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Sent on Wednesday, 2008 Nov 19.
Search brain cancer
Click on the following url to view complete results in pubmed. (Results may change over time.)
http://www.ncbi.nlm.nih.gov/entrez/cubby.fcgi?call=0dYEPwvta4LBy_ePW3-4X0g5kUSpMpAnaGCscXMqxrEMo9GGvAzZeVOhjNqcDGk&WebCubbyUser=0jUZ_BJTQWEcVG_un8kbD6zb%40990F1EB9924A4BF1_0003SID
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==================== Entrez pubmed Results ======================
Items 1 - 5 of 91
1: J Theor Biol. 2008 Oct 29; [Epub ahead of print]
Chromosome-specific spatial periodicities in gene expression revealed by
spectral analysis.
Hanin L, Awadalla SS, Cox P, Glazko G, Yakovlev A.
Department of Mathematics, Idaho State University, 921 S. 8th Avenue, Stop 8085,
Pocatello, ID 83209-8085, USA.
Recent years have seen an unprecedented surge of research activity in studies of
gene expression. This extensive work, however, has been almost uniformly focused
on genome-wide gene expression and has largely ignored the fundamental fact that
every gene has a specific chromosome location. We propose a novel method of
spectral analysis for detecting hidden periodicities in gene expression signals
ordered along the length of each chromosome. Using this method, we have
discovered that each chromosome in rodents and humans has a unique periodic
pattern of gene expression. The uncovered spatial periodicities in gene
expression are tissue-specific in the sense that the largest differences in
humans were observed between two normal tissues (brain and mammary gland) as
well as between their tumor counterparts (glioma and breast cancer). The
smallest differences resulted from the comparison of tumors (glioma and breast
cancer) with their normal counterparts. All such effects do not extend to all
chromosomes but are limited to only some of them. The estimated periods and
amplitudes are identical for the genes located on the positive and negative DNA
strands. While precise molecular mechanisms of chromosome-specific periodicities
in gene expression have yet to be unraveled, their universal presence in
different tissues adds another dimension to the current understanding of the
genome organization.
PMID: 19014953 [PubMed - as supplied by publisher]
2: Johns Hopkins Med Lett Health After 50. 2008 Nov;20(9):1-2.
Understanding brain tumors.
[No authors listed]
PMID: 18998612 [PubMed - indexed for MEDLINE]
3: Cancer Cell. 2008 Nov 4;14(5):382-93.
miR-296 regulates growth factor receptor overexpression in angiogenic
endothelial cells.
Wurdinger T, Tannous BA, Saydam O, Skog J, Grau S, Soutschek J, Weissleder R,
Breakefield XO, Krichevsky AM.
Department of Neurology, Massachusetts General Hospital and Neuroscience
Program, Harvard Medical School, Boston, MA 02115, USA.
A key step in angiogenesis is the upregulation of growth factor receptors on
endothelial cells. Here, we demonstrate that a small regulatory microRNA,
miR-296, has a major role in this process. Glioma cells and angiogenic growth
factors elevate the level of miR-296 in primary human brain microvascular
endothelial cells in culture. The miR-296 level is also elevated in primary
tumor endothelial cells isolated from human brain tumors compared to normal
brain endothelial cells. Growth factor-induced miR-296 contributes significantly
to angiogenesis by directly targeting the hepatocyte growth factor-regulated
tyrosine kinase substrate (HGS) mRNA, leading to decreased levels of HGS and
thereby reducing HGS-mediated degradation of the growth factor receptors VEGFR2
and PDGFRbeta. Furthermore, inhibition of miR-296 with antagomirs reduces
angiogenesis in tumor xenografts in vivo.
Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
PMID: 18977327 [PubMed - indexed for MEDLINE]
4: Anasthesiol Intensivmed Notfallmed Schmerzther. 2008 Oct;43(10):682-90; quiz
691. Epub 2008 Oct 28.
[Decompressive craniectomy in traumatic brain injury and malignant brain
infarction]
[Article in German]
Greiner C.
Klinik fur Neurochirurgie und Wirbelsaulenchirurgie, Marienhospital Osnabruck.
neuro@mho.de
High intracranial pressure (ICP) is the most frequent cause of death and
disability after severe traumatic brain injury and malignant cerebral
infarction. After failure of general therapeutic maneuvers and first line
therapies, "second tier" therapies have to be considered. Decompressive
craniectomy is an advanced treatment option for controlling intracranial
pressure (ICP). In this review indications and techniques of decompressive
craniectomy are described and current literature is discussed. The author
concludes that decompressive craniectomy is no routine, but should be considered
in individual cases.
Publication Types:
English Abstract
PMID: 18958822 [PubMed - indexed for MEDLINE]
5: J Cell Biol. 2008 Nov 3;183(3):385-91. Epub 2008 Oct 27.
Sonic Hedgehog signaling impairs ionizing radiation-induced checkpoint
activation and induces genomic instability.
Leonard JM, Ye H, Wetmore C, Karnitz LM.
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN
55905, USA.
The Sonic Hedgehog (Shh) pathway plays important roles in embryogenesis, stem
cell maintenance, tissue repair, and tumorigenesis. Haploinsufficiency of
Patched-1, a gene that encodes a repressor of the Shh pathway, dysregulates the
Shh pathway and increases genomic instability and the development of spontaneous
and ionizing radiation (IR)-induced tumors by an unknown mechanism. Here we show
that Ptc1(+/-) mice have a defect in the IR-induced activation of the ATR-Chk1
checkpoint signaling pathway. Likewise, transient expression of Gli1, a
downstream target of Shh signaling, disrupts Chk1 activation in human cells by
preventing the interaction of Chk1 with Claspin, a Chk1 adaptor protein that is
required for Chk1 activation. These results suggest that inappropriate Shh
pathway activation promotes tumorigenesis by disabling a key signaling pathway
that helps maintain genomic stability and inhibits tumorigenesis.
Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
PMID: 18955550 [PubMed - indexed for MEDLINE]