated with the
cytotoxic effects of ACNU in GBM cells. In the presence of ACNU alone,
dexamethasone alone, and the combination of both agents, messenger RNA
expression of MGMT was induced to varying degrees with the highest increases
seen in the later conditions. This dexamethasone-dependent induction of the
MGMT gene was even observed in U87MG cells in which the promoter is
methylated, although the absolute expression of MGMT mRNA was the lowest in
that cell line. The induction of MGMT by dexamethasone was associated with
an increased resistance of these cells to ACNU. CONCLUSIONS: These results
indicate that dexamethasone-mediated upregulation of MGMT limits the
efficiency of alkylating agents in the treatment of malignant gliomas.
PMID: 15481722 [PubMed - in process]
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| 9: J Neurosurg. 2004 Oct;101(4):653-8. |
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Mismatch repair protein hMSH2 in primary drug resistance
in in vitro human malignant gliomas.
Rellecke P, Kuchelmeister K, Schachenmayr W, Schlegel J.
Institute of Pathology, Technical University, Munich.
OBJECT: The mismatch repair (MMR) system has previously been implicated in
acquired chemoresistance in malignant gliomas in humans. Its impact on the
primary chemoresistance in glioblastoma multiforme (GBM) has not been
determined in detail, however. METHODS: The authors investigated the
expression of both the MMR genes (hMSH2, hMLH1, hPMS1, hPMS2, and hMSH6) at
the transcriptional level through reverse transcription-polymerase chain
reaction and the hMSH2 protein through Western blot and immunohistochemical
analysis of tumor tissue and primary cell cultures of 25 in vitro human de
novo GBMs without prior experimental treatment. Results of these analyses
were compared with data on in vitro chemoresistance to nine drugs that are
in general use in glioma therapy. All MMR genes were expressed in the GBMs,
with no significant difference among the individual tumors except in one
respect; that is, GBMs showed either relatively high levels or barely
detectable levels of hMSH2 messenger (m)RNA and protein expression. All
multiresistant tumors demonstrated high hMSH2 expression, and all but two of
the sensitive tumors exhibited low hMSH2 mRNA levels. CONCLUSIONS: Analysis
of the data indicates that functional alterations of the MMR system are
involved in the primary drug resistance in in vitro human malignant gliomas.
Analysis of hMSH2 expression might therefore predict therapeutic responses
in humans with GBMs.
PMID: 15481721 [PubMed - in process]
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| 10: J Neurosurg. 2004 Oct;101(4):621-6. |
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Craniotomy for supratentorial brain tumors: risk factors
for brain swelling after opening the dura mater.
Rasmussen M, Bundgaard H, Cold GE.
Department of Neuroanesthesia, Arhus University Hospital, Arhus, Denmark.
OBJECT: Cerebral swelling often occurs during craniotomy for cerebral
tumors. The primary aim in this study was to determine risk factors
(intracranial pressure [ICP], patient characteristics, histopathological
features, neuroimaging characteristics, anesthetic regimen, and
perioperative physiological data) predictive of brain swelling through the
dural opening. As a secondary aim the authors attempted to define subdural
ICP thresholds associated with brain swelling. METHODS: The study population
consisted of 692 patients (mean age 50+/-15 years) scheduled for elective
craniotomy for supratentorial brain tumors. Brain swelling through the dural
opening was estimated according to a four-point scale. The patients were
dichotomized as those without cerebral swelling (that is, brain below the
dura mater [59 patients] or brain at the level of the dura mater [386
patients]) and those with cerebral swelling (that is, moderate brain
swelling [205 patients] or pronounced brain swelling [42 patients]).
Logistic regression analysis was used to identify subdural ICP (odds ratio
[OR] 1.9, 95% confidence interval [CI] 1.72-2.1, p < 0.0001), midline
shift (OR 1.06, 95% CI 1.02-1.11, p = 0.008), a diagnosis of glioblastoma
multiforme (OR 2.1, 95% CI 1.01-4.3, p = 0.047), and metastasis (OR 2.9, 95%
CI 1.3-6.9, p = 0.01) as independent risk factors of intraoperative brain
swelling. Thresholds for ICP associated with brain swelling were defined as
follows: at an ICP less than 5 mm Hg, brain swelling rarely occurred (5%
probability); at an ICP greater than 13 mm Hg, brain swelling occurred with
95% probability; and at an ICP greater than 26 mm Hg, severe brain swelling
occurred with 95% probability. CONCLUSIONS: Subdural ICP is the strongest
predictor of intraoperative brain swelling. It is possible to define
thresholds of cerebral swelling and the authors recommend subdural ICP
measurement as a tool to initiate preventive measures to reduce ICP before
opening the dura mater.
PMID: 15481716 [PubMed - in process]
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| 11: Neurology. 2004 Oct 12;63(7):1281-4. |
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How effective is BCNU in recurrent glioblastoma in the
modern era? A phase II trial.
Brandes AA, Tosoni A, Amista P, Nicolardi L, Grosso D, Berti F, Ermani M.
Department of Medical Oncology, Azienda Ospedale-Universita, Ospedale
Busonera, Via Gattamelata 64, 35100 Padova, Italy. aabrandes@unipd.it
BACKGROUND: The initial studies on nitrosoureas were performed >30 years
ago. These drugs remain the standard chemotherapy for glioblastoma. However,
because the criteria used to evaluate the activity of nitrosoureas in a
neuro-oncologic setting have changed, new data on their activity are needed.
METHODS: The authors conducted a phase II study on 40 patients with
recurrent glioblastoma following surgery and standard radiotherapy. They
analyzed progression-free survival at 6 months (PFS-6), time to progression
(TTP), response rate, and toxicity. Patients were treated with 80 mg/m2
carmustine on days 1 to 3, every 8 weeks for a maximum of six cycles.
RESULTS: Median TTP was 13.3 weeks (95% CI, 10.26 to 16.86 weeks), and PFS-6
was 17.5% (95% CI, 8.9 to 34.3). Response to chemotherapy, age < or =40
years, and performance status > or =90 were significant prognostic
factors for TTP; however, with multivariate analysis, only response to
chemotherapy was significant. The major side effects were reversible
hematologic and long-lasting hepatic and pulmonary toxicity. CONCLUSION: The
activity of this BCNU regimen is comparable with that reported in the past
and with the newest therapies, such as temozolomide. However, BCNU toxicity
is high and recovery is slow, thus compromising the administration of
further drugs in patients with progressive disease.
PMID: 15477552 [PubMed - in process]
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| 12: Surg Neurol. 2004 Sep;62(3):238-43; discussion 243-4. |
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Attenuation of vascularity by preoperative radiosurgery
facilitates total removal of a hypervascular hemangioblastoma at the
cerebello-pontine angle: case report.
Kamitani H, Hirano N, Takigawa H, Yokota M, Miyata H, Ohama E, Watanabe
T.
Department of Neurosurgery, Institute of Neurological Sciences, Faculty of
Medicine, Tottori University, Yonago, Tottori, Japan.
BACKGROUND: The surgical removal of solid, large, and deep-seated
hemangioblastomas remains challenging because it is difficult to control
bleeding during the procedure. We used preoperative radiosurgery in a solid,
highly vascular hemangioblastoma at the left cerebello-pontine angle and
present our angiographic, operative, and histologic findings. CASE
DESCRIPTION: A 37-year-old paraplegic woman with multiple hemangioblastomas
was re-admitted to our clinic with cerebellar ataxia 6 years after resection
of a tumor at the fourth ventricle. A vertebral artery angiogram revealed
that the 3.5 cm diameter hemangioblastoma at the left cerebello-pontine
angle was highly vascular and fed by the left anterior inferior cerebellar
artery and posterior inferior cerebellar artery. Nine months before surgical
removal it was treated with stereotactic radiosurgery (gamma knife, margin
dose 28 Gy) to inhibit tumor progression and to reduce its vascularity. The
tumor was totally removed via the left lateral suboccipital approach;
bleeding was well controlled and there were no complications. Pathologic
examination of the content of the excised tumor revealed coagulation
necrosis with hyaline degeneration of the tumor vessels, resulting in a
marked decrease in its vascularity. CONCLUSION: Preoperative radiosurgery
led to a marked reduction in the vascularity of this hypervascular
hemangioblastoma and was useful for controlling bleeding from the tumor
during resection. We succeeded to remove the vascular-rich hemangioblastma
after the intentional preoperative radiosurgery. The pathologic changes
induced by radiotherapy were confirmed by operative finding.
Publication Types:
PMID: 15336869 [PubMed - indexed for MEDLINE]
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| 13: Surg Neurol. 2004 Sep;62(3):227-33; discussion 233. |
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Sellar repair with fibrin sealant and collagen fleece
after endoscopic endonasal transsphenoidal surgery.
Cappabianca P, Cavallo LM, Valente V, Romano I, D'Enza AI, Esposito F, de
Divitiis E.
Department of Neurological Sciences, Unit of Neurosurgery, Universita degli
Studi di Napoli Federico II, Naples, Italy.
OBJECTIVE: To determine, in patients undergoing sellar repair after
endoscopic endonasal transsphenoidal surgery, the clinical efficacy of a
combination of fibrin sealant/collagen fleece compared to the use of fibrin
sealant or collagen fleece alone, in preventing CSF-related (cerebrospinal
fluid) postoperative complications. METHODS: From a retrospective analysis
of our series of 242 consecutive endoscopic transsphenoidal procedures, in
56 out of the 90 cases in which the sella had been repaired, fibrin sealant
and/or collagen fleece was employed, both in combination with one or
multiple layers of other materials. The incidence of postoperative CSF leaks
and the need for a postoperative lumbar drainage in the groups of fibrin
sealant or collagen fleece treated patients were compared to the group of
patients treated with the fibrin sealant/collagen fleece combination.
RESULTS: In 2 out of 16 fibrin sealant treated patients a postoperative CSF
leak presented, and in 6 out of these 16 subjects a postoperative lumbar
drainage was necessary; patients who received a fibrin sealant/collagen
fleece combination exhibited no detectable postoperative CSF leak, and no
postoperative lumbar drainage was used. CONCLUSIONS: Closure of the sella
turcica with fibrin sealant in combination with a collagen fleece is a safe
and effective method to prevent CSF fistulas. When used in combination, the
collagen fleece enhances the sealing and tissue regeneration properties of
the fibrin sealant, thus reducing the incidence of postoperative CSF leaks,
obviating the need for a lumbar drain placement.
PMID: 15336865 [PubMed - indexed for MEDLINE]
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| 14: Surg Neurol. 2004 Sep;62(3):195-9; discussion 199-200. |
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Cytological and bacteriological studies of intraoperative
autologous blood in neurosurgery.
Kudo H, Fujita H, Hanada Y, Hayami H, Kondoh T, Kohmura E.
Departments of Neurosurgery and Anesthesiology, Rokko Island Hospital, Kobe,
Japan.
BACKGROUND: To ensure the safety of salvaged blood in neurologic surgery,
reinfused blood through the Cell Saver System (CSS) (Hemonetics) was
investigated cytologically and bacteriologically. METHODS: Specimens of
reinfused blood were cytologically examined with Papanicolaou or Giemsa
stains. Reinfused blood and air in the operating theater were investigated
by microbiologic techniques. The concentration of dust particles in the
theater was determined. RESULTS: Tumor cells were positive in reinfused
blood in 5 of 9 specimens with glioblastoma, in 2 of 8 with pituitary
adenoma, and 1 of 13 with meningioma. The probability of migration of
meningioma cells into reinfused blood was significantly low in comparison
with that of glioma cells. Of the 30 specimens studied microbiologically,
the bacterial growth was detected in salvaged blood of 14 specimens (46.7%)
and in the air of the operating theater for 8 specimens (26.7%). In
craniotomy, the contamination rate was 10 of 26 specimens of reinfused blood
(38.5%). Most microorganisms were found to be staphylococci. No
statistically significant correlation could be found between salvaged blood
and air as to contamination or between reinfused blood and the concentration
of dust particles in the theater as to bacteriologic results. No infectious
complications were found after the operation, though salvaged blood through
the CSS was reinfused in 37 patients without glioblastoma or transsphenoidal
approach. CONCLUSIONS: The CSS cannot always entrap tumor cells. Salvaged
blood should not be reinfused in the patients with glioblastoma or
transsphenoidal surgery. None of the patients with reinfusion had any
infectious complications. Reinfusion of salvaged blood seems to be safe in
neurosurgery.
Publication Types:
PMID: 15336856 [PubMed - indexed for MEDLINE]
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Volume 3, Supplement 8 - 20 October 2004