| 1: Cancer. 2005 Jul
1;104(1):143-8. |
|
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A multicenter retrospective study of chemotherapy for
recurrent intracranial ependymal tumors in adults by the Gruppo Italiano
Cooperativo di Neuro-Oncologia.
Brandes
AA, Cavallo
G, Reni
M, Tosoni
A, Nicolardi
L, Scopece
L, Franceschi
E, Sotti
G, Talacchi
A, Turazzi
S, Ermani
M.
Department of Medical Oncology, Azienda Ospedale-Universita of Padova,
Padova, Italy. aabrandes@unipd.it
BACKGROUND: No data on the role of chemotherapy in recurrent ependymal
tumors are available in adults. The aim of the current study was to
investigate outcomes after salvage chemotherapy in this setting. METHODS: A
retrospective review was made of the charts of 28 adults (> or = 18 years)
with progressive or recurrent ependymal tumors after surgery and
radiotherapy, who received chemotherapy between 1993 and 2003 in 3
institutions of the Gruppo Italiano Cooperativo di Neuro-Oncologia network.
RESULTS: Thirteen patients (46.3%) received cisplatin-based chemotherapy (Group
A) and 15 (53.7%) received regimens without cisplatin (Group B).
Platinum-based chemotherapy yielded 2 complete responses (CR) (15.4%) and 2
(15.4%) partial responses (PR), whereas 7 patients (53.8%) remained stable
(SD). After regimens without cisplatin, there were no CR, 2 PR (13.3%), and
11 SD (73.3%). The overall median time to progression was 9.9 months (95%
confidence interval [95% CI], 7.5-21.7 months), 9.9 months (5.2-not reached)
for Group A and 10.9 months (95% CI, 7.17-23.9 months) for Group B. The
overall median survival (OS) was 40.7 months (95% CI, 16-not reached), 31
months (21-not reached) for Group A and 40.7 months (13.4-not reached) for
Group B. CONCLUSIONS: Cisplatin-based chemotherapy achieved a higher
response rate, but did not prolong disease progression-free survival or OS.
More active regimens for the salvage treatment of ependymal tumors have yet
to be found.
Publication Types:
PMID: 15912507 [PubMed - indexed for MEDLINE]
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| 2: Cancer. 2005 Jul
1;104(1):126-34. |
|
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Lack of benefit of spinal irradiation in the primary
treatment of intracranial germinoma: a multiinstitutional, retrospective
review of 180 patients.
Shikama
N, Ogawa
K, Tanaka
S, Toita
T, Nakamura
K, Uno
T, Ohnishi
H, Itami
J, Tada
T, Saeki
N.
Department of Radiology, Shinshu University, School of Medicine, Matsumoto,
Japan. shikama@hsp.md.shinshu-u.ac.jp
BACKGROUND: The current study assessed the contribution of spinal
irradiation to the treatment outcome of patients with intracranial germinoma.
METHODS: Clinical data from 180 patients with intracranial germinoma, who
were treated with radiotherapy and/or chemotherapy from 1980 to 2001, were
collected from 6 institutions. The patients' median age was 16 years (range,
1-47 yrs), and the male-to-female ratio was 133:47. Pathologic verification
was obtained in 88 patients. A solitary tumor was seen in 129 patients, and
multifocal or disseminated tumors were detected in 51 patients. The median
tumor size was 2.5 cm (range, 0.6-7.0 cm). Local field and/or whole brain
irradiation was performed in 114 patients, and craniospinal irradiation was
performed in 66 patients. Fifty-five patients were treated with chemotherapy.
The median follow-up time was 89 months (range, 3-297 mos). RESULTS:
Eight-year overall and event-free survival rates were 91% and 89%,
respectively. The 8-year recurrence rates at the primary site, intracranial
space, and the spinal space were 1%, 6%, and 6%, respectively. Cox
regression analysis showed that spinal irradiation (hazard ratio, 1.050; 95%
confidence interval [CI], 0.355-3.170) did not contribute to a favorable
event-free survival. CONCLUSIONS: Spinal irradiation did not contribute to
favorable event-free survival in patients with intracranial germinoma.
Publication Types:
- Evaluation Studies
- Multicenter Study
PMID: 15895370 [PubMed - indexed for MEDLINE]
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| 3: Cancer. 2005 Jul
1;104(1):135-42. |
|
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Recurrent central neurocytomas.
Bertalanffy
A, Roessler
K, Koperek
O, Gelpi
E, Prayer
D, Knosp
E.
Neurosurgical Department, Medical University of Vienna, Vienna, Austria.
alexander.bertalanffy@univie.ac.at
BACKGROUND: Since the first description of Central neurocytomas (CNs) as a
benign tumor entity in 1982, there has been great enthusiasm regarding the
benign course and the curative surgical approach to this disease. The
current study was performed to investigate the frequency of disease
recurrence during long-term follow-up. METHODS: A retrospective analysis of
the medical files with emphasis on clinicoradiologic findings and histologic
and immunohistochemical features was performed. RESULTS: Between 1985-2003.
surgical resection was performed in 14 patients with CNs ages 16-43 years (7
were female and 7 were male). Two patients (14%) died postoperatively and
one patient had a malignant disease course (7%). In the remaining 11
patients, one patient with an incompletely resected CN had disease
progression after 37 months but at the time of last follow-up had had stable
disease for 10 years. In addition, the authors reported 5 patients with
disease recurrence occurring at a median of 67 months after surgery (range,
51-79 months after surgery), all of which occurred after complete surgical
resection was performed. The observation period for the remaining 5 patients
was short (median of 34 months [range, 5-44 months]). Extensive histologic
and immunohistochemical workup did not identify any significant prognostic
parameters. The MIB-1 proliferation index ranged from 0.8-11% (median of
4.6%), but was reported to be 46.8% in the malignant transformed tumor. All
patients with disease recurrence responded well to different forms of focal
radiation therapy (gamma knife radiosurgery in three patients and
interstitial irradiation in one patient) and for one patient with a recently
detected recurrence, gamma knife radiosurgery was planned. CONCLUSIONS: CNs
appear to have a higher tendency to recur during long-term follow-up than
previously reported, even after complete resection. Therefore, periodic
neuroradiologic follow-up examinations should be considered mandatory in all
patients, even after several years.
PMID: 15880432 [PubMed - indexed for MEDLINE]
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| 4: Clin
Cancer Res. 2005 Aug 15;11(16):5965-70. |
|
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PEX-producing human neural stem cells inhibit tumor
growth in a mouse glioma model.
Kim
SK, Cargioli
TG, Machluf
M, Yang
W, Sun
Y, Al-Hashem
R, Kim
SU, Black
PM, Carroll
RS.
Department of Neurosurgery, Brigham and Women's Hospital and Children's
Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
A unique characteristic of neural stem cells is their capacity to track
glioma cells that have migrated away from the main tumor mass into the
normal brain parenchyma. PEX, a naturally occurring fragment of human
metalloproteinase-2, acts as an inhibitor of glioma and endothelial cell
proliferation, migration, and angiogenesis. In the present study, we
evaluated the antitumor activity of PEX-producing human neural stem cells
against malignant glioma. The HB1.F3 cell line (immortalized human neural
stem cell) was transfected by a pTracer vector with PEX. The retention of
the antiproliferative activity and migratory ability of PEX-producing HB1.F3
cells (HB1.F3-PEX) was confirmed in vitro. For the in vivo studies,
DiI-labeled HB1.F3-PEX cells were stereotactically injected into established
glioma tumor in nude mice. Tumor size was subsequently measured by magnetic
resonance imaging and at the termination of the studies by histologic
analysis including tumor volume, microvessel density, proliferation, and
apoptosis rate. Histologic analysis showed that DiI-labeled HB1.F3-PEX cells
migrate at the tumor boundary and cause a 90% reduction of tumor volume (P
< 0.03). This reduction in tumor volume in animals treated with
HB1.F3-PEX was associated with a significant decrease in angiogenesis
(44.8%, P < 0.03) and proliferation (23.6%, P < 0.03). These results
support the use of neural stem cells as delivery vehicle for targeting
therapeutic genes against human glioma.
PMID: 16115940 [PubMed - in process]
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| 5: Clin
Cancer Res. 2005 Aug 15;11(16):5900-11. |
|
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Immunologic evaluation of personalized peptide
vaccination for patients with advanced malignant glioma.
Yajima
N, Yamanaka
R, Mine
T, Tsuchiya
N, Homma
J, Sano
M, Kuramoto
T, Obata
Y, Komatsu
N, Arima
Y, Yamada
A, Shigemori
M, Itoh
K, Tanaka
R.
Department of Neurosurgery, Brain Research Institute, Niigata University,
Niigata, Japan.
PURPOSE: The primary goal of this phase I study was to assess the safety and
immunologic responses of personalized peptide vaccination for patients with
advanced malignant glioma. EXPERIMENTAL DESIGN: Twenty-five patients with
advanced malignant glioma (8 grade 3 and 17 grade 4 gliomas) were evaluated
in a phase I clinical study of a personalized peptide vaccination. For
personalized peptide vaccination, prevaccination peripheral blood
mononuclear cells and plasma were provided to examine cellular and humoral
responses to 25 or 23 peptides in HLA-A24+ or HLA-A2+ patients, respectively;
then, only the reactive peptides (maximum of four) were used for in vivo
administration. RESULTS: The protocols were well tolerated with local
redness and swelling at the injection site in most cases. Twenty-one
patients received more than six vaccinations and were evaluated for both
immunologic and clinical responses. Increases in cellular or humoral
responses specific to at least one of the vaccinated peptides were observed
in the postvaccination (sixth) samples from 14 or 11 of 21 patients,
respectively. More importantly, significant levels of peptide-specific IgG
were detected in the postvaccination tumor cavity or spinal fluid of all of
the tested patients who showed favorable clinical responses. Clinical
responses were 5 partial responses, 8 cases of stable disease, and 8 cases
of progressive disease. The median overall survival for patients with
recurrent glioblastoma multiforme in this study (n = 17) was 622 days.
CONCLUSIONS: Personalized peptide vaccinations were recommended for the
further clinical study to malignant glioma patients.
PMID: 16115932 [PubMed - in process]
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| 6: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):247-52. |
|
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Toxicity, biodistribution, and convection-enhanced
delivery of the boronated porphyrin BOPP in the 9L intracerebral rat glioma
model.
Ozawa
T, Afzal
J, Lamborn
KR, Bollen
AW, Bauer
WF, Koo
MS, Kahl
SB, Deen
DF.
Department of Neurological Surgery, University of California, San Francisco,
San Francisco, CA, USA.
Purpose: To investigate the toxicity, biodistribution, and
convection-enhanced delivery (CED) of a boronated porphyrin (BOPP) that was
designed for boron neutron capture therapy and photodynamic therapy. Methods
and Materials: For the toxicity study, Fischer 344 rats were injected with
graded concentrations of BOPP (35-100 mg/kg) into the tail vein. For boron
biodistribution studies, 9L tumor-bearing rats received BOPP either
systematically (intravenously) or locally. Results: All rats that received
70 mg/kg BOPP and 70% of rats that received </=60 mg/kg BOPP i.v. either
had to be euthanized or died within 4 days of injection. In the
biodistribution study, boron levels were relatively high in liver, kidney,
spleen, and adrenal gland tissue, and moderate levels were found in all
other organs. The maximum tumor boron concentration was 21.4 mug/g at 48 h
after i.v. injection; this concentration of boron in brain tumors is at the
low end of the range considered optimal for therapy. In addition, the tumor/blood
ratio (approximately 1.2) was not optimal. When BOPP was delivered directly
into intracerebral 9L tumors with CED, we obtained tumor boron
concentrations much greater than those obtained by i.v. injection.
Convection-enhanced delivery of 1.5 mg BOPP produced an average tumor boron
level of 519 mug/g and a tumor/blood ratio of approximately 1850:1.
Conclusions: Our study demonstrates that changing the method of BOPP
delivery from i.v. to CED significantly enhances the boron concentration in
tumors and produces very favorable tumor/brain and tumor/blood ratios.
PMID: 16111595 [PubMed - in process]
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| 7: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):230-7. |
|
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Combined effects of radiation and interleukin-13
receptor-targeted cytotoxin on glioblastoma cell lines.
Kawakami
K, Kawakami
M, Liu
Q, Puri
RK.
Laboratory of Molecular Tumor Biology, Division of Cellular and Gene
Therapies, Center for Biologics Evaluation and Research, Food and Drug
Administration, Bethesda, MD.
Purpose: Interleukin-13 receptor-targeted cytotoxin (IL13-PE38) is highly
cytotoxic to human glioblastoma (GBM) cells. Although this molecule is being
tested in a multicenter Phase III clinical trial (PRECISE Study) in patients
with recurrent disease, the activity of IL13-PE38 when combined with
radiation therapy has not been investigated. Methods and Materials:
Cytotoxicity of IL13-PE38 to GBM cell lines was assessed by protein
synthesis inhibition and clonogenic assays, and the growth of GBM cells
receiving radiation was assessed by thymidine uptake assays. Expression of
IL-13 receptor alpha2 (IL-13Ralpha2) messenger ribonucleic acid (mRNA) in
GBM cells exposed to radiation was assessed by quantitative reverse
transcriptase/polymerase chain reaction (RT-PCR) and IL-13R density by
radiolabeled IL-13 binding assays. Results: Prior irradiation of GBM cell
lines followed by IL13-PE38 treatment did not enhance cytotoxicity; however,
concomitant 5 Gy irradiation and IL13-PE38 treatment was highly cytotoxic to
T98G, M059K, A172, and LN-229 cell lines as determined by cell viability
assays. There was a statistically significant decrease in number of viable
cells in IL13-PE38 and irradiated cells compared with irradiated cells alone
(p < 0.05) or IL13-PE38 treated cells alone (p < 0.05). In contrast,
U251, SN19, and U87MG cell lines did not show any combined effect. These
results were confirmed by clonogenic assays. Although three GBM cell
lines-U251, SN19, and A172-showed 2.8- to 13.9-fold upregulation of
IL-13Ralpha2 mRNA expression at 6-24 h after exposure to 5 Gy radiation,
specific binding of radiolabeled IL-13 to these cell lines did not improve.
Conclusions: Our results suggest that concomitant radiation therapy and
IL13-PE38 treatment may be beneficial for the treatment of patients with
GBM. This strategy may be worth exploring in animal models of human glioma.
PMID: 16111594 [PubMed - in process]
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| 8: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):64-74. |
|
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L-(methyl-11C) methionine positron emission tomography
for target delineation in resected high-grade gliomas before radiotherapy.
Grosu
AL, Weber
WA, Riedel
E, Jeremic
B, Nieder
C, Franz
M, Gumprecht
H, Jaeger
R, Schwaiger
M, Molls
M.
Department of Radiation Oncology, Klinikum Rechts der Isar, Technical
University of Munich, Munich, Germany.
Purpose: Using magnetic resonance imaging (MRI), residual tumor cannot be
differentiated from nonspecific postoperative changes in operated patients
with brain gliomas. The higher specificity and sensitivity of l-(methyl-11C)-labeled
methionine positron emissions tomography (MET-PET) in gliomas has been
demonstrated in previous studies and is the rationale for the integration of
this investigation in gross tumor volume delineation. The goal of this trial
was to quantify the affect of MET-PET vs. with MRI in gross tumor volume
definition for radiotherapy planning of high-grade gliomas. Methods and
Materials: The trial included 39 patients with resected malignant gliomas.
MRI and MET-PET data were coregistered based on mutual information. The
residual tumor volume on MET-PET and the volume of tissue abnormalities on
T(1)-weighted MRI (gadolinium [Gd] enhancement) and T(2)-weighted MRI (hyperintensity
areas) were compared using MET-PET/MRI fusion images. Results: The MET-PET
vs. Gd-enhanced T(1)-weighted MRI analysis was performed on 39 patients. In
5 patients (13%), MET uptake corresponded exactly with Gd enhancement, and
in 29 (74%) of 39 patients, the region of MET uptake was larger than that of
the Gd enhancement. In 27 (69%) of the 39 patients, the Gd enhancement area
extended beyond the MET enhancement. MET uptake was detected up to 45 mm
beyond the Gd enhancement. MET-PET vs. T(2)-weighted MRI was investigated in
18 patients. MET uptake did not correspond exactly with the hyperintensity
areas on T(2)-weighted MRI in any patient. In 9 (50%) of 18 patients, MET
uptake extended beyond the hyperintensity area on the T(2)-weighted MRI, and
in 18 (100%), at least some hyperintensity on the T(2)-weighted MRI was
located outside the MET enhancement area. MET uptake was detected up to 40
mm beyond the hyperintensity area on T(2)-weighted MRI. Conclusion: In
operated patients with brain gliomas, the size and location of residual MET
uptake differs considerably from abnormalities found on postoperative MRI.
Because postoperative changes cannot be differentiated from residual tumor
by MRI, MET-PET, with a greater specificity for tumor tissue, can help to
outline the gross tumor volume with greater accuracy.
PMID: 16111573 [PubMed - in process]
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| 9: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):56-63. |
|
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MRI changes due to early-delayed conformal radiotherapy
and postsurgical effects in patients with brain tumors.
Armstrong
CL, Hunter
JV, Hackney
D, Shabbout
M, Lustig
RW, Goldstein
B, Werner-Wasik
M, Curran
WJ Jr.
Department of Neurology, University of Pennsylvania Medical School,
Philadelphia, PA; Division of Oncology, The Children's Hospital of
Philadelphia, Philadelphia, PA.
Purpose: Discernment of radiotherapy (XRT) effects vs. tumor activity is
difficult in brain tumor patients during the months after XRT when white
matter hyperintensities sometimes emerge. We examined brain scans in
XRT-treated vs. untreated patients for early-delayed post-XRT effects.
Methods and Materials: Brain regions susceptible to XRT injury were examined
on magnetic resonance imaging (MRI) for T2-weighted hyperintensities and
atrophy in 37 adults with low-grade primary brain tumors (13 nonirradiated
and 24 irradiated). Cases evidencing recurrence/growth over the study period
were censored. Interactions with age, mood, fatigue, medications, tumor type
and grade, extent of resection, and laterality of MRI changes were examined.
Results: Hyperintensity and atrophy ratings over time for the treated and
untreated groups were not significantly different. White matter atrophy
increased unrelated to XRT. In all patients combined, white matter atrophy
and hyperintensities were greater at all time points and more lateralized in
surgically treated patients. Conclusions: Radiotherapy status was not
related to changes in MRI ratings during the weeks/months after XRT.
Findings contradict assumptions about radiographically evidenced
early-delayed XRT effects. Increases in T2-weighted hyperintensities during
the 1-6-month period postconformal radiotherapy for low-grade tumors are
likely not related to early-delayed XRT effects.
PMID: 16111572 [PubMed - as supplied by publisher]
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| 10: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):47-55. |
|
-
The American Society for Therapeutic Radiology and
Oncology (ASTRO) evidence-based review of the role of radiosurgery for
malignant glioma.
Tsao
MN, Mehta
MP, Whelan
TJ, Morris
DE, Hayman
JA, Flickinger
JC, Mills
M, Rogers
CL, Souhami
L.
The American Society for Therapeutic Radiology and Oncology, Fairfax, VA.
Purpose: To systematically review the evidence for the use of stereotactic
radiosurgery or stereotactic fractionated radiation therapy in adult
patients with malignant glioma. Methods: Key clinical questions to be
addressed in this evidence-based review were identified. Outcomes considered
were overall survival, quality of life or symptom control, brain tumor
control or response and toxicity. MEDLINE (1990-2004 June Week 2), CANCERLIT
(1990-2003), CINAHL (1990-2004 June Week 2), EMBASE (1990-2004 Week 25), and
the Cochrane library (2004 issue 2) databases were searched using OVID. In
addition, the Physician Data Query clinical trials database, the proceedings
of the American Society of Clinical Oncology (1997-2004), ASTRO (1997-2004),
and the European Society of Therapeutic Radiology and Oncology (ESTRO)
(1997-2003) were searched. Data from the literature search were reviewed and
tabulated. This process included an assessment of the level of evidence.
Results: For patients with newly diagnosed malignant glioma, radiosurgery as
boost therapy with conventional external beam radiation was examined in one
randomized trial, five prospective cohort studies, and seven retrospective
series. There is Level I evidence that the use of radiosurgery boost
followed by external beam radiotherapy and carmustine (BCNU) does not confer
benefit with respect to overall survival, quality of life, or patterns of
failure as compared with external beam radiotherapy and BCNU. There is Level
I-III evidence of toxicity associated with radiosurgery boost as compared
with external beam radiotherapy alone. The results of the prospective and
retrospective studies may be influenced by selection bias. Radiosurgery used
as salvage for recurrent or progressive malignant glioma after conventional
external beam radiotherapy failure was reported in zero randomized trials,
three prospective cohort studies, and five retrospective series. The
available data are sparse and insufficient to make absolute recommendations.
Stereotactic fractionated radiation therapy has been reported as boost
therapy with external beam radiotherapy for patients with newly diagnosed
malignant glioma in only three prospective studies. As primary therapy alone
without conventional external beam radiotherapy for newly diagnosed
malignant glioma patients, stereotactic fractionated radiation therapy has
been reported in only one prospective study. There were only three
prospective series and two retrospective studies reported for patients with
recurrent or progressive malignant glioma. Conclusions: For patients with
malignant glioma, there is Level I-III evidence that the use of radiosurgery
boost followed by external beam radiotherapy and BCNU does not confer
benefit in terms of overall survival, local brain control, or quality of
life as compared with external beam radiotherapy and BCNU. The use of
radiosurgery boost is associated with increased toxicity. For patients with
malignant glioma, there is insufficient evidence regarding the
benefits/harms of using radiosurgery at the time progression or recurrence.
There is also insufficient evidence regarding the benefits/harms in the use
of stereotactic fractionated radiation therapy for patients with newly
diagnosed or progressive/recurrent malignant glioma.
PMID: 16111571 [PubMed - in process]
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| 11: Int
J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):37-46. |
|
-
The American Society for Therapeutic Radiology and
Oncology (ASTRO) evidence-based review of the role of radiosurgery for brain
metastases.
Mehta
MP, Tsao
MN, Whelan
TJ, Morris
DE, Hayman
JA, Flickinger
JC, Mills
M, Rogers
CL, Souhami
L.
The American Society for Therapeutic Radiology and Oncology, Fairfax, VA.
Purpose: To systematically review the evidence for the use of stereotactic
radiosurgery in adult patients with brain metastases. Methods: Key clinical
questions to be addressed in this evidence-based review were identified.
Outcomes considered were overall survival, quality of life or symptom
control, brain tumor control or response and toxicity. MEDLINE (1990-2004
June Week 2), CANCERLIT (1990-2003), CINAHL (1990-2004 June Week 2), EMBASE
(1990-2004 Week 25), and the Cochrane library (2004 issue 2) databases were
searched using OVID. In addition, the Physician Data Query clinical trials
database, the proceedings of the American Society of Clinical Oncology
(ASCO) (1997-2004), ASTRO (1997-2004), and the European Society of
Therapeutic Radiology and Oncology (ESTRO) (1997-2003) were searched. Data
from the literature search were reviewed and tabulated. This process
included an assessment of the level of evidence. Results: For patients with
newly diagnosed brain metastases, managed with whole-brain radiotherapy
alone vs. whole-brain radiotherapy and radiosurgery boost, there were three
randomized controlled trials, zero prospective studies, and seven
retrospective series (which satisfied inclusion criteria). For patients with
up to three (<4 cm) newly diagnosed brain metastases (and in one study up
to four brain metastases), radiosurgery boost with whole-brain radiotherapy
significantly improves local brain control rates as compared with
whole-brain radiotherapy alone (Level I-III evidence). In one large
randomized trial, survival benefit with whole-brain radiotherapy was
observed in patients with single brain metastasis. In this trial, an overall
increased ability to taper down on steroid dose and an improvement in
Karnofsky performance status was seen in patients who were treated with
radiosurgery boost as compared with patients treated with whole-brain
radiotherapy alone. However, Level I evidence regarding overall quality of
life outcomes using a validated instrument has not been reported. All
randomized trials showed improved local control with the addition of
radiosurgery to whole-brain radiotherapy. For patients with multiple brain
metastases, there is no overall survival benefit with the use of
radiosurgery boost to whole-brain radiotherapy (Level I-III evidence).
Radiosurgery boost is associated with a small risk of early or late
toxicity. In patients treated with radiosurgery alone (withholding
whole-brain radiotherapy) as initial treatment, there were 2 randomized
trials, 2 prospective cohort studies, and 16 retrospective series. There is
Level I to Level III evidence that the use of radiosurgery alone does not
alter survival as compared to the use of whole-brain radiotherapy. However,
there is Level I to Level III evidence that omission of whole-brain
radiotherapy results in poorer intracranial disease control, both local and
distant (defined as remaining brain, outside the radiosurgery field).
Quality of life outcomes have not been adequately reported. Radiosurgery is
associated with a small risk of early or late toxicity. Radiosurgery as
salvage for patients with brain metastases was reported in zero randomized
trials, one prospective study, and seven retrospective series. Conclusions:
Based on Level I-III evidence, for selected patients with small (up to 4 cm)
brain metastases (up to three in number and four in one randomized trial),
the addition of radiosurgery boost to whole-brain radiotherapy improves
brain control as compared with whole-brain radiotherapy alone. In patients
with a single brain metastasis, radiosurgery boost with whole-brain
radiotherapy improves survival. There is a small risk of toxicity associated
with radiosurgery boost as compared with whole-brain radiotherapy alone. In
selected patients treated with radiosurgery alone for newly diagnosed brain
metastases, overall survival is not altered. However, local and distant
brain control is significantly poorer with omission of upfront whole-brain
radiotherapy (Level I-III evidence). Whether neurocognition or quality of
life outcomes are different between initial radiosurgery alone vs.
whole-brain radiotherapy (with or without radiosurgery boost) is unknown,
because this has not been adequately tested. There was no statistically
significant difference in overall toxicity between those treated with
radiosurgery alone vs. whole-brain radiotherapy and radiosurgery boost based
on an interim report from one randomized study. There is insufficient
evidence as to the clinical benefit/risks radiosurgery used in the setting
of recurrent or progressive brain metastases, although radiographic
responses are well-documented.
PMID: 16111570 [PubMed - in process]
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| 12: J Neurosurg.
2005 Jul;103(1):79-86. |
|
Inhibition of tumor growth and prolonged survival of rats
with intracranial gliomas following administration of clotrimazole.
Khalid
MH, Tokunaga
Y, Caputy
AJ, Walters
E.
Department of Biochemistry and Molecular Biology, Howard University College
of Medicine, Washington, DC 20059, USA. humayunkhalid@hotmail.com
OBJECT: Clotrimazole, an imidazole derivative and inhibitor of cytochrome
P-450, inhibits the proliferation of cancer cells by downregulating the
movement of intracellular Ca++ and K+ and by interfering with the
translation initiation process. Clotrimazole inhibits the proliferation of
human glioblastoma multiforme cells; it induces morphological changes toward
differentiation and blocks the cell cycle in the G1/G1 phase. In vitro,
clotrimazole enhances the antitumor effect of cisplatin by inducing
wild-type p53-mediated apoptosis. The authors examined the effect of
clotrimazole on tumor growth, sensitivity to cisplatin, and survival of rats
with intracranial gliomas. METHODS: Cultured C6 and 9L glioma cells were
exposed to clotrimazole, and cell growth was assessed using the
3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide colorimetric
assay. Clotrimazole produced a dose- and time-dependent inhibition of cell
proliferation. The growth inhibitory effect of clotrimazole could not be
overcome by exogenous stimulation with epidermal growth factor. Both C6 and
9L glioma cells were implanted into the rat brain and after 5 days, the
animals were treated with a daily single dose of clotrimazole for 8
consecutive days. Clotrimazole treatment caused a significant inhibition of
intracranial tumor growth. The survival of rats with 9L gliomas was analyzed
after 10 days of treatment with clotrimazole, cisplatin, or a combination of
clotrimazole and cisplatin. Rats treated with either drug displayed a
significantly prolonged survival time; however, the combination treatment
resulted only in an additional survival benefit. CONCLUSIONS: Clotrimazole
effectively inhibits cell proliferation and tumor growth, and prolongs
survival of rats with intracranial gliomas. Clotrimazole may be considered a
potential anticancer drug for treatment of intracranial gliomas.
PMID: 16121977 [PubMed - in process]
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| 13: Mayo
Clin Proc. 2005 Aug;80(8):1098. |
|
Retrograde jejunojejunal intussusception secondary to
metastatic melanoma.
Bilello
JF, Peterson
WM.
Department of Surgery, University Medical Center, University of California
San Francisco-Fresno Campus, Fresno, USA.
Publication Types:
PMID: 16092592 [PubMed - indexed for MEDLINE]
-
| 14: Mayo
Clin Proc. 2005 Aug;80(8):1050-7. |
|
Medication-induced hyperprolactinemia.
Molitch
ME.
Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern
University Feinberg School of Medicine, Chicago, IL 60611, USA.
molitch@northwestern.edu
Medication use is a common cause of hyperprolactinemia, and it is important
to differentiate this cause from pathologic causes, such as prolactinomas.
To ascertain the frequency of this clinical problem and to develop treatment
guidelines, the medical literature was searched by using PubMed and the
reference lists of other articles dealing with hyperprolactinemia due to
specific types of medications. The medications that most commonly cause
hyperprolactinemia are antipsychotic agents; however, some newer atypical
antipsychotics do not cause this condition. Other classes of medications
that cause hyperprolactinemia include antidepressants, antihypertensive
agents, and drugs that increase bowel motility. Hyperprolactinemia caused by
medications is commonly symptomatic, causing galactorrhea, menstrual
disturbance, and impotence. It is Important to ensure that
hyperprolactinemia in an Individual patient is due to medication and not to
a structural lesion in the hypothalamic/pituitary area; this can be
accomplished by (1) stopping the medication temporarily to determine whether
prolactin levels return to normal, (2) switching to a medication that does
not cause hyperprolactinemia (in consultation with the patient's
psychiatrist for psychoactive medications), or (3) performing magnetic
resonance imaging or computed tomography of the hypothalamic/pituitary area.
If the patient's hyperprolactinemia is symptomatic, treatment strategies
include switching to an alternative medication that does not cause
hyperprolactinemia, using estrogen or testosterone replacement, or, rarely,
cautiously adding a dopamine agonist.
Publication Types:
PMID: 16092584 [PubMed - indexed for MEDLINE]
-
| 15: Oncogene. 2005 Aug
29;24(37):5722-30. |
|
-
Tgf-Beta, neuronal stem cells and glioblastoma.
Golestaneh
N, Mishra
B.
1School of Medicine, Laboratory of Developmental Neurobiology, Georgetown
University, Medical Dental Building NW, Room 211-213, 3900 Reservoir Road
NW, Washington, DC 20007, USA.
Transforming growth factor beta (TGF-beta) signaling leads to a number of
biological end points involving cell growth, differentiation, and
morphogenesis. Typically, the cellular effect accompanies an induction of
mesodermal cell fate and inhibition of neural cell differentiation. However,
during pathological conditions, these defined effects of TGF-beta can be
reversed; for example, the growth-inhibitory effect is replaced with its
tumor promoting ability. A multitude of factors and cross-signaling pathways
have been reported to be involved in modulating the dual effects of
TGF-beta. In this review, we focus on the potential role of TGF-beta signal
transduction during development of neural progenitor cells and its relation
to glioblastoma development from neural stem cells.Oncogene (2005) 24,
5722-5730. doi:10.1038/sj.onc.1208925.
PMID: 16123805 [PubMed - in process]
-
| 16: Surg Neurol.
2005 Aug;64(2):154-9. |
|
-
Intracranial capillary hemangioma: case report and review
of the literature.
Simon
SL, Moonis
G, Judkins
AR, Scobie
J, Burnett
MG, Riina
HA, Judy
KD.
Department of Neurosurgery, The Hospital of the University of Pennsylvania,
Philadelphia, PA 19104, USA. ssimonpa@yahoo.com
BACKGROUND: Capillary hemangiomas are benign vascular lesions that commonly
present at birth or in early infancy on the face, scalp, back, or chest. The
authors present an exceedingly rare case of an intracranial capillary
hemangioma arising in an adult. Only 4 biopsy-proven cases have been
reported in the pediatric population previous to this case report. CASE
DESCRIPTION: A 31-year-old pregnant woman presented at 38 weeks of gestation
with severe headaches, nausea, and vomiting. Imaging revealed an extra-axial
mass lesion arising from the tentorium with both supra- and infratentorial
components. The patient underwent a resection of her tumor, which was
diagnosed as a capillary hemangioma by histopathologic examination. The
patient required 2 further resections after the lesion exhibited a rapid
regrowth from residual tumor in the left transverse sinus. The patient has
remained free of disease 41 months out from her third surgery. CONCLUSIONS:
Intracranial capillary hemangiomas are exceedingly rare entities, with a
capability for rapid growth. When gross total resection cannot be achieved,
these patients should be observed closely, and the use of adjuvant
radiotherapy should be considered.
Publication Types:
PMID: 16051010 [PubMed - indexed for MEDLINE]
-
| 17: Surg Neurol.
2005 Aug;64(2):101-2. |
|
-
Research news and notes.
Roitberg
B.
Department of Neurosurgery, University of Illinois, Chicago, IL 60612, USA.
roitberg@uic.edu
PMID: 16050995 [PubMed - indexed for MEDLINE]
|
Volume 4, Number 36 - 30 August 2005