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Sent on Friday, 2008 Nov 07.
Search brain cancer
Click on the following url to view complete results in pubmed. (Results may change over time.)
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==================== Entrez pubmed Results ======================
Items 1 - 5 of 43
1: Dev Dyn. 2008 Nov 4; [Epub ahead of print]
Semaphorin and neuropilin expression during early morphogenesis of Xenopus
laevis.
Koestner U, Shnitsar I, Linnemannstons K, Hufton AL, Borchers A.
Department of Developmental Biochemistry, Center for Molecular Physiology of the
Brain (CMPB), GZMB, University of Gottingen, Gottingen, Germany.
Semaphorins are major regulators of morphogenesis and are involved in a variety
of processes ranging from the guidance of cell migration to the development of
cancer. Since semaphorins were first characterized as repulsive neuronal
guidance cues, their expression has been best documented in the nervous system.
However, broader studies are lacking. Here, we describe the expression of 13
members of the semaphorin family and two neuropilin receptors during early
Xenopus laevis development. No particular expression pattern defines any of the
semaphorin classes, but many are dynamically expressed in distinct areas
undergoing morphogenetic cell movements like the developing mesoderm and the
migrating neural crest. Furthermore, the complementary expression patterns of
Sema3A/Nrp1 and Sema3F/Nrp2 are maintained across hundreds of millions of years,
possibly indicating a conserved role in the guidance of migrating neural crest
cells. Developmental Dynamics, 2008. (c) 2008 Wiley-Liss, Inc.
PMID: 18985750 [PubMed - as supplied by publisher]
2: Glia. 2008 Nov 4; [Epub ahead of print]
Oct4 is expressed in human gliomas and promotes colony formation in glioma
cells.
Du Z, Jia D, Liu S, Wang F, Li G, Zhang Y, Cao X, Ling EA, Hao A.
Key Laboratory of the Ministry of Education for Experimental Teratology,
Shandong University School of Medicine, Jinan, China.
There is increasing evidence that self-renewal capacity of cancer cells is
critical for carcinogenesis; hence, it is vital to examine the expression and
involvement of self-renewal regulatory genes in these cells. Here, we reported
that Oct4, a well-known regulator of self-renewal in embryonic stem cells, was
highly expressed in human gliomas and glioma cell lines, and the expression
levels were increased in parallel with increasing glioma grades. In in vitro
cell cultures, Oct4 was only expressed in rat C6 glioma cells and rat neural
stem cells but not in rat brain differentiated cells. Downregulation of Oct4
expression by RNA interference in C6 cells was associated with reduced cell
proliferation and colony formation. Further analysis revealed that Oct4 could
upregulate phosphorylation of Stat3 to promote tumor cell proliferation.
Overexpression of Oct4 in C6 cells increased the expression of nestin but
decreased the expression of GFAP suggesting that Oct4 might inhibit the
differentiation of glioma cells. Our findings may provide further evidence for
the stem cell theory of carcinogenesis. In contrast, the results might also
imply that Oct4 contributes to the existence of undifferentiated cells in
gliomas. (c) 2008 Wiley-Liss, Inc.
PMID: 18985733 [PubMed - as supplied by publisher]
3: Dig Dis Sci. 2008 Nov 5; [Epub ahead of print]
Octreotide Uptake in Intracranial Metastasis of Pancreatic Ductal Adenocarcinoma
Origin in a Patient with a Prolonged Clinical Course.
Marepaily R, Micheals D, Sloan A, Hatfield J, Adsay V, Joyrich R, Ullah N, Tobi
M.
Department of Internal Medicine, Neurosurgery, Nuclear Medicine and Pathology,
John D. Dingell VAMC and Wayne State University School of Medicine, Detroit, MI,
USA.
We describe a case with prolonged survival of 2 years in a female patient with
pancreatic ductal adenocarcinoma who, at diagnosis, already had liver spread and
eventually succumbed to brain metastases which scanned positive with
[(111)In-DTPA] octreotide scintiscan (OctreoScan). Subsequently, the patient
underwent a craniotomy for resection of the metastases, but her condition
deteriorated. A chromogranin A stain was negative, showing that there was no
neuroendocrinal component to the cerebral secondaries. In contrast, tumor
labeling with a monoclonal antibody associated with a favorable prognosis in
pancreatic neoplasms was positive. There is mounting evidence that somatostatin
receptor status confers a relatively favorable prognosis in pancreatic
adenocarcinoma, although OctreoScan-positive brain metastases have not been
previously reported.
PMID: 18985450 [PubMed - as supplied by publisher]
4: Acta Neuropathol. 2008 Nov 5; [Epub ahead of print]
Analysis of the IDH1 codon 132 mutation in brain tumors.
Balss J, Meyer J, Mueller W, Korshunov A, Hartmann C, von Deimling A.
Clinical Cooperation Unit Neuropathology G380, German Cancer Research Center,
69120, Heidelberg, Germany.
A recent study reported on mutations in the active site of the isocitrate
dehydrogenase (IDH1) gene in 12% of glioblastomas. All mutations detected
resulted in an amino acid exchange in position 132. We analyzed the genomic
region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors
including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7
pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult
glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83
oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial
primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23
pituitary adenomas. A total of 221 somatic IDH1 mutations were detected and the
highest frequencies occurred in diffuse astrocytomas (68%), oligodendrogliomas
(69%), oligoastrocytomas (78%) and secondary glioblastomas (88%). Primary
glioblastomas and other entities were characterized by a low frequency or
absence of mutations in amino acid position 132 of IDH1. The very high frequency
of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas
suggests a role in early tumor development.
PMID: 18985363 [PubMed - as supplied by publisher]
5: PLoS ONE. 2008;3(11):e3655. Epub 2008 Nov 5.
CD133 is a marker of bioenergetic stress in human glioma.
Griguer CE, Oliva CR, Gobin E, Marcorelles P, Benos DJ, Lancaster JR Jr,
Gillespie GY.
Department of Surgery, Division of Neurosurgery, University of Alabama at
Birmingham, Birmingham, AL, USA. cgriguer@uab.edu
Mitochondria dysfunction and hypoxic microenvironment are hallmarks of cancer
cell biology. Recently, many studies have focused on isolation of brain cancer
stem cells using CD133 expression. In this study, we investigated whether CD133
expression is regulated by bioenergetic stresses affecting mitochondrial
functions in human glioma cells. First, we determined that hypoxia induced a
reversible up-regulation of CD133 expression. Second, mitochondrial dysfunction
through pharmacological inhibition of the Electron Transport Chain (ETC)
produced an up-regulation of CD133 expression that was inversely correlated with
changes in mitochondrial membrane potential. Third, generation of stable glioma
cells depleted of mitochondrial DNA showed significant and stable increases in
CD133 expression. These glioma cells, termed rho(0) or rho(0), are characterized
by an exaggerated, uncoupled glycolytic phenotype and by constitutive and stable
up-regulation of CD133 through many cell passages. Moreover, these rho(0) cells
display the ability to form "tumor spheroids" in serumless medium and are
positive for CD133 and the neural progenitor cell marker, nestin. Under
differentiating conditions, rho(0) cells expressed multi-lineage properties.
Reversibility of CD133 expression was demonstrated by transfering parental
mitochondria to rho(0) cells resulting in stable trans-mitochondrial "cybrid"
clones. This study provides a novel mechanistic insight about the regulation of
CD133 by environmental conditions (hypoxia) and mitochondrial dysfunction
(genetic and chemical). Considering these new findings, the concept that CD133
is a marker of brain tumor stem cells may need to be revised.
Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
PMID: 18985161 [PubMed - in process]