| 1: Arch
Pathol Lab Med. 2005 Jul;129(7):e173-5. |
|
-
A 37-year-old woman with dural-based intracranial masses.
Haynik
DM, Prayson
RA.
Department of Anatomic Pathology, Cleveland Clinic Foundation, Cleveland,
Ohio 44195, USA.
Publication Types:
PMID: 15974832 [PubMed - indexed for MEDLINE]
  
-
| 2: Cancer. 2005 May
15;103(10):2132-42. |
|
-
Expression and structure of interleukin 4 receptors in
primary meningeal tumors.
Puri
S, Joshi
BH, Sarkar
C, Mahapatra
AK, Hussain
E, Sinha
S.
Department of Biochemistry, All India Institute of Medical Sciences, New
Delhi, India.
BACKGROUND: It was reported previously that malignant human tumors, like
glioma and medulloblastoma, express high-density interleukin (IL-4) receptor
mRNA and protein. Because IL-4 receptors (R) are sensitive targets for
targeted therapeutics, knowledge of the expression of these receptors in
other central nervous system tumors is of great interest. In this study, the
authors examined the expression and subunit composition of IL-4R complex in
primary human meningiomas. METHODS: Reverse transcription-polymerase chain
reaction (RT-PCR) analysis for IL-13Ralpha1, IL-4Ralpha and IL-2Rgammac was
performed on total RNA extracted from 35 meningiomas and a normal human
brain tissue sample. Results were confirmed in nine randomly selected tumors
by quantitative real-time PCR and in situ immunofluorescence assay. RESULTS:
Transcripts for the IL-4Ralpha and IL-13Ralpha1 chains were overexpressed in
meningiomas compared with normal brain tissue. The levels of IL-4Ralpha mRNA
appeared to be higher compared with the levels of IL-13Ralpha1 mRNA. The
results also showed that tumors with higher disease grade tended to have
increased mRNA expression for the IL-4Ralpha chain. This IL-4Ralpha mRNA
overexpression appeared to be more frequent in younger patients (age < 37
years). The transcripts for IL-2Rgammac chain were not detected in any of
the tumor samples or in normal brain tissue. Quantitative real-time PCR
confirmed the results of the RT-PCR analysis. Meningiomas also demonstrated
a bright immunofluorescent staining for the IL-4Ralpha and IL-13Ralpha1
chains but no staining for IL-2Rgammac. CONCLUSIONS: Expression of the
IL-4Ralpha and IL-13Ralpha1 chains and absence of IL-2gammac expression
established that meningiomas expressed type II IL-4Rs. These receptors may
serve as a target for cytotoxin/immunotoxin therapy in patients with
meningioma who are not amenable to surgical resection or for recurrent
tumors.
PMID: 15830341 [PubMed - indexed for MEDLINE]
-
| 3: Cancer. 2005 May
15;103(10):2143-53. |
|
-
Perineural spread of cutaneous malignancy to the brain: a
review of the literature and five patients treated with stereotactic
radiotherapy.
Fowler
BZ, Crocker
IR, Johnstone
PA.
Department of Radiation Oncology, Emory University School of Medicine,
Atlanta, Georgia 30322, USA.
BACKGROUND: The retrospective analysis was performed to investigate the role
of stereotactic radiotherapy (SRT) techniques for patients with intracranial
perineural spread (PNS) of a primary cutaneous malignancy. METHODS: Five
patients were identified who received SRT from 1993 to 2003 for cutaneous
malignancies with intracranial PNS to the cavernous sinus (n = 3) or
Meckel's cave (n = 2). Patients were treated with GammaKnife stereotactic
radiosurgery (n = 2), linear accelerator (linac)-based fractionated SRT (n =
2), or linac-based stereotactic radiosurgery (n = 1). RESULTS: The median
overall survival (OS) periods from diagnoses of cutaneous malignancy and
intracranial PNS were 63.0 months (range, 22.0-102.2 months) and 25.5 months
(range, 22.0-55.2 months), respectively. The median OS from SRT was 24.2
months (range, 19.5-53.2 months). One patient was alive and without evidence
of disease at 53 months of follow-up. The median durations of local and
regional control from SRT were 19.5 months (range, 1.5-53.2 months) and 7.0
months (range, 1.5-53.2 months), respectively. CONCLUSIONS: Previous reports
generally have recommended that patients with intracranial PNS receive
palliative external-beam radiotherapy. Results from the current study
suggest that some of these patients may have prolonged survival, or even may
be cured. Judicious use of SRT should be considered in their management.
Publication Types:
- Case Reports
- Review
- Review, Tutorial
PMID: 15816051 [PubMed - indexed for MEDLINE]
-
| 4: Childs
Nerv Syst. 2005 Jul 13; [Epub ahead of print] |
|
-
Editorial on Current surgical management of
craniopharyngiomas.
Tomita
T.
Division of Neurosurgery, Children's Memorial Hospital, 2300 Children's
Plaza, Chicago, IL, 60614, USA, ttomita@childrensmemorial.org.
PMID: 16012874 [PubMed - as supplied by publisher]
-
| 5: J
Clin Oncol. 2005 Jul 11; [Epub ahead of print] |
|
-
Clinicopathologic and Genetic Profile of Intracranial
Marginal Zone Lymphoma: A Primary Low-Grade CNS Lymphoma That Mimics
Meningioma.
Tu
PH, Giannini
C, Judkins
AR, Schwalb
JM, Burack
R, O'neill
BP, Yachnis
AT, Burger
PC, Scheithauer
BW, Perry
A.
Division of Neuropathology and Section of Hematopathology, Washington
University School of Medicine, St Louis, MO; Division of Neuropathology and
Department of Neurology, Mayo Clinic, Rochester, MN; Department of
Pathology, Children's Hospital of Philadelphia, University of Pennsylvania
School of Medicine, Philadelphia, PA; Division of Neurosurgery, University
of Toronto, Toronto, Ontario, Canada; Division of Neuropathology, University
of Florida College of Medicine, Gainesville, FL; and Department of
Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD.
PURPOSE: Although rare overall, marginal zone B-cell lymphoma (MZBCL) is the
most common primary low-grade CNS lymphoma reported in the literature. The
aim of this study is to elucidate the biology and genetic features of this
unusual tumor. PATIENTS AND METHODS: Fifteen CNS MZBCLs were studied
clinically, pathologically, and genetically, including fluorescent in situ
hybridization analyses with commercially available MALT1 and IgH break-apart
and centromere 3, 7, 12, and 18 probes. RESULTS: CNS MZBCLs preferentially
affect middle-aged women (female-to-male ratio, 4:1), with 93% presenting as
dural-based masses mimicking meningioma. Ten patients with 1 to 7.6 years of
follow-up after diagnosis showed no evidence of disease after radiation
and/or chemotherapy. Like MZBCLs outside of the CNS, they consisted of
CD20(+), CD3(-) small B lymphocytes with varying degrees of plasmacytic
differentiation and predominantly kappa light-chain restriction (78%).
Lymphoid follicles with follicular colonization were seen in three patients
and deposition of amyloid was noted in samples from two patients, one of
which was tumefactive. Neither Bcl-6 protein nor Epstein-Barr virus-encoded
RNA was expressed. Trisomy 3 was detected in six of 12 patients, with no
rearrangements of MALT1 or IgH and no trisomies of 7, 12, or 18 detected.
CONCLUSION: Our data suggest that intracranial MZBCL is an indolent primary
CNS lymphoma that typically presents as a meningioma-like dural-based mass.
Trisomy 3, but not MALT1 or IgH translocation, is a common genetic
abnormality that may contribute to the pathogenesis of this CNS lymphoma.
PMID: 16009945 [PubMed - as supplied by publisher]
-
| 6: Oncogene. 2005 Jun 20;
[Epub ahead of print] |
|
-
Role of p38 mitogen-activated kinase and c-Jun terminal
kinase in migration response to lysophosphatidic acid and
sphingosine-1-phosphate in glioma cells.
Malchinkhuu
E, Sato
K, Horiuchi
Y, Mogi
C, Ohwada
S, Ishiuchi
S, Saito
N, Kurose
H, Tomura
H, Okajima
F.
1Laboratory of Signal Transduction, Institute for Molecular and Cellular
Regulation, Gunma University, 3-39-15, Showa-machi, Maebashi 371-8512,
Japan.
A potential role for 1-oleoyl-sn-glycero-3-phosphate or lysophosphatidic
acid (LPA) and sphingosine-1-phosphate (S1P) in the regulation of malignant
diseases has been widely considered. In this study, we found that in
transformed astroglial cells, the expression profile of lysophospholipid
receptor mRNA and the action modes of LPA and S1P on cell motility were
changed: there was a change in the acquisition of the ability of LPA to
stimulate cell migration and a change in the migratory response to S1P from
stimulation through S1P(1) to inhibition through S1P(2). LPA-induced cell
migration was almost completely inhibited by either pertussis toxin, LPA(1)
receptor antagonists including Ki16425
(3-(4-[4-([1-(2-chlorophenyl)ethoxy]carbonyl amino)-3-methyl-5-isoxazolyl]
benzylsulfonyl)propanoic acid) or an inhibitor of phosphatidylinositol
3-kinase (PI3K) wortmannin. The LPA-induced action was also suppressed,
although incompletely, by several specific inhibitors for intracellular
signaling pathways including Rac1, Cdc42, p38 mitogen-activated protein
kinase (p38MAPK) and c-Jun terminal kinase (JNK), but not extracellular
signal-regulated kinase. Nearly complete inhibition of migration response to
LPA, however, required simultaneous inhibition of both the p38MAPK and JNK
pathways. Inhibition of Rac1 suppressed JNK but not p38MAPK, while the
activity of p38MAPK was abolished by a dominant-negative form of Cdc42.
These findings suggest that, in glioma cells, the PI3K/Cdc42/p38MAPK and
PI3K/Rac1/JNK pathways are equally important for LPA(1) receptor-mediated
migration.Oncogene advance online publication, 20 June 2005;
doi:10.1038/sj.onc.1208805.
PMID: 16007180 [PubMed - as supplied by publisher]
-
| 7: Oncogene. 2005 Jun 27;
[Epub ahead of print] |
|
-
Sodium butyrate sensitizes human glioma cells to
TRAIL-mediated apoptosis through inhibition of Cdc2 and the subsequent
downregulation of survivin and XIAP.
Kim
EH, Kim
HS, Kim
SU, Noh
EJ, Lee
JS, Choi
KS.
1Institute for Medical Sciences, Ajou University School of Medicine, Suwon,
South Korea.
In TNF-related apoptosis-inducing ligand (TRAIL)-resistant glioma cells,
co-treatment with nontoxic doses of sodium butyrate and TRAIL resulted in a
marked increase of TRAIL-induced apoptosis. This combined treatment was also
cytotoxic to glioma cells overexpressing Bcl-2 or Bcl-xL, but not to normal
human astrocytes, thus offering an attractive strategy for safely treating
resistant gliomas. Cotreatment with sodium butyrate facilitated completion
of proteolytic processing of procaspase-3 that was partially blocked by
treatment with TRAIL alone. We also found that treatment with sodium
butyrate significantly decreased the protein levels of survivin and X-linked
inhibitor of apoptosis protein (XIAP), two major caspase inhibitors.
Overexpression of survivin and XIAP attenuated sodium butyrate-stimulated
TRAIL-induced apoptosis, suggesting its involvement in conferring TRAIL
resistance to glioma cells. Furthermore, the kinase activities of Cdc2 and
Cdk2 were significantly decreased following sodium butyrate treatment,
accompanying downregulation of cyclin A and cyclin B, as well as
upregulation of p21. Forced expression of Cdc2 plus cyclin B, but not Cdk2
plus cyclin A, attenuated sodium butyrate/TRAIL-induced apoptosis,
overriding sodium butyrate-mediated downregulation of survivin and XIAP.
Therefore, Cdc2-mediated downregulation of survivin and XIAP by sodium
butyrate may contribute to the recovery of TRAIL sensitivity in glioma
cells.Oncogene advance online publication, 27 June 2005;
doi:10.1038/sj.onc.1208851.
PMID: 16007142 [PubMed - as supplied by publisher]
-
| 8: Oncogene. 2005 Jul 4; [Epub
ahead of print] |
|
-
PI3K-AKT pathway negatively controls EGFR-dependent
DNA-binding activity of Stat3 in glioblastoma multiforme cells.
Ghosh
MK, Sharma
P, Harbor
PC, Rahaman
SO, Haque
SJ.
1Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic
Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.
Glioblastoma multiforme (GBM) cells frequently harbor amplification and/or
gain-of-function mutation of the EGFR gene leading to the activation of
multiple signaling pathways. Blockade of EGFR activation inhibited the
activation of both AKT and Stat3 in U87 and D54 GBM cells and induced
spontaneous apoptosis, which were associated with reduction in the
steady-state level of Mcl-1. Surprisingly, inhibition of PI3 kinase (PI3K)
activity, which in turn inhibited AKT activation, significantly increased
the DNA-binding activity of Stat3 in U87 and D54 cells. This was not due to
an increase in the level of tyrosine-phosphorylated Stat3. Conversely,
ectopic expression of constitutively activated AKT significantly decreased
the DNA-binding activity of Stat3 in 293T cells. Interestingly, blockade of
protein phosphatase 2A activity in GBM or 293T cells by calyculin A, which
activated AKT, stabilized the phosphorylation of multiple Ser/Thr residues
that were located in the transactivation domain (TAD) of Stat3 and this in
turn completely ablated the DNA-binding activity of Stat3. Collectively,
these results suggest that both Stat3 and AKT provide survival signals in
U87 and D54 cells, and Ser/Thr phosphorylation of Stat3-TAD by the PI3K-AKT
pathway negatively controls the DNA-binding function of Stat3.Oncogene
advance online publication, 4 July 2005; doi:10.1038/sj.onc.1208894.
PMID: 16007122 [PubMed - as supplied by publisher]
-
| 9: Pediatr
Hematol Oncol. 2005 Jul-Aug;22(5):361-71. |
|
Recent advances in the treatment of childhood brain
tumors.
Khatua
S, Jalali
R.
Division of Pediatric Oncology, Tata Memorial Center, Mumbai, India.
Pediatric brain tumors are the commonest cause of cancer-related death in
children. The last four decades have seen only a 35% increase in 5-year
survival rate of children with these tumors. The therapeutic successes
achieved are due to advances in neuroimaging, surgical techniques,
radiotherapy, and induction of newer chemotherapeutic agents along with
molecular targeted therapy. Neuroimaging advances include the use of MRA,
MRS, DSA, and PET scans. With the use of stereotactic surgery,
intraoperative mapping, and imaging, surgical resection has improved with
significant decrease in morbidity. A major development has been the use of
precision guided radiotherapy utilizing technologies like 3D-CRT, SRS, and
IMRT, thereby decreasing radiation to normal tissues. Induction of newer
drugs and high-dose chemotherapy with peripheral stem cell support has
improved survival and delayed radiation in younger children and infants with
brain tumors. Intense ongoing research is profiling novel molecular targets
for therapeutic intervention. Newer therapeutic strategies like blood brain
barrier disruption, immunotherapy, and gene therapy are in clinical trials.
This review article intends to give the reader an overview of current
therapeutic strategies and research involved in the treatment of children
with brain tumors.
PMID: 16020126 [PubMed - in process]-
|
Volume 4, Number 30 - 19 July 2005