BioMedLib Search Engine
[ goto HOMEPAGE ]
Search the biomedical literature, for the most relevant articles.
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Clarify the query
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
astrocytoma grade i 2005:2010[pubdate] *count=100
1412 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
grade i
' expands to
5 meanings
. Choose the one you intended:
Concept C0205615: well differentiated qualifier value;
details
Concept C0687695: grade 1 qualifier value;
details
Concept C1883546: who central nervous system grade i;
details
Concept : ;
details
Concept : ;
details
'
astrocytoma
' expanded to all its synonyms;
details
Email the results to the following email address:
Export the checked citations in RIS format (RIS format is used by RefWorks, Endnote, among others).
Items 1 to 100 of about 1412
1.
Gu J, Zhang C, Chen R, Pan J, Wang Y, Ming M, Gui W, Wang D:
Clinical implications and prognostic value of EMMPRIN/CD147 and MMP2 expression in pediatric gliomas.
Eur J Pediatr
; 2009 Jun;168(6):705-10
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Clinical implications and prognostic
value of
EMMPRIN/CD147 and MMP2 expression in pediatric
gliomas
.
Extracellular matrix metalloproteinase inducer (EMMPRIN), a member of the immunoglobulin superfamily, is present on the surface
of tumor
cells where it stimulates adjacent fibroblasts to produce matrix metalloproteinases (MMPs).
We have analyzed the clinicopathological characteristics of EMMPRIN and MMP2 expression in normal brain tissue and pediatric
gliomas
and evaluated their prognostic
value
in diagnosing the latter.
Immunochemistry analysis revealed EMMPRIN and MMP2 expression in cryo-sections of pediatric
gliomas
(45 samples) and normal brain tissue (20 samples).
Both EMMPRIN and MMP2 were expressed in normal brain and
glioma
tissues with different levels of malignancy.
The intensively positive expression rates of EMMPRIN (22/27) and MMP2 (21/27) in anaplastic
astrocytoma
and glioblastoma tissues were significantly higher than those in normal brain and low-
grade astrocytoma
tissues (2/28 and (1/2)8, respectively).
The positive expression of EMMPRIN and MMP2 was associated with higher
grade
gliomas
.
Based on these results, we conclude that EMMPRIN and MMP2 are expressed differently in normal brain and pediatric
gliomas
.
The detection of their co-expression may facilitate the prediction of pediatric
gliomas
prognosis.
[MeSH-major]
Antigens, CD147 / metabolism.
Astrocytoma
/ metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Matrix Metalloproteinase 2 / metabolism
[MeSH-minor]
Child. Child, Preschool.
Disease
Progression. Female. Humans. Immunohistochemistry. Infant. Male. Prognosis
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Pathol. 2002 Apr;160(4):1215-21
[
11943706.001
]
[Cites]
Brain Pathol. 1993 Jul;3(3):255-68
[
8293185.001
]
[Cites]
Int J Cancer. 2003 Feb 20;103(5):647-51
[
12494473.001
]
[Cites]
Am J Pathol. 1999 Feb;154(2):417-28
[
10027400.001
]
[Cites]
Cancer Res. 2004 Feb 15;64(4):1229-32
[
14983875.001
]
[Cites]
Am J Pathol. 2001 Jun;158(6):1921-8
[
11395366.001
]
[Cites]
Brain Pathol. 2007 Jul;17(3):276-81
[
17465990.001
]
[Cites]
Cancer Res. 2001 Mar 1;61(5):2276-81
[
11280798.001
]
[Cites]
Pathol Int. 2006 Jul;56(7):359-67
[
16792544.001
]
[Cites]
Rev Recent Clin Trials. 2006 May;1(2):119-31
[
18473963.001
]
[Cites]
Int J Cancer. 2002 May 10;99(2):157-66
[
11979428.001
]
[Cites]
Mol Cancer Res. 2005 Oct;3(10):541-51
[
16254188.001
]
[Cites]
Cancer Gene Ther. 2003 Nov;10(11):823-32
[
14605668.001
]
[Cites]
Cancer. 2004 Nov 1;101(9):1994-2000
[
15372476.001
]
[Cites]
Br J Cancer. 1996 Jun;73(11):1401-8
[
8645587.001
]
[Cites]
Cancer Res. 2005 Apr 15;65(8):3193-9
[
15833850.001
]
[Cites]
Int J Cancer. 2003 Sep 20;106(5):745-51
[
12866035.001
]
[Cites]
Cancer Immunol Immunother. 2008 Sep;57(9):1367-79
[
18273614.001
]
[Cites]
Am J Pathol. 1996 Jul;149(1):273-82
[
8686751.001
]
[Cites]
Cancer Res. 2007 May 1;67(9):4088-97
[
17483319.001
]
[Cites]
Am J Pathol. 2005 Jan;166(1):209-19
[
15632013.001
]
[Cites]
Oncogene. 2007 Aug 9;26(36):5229-37
[
17325663.001
]
[Cites]
Int J Cancer. 2006 Oct 15;119(8):1800-10
[
16721788.001
]
[Cites]
N Engl J Med. 2005 Mar 10;352(10 ):987-96
[
15758009.001
]
(PMID = 18795327.001).
[ISSN]
1432-1076
[Journal-full-title]
European journal of pediatrics
[ISO-abbreviation]
Eur. J. Pediatr.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / BSG protein, human; 136894-56-9 / Antigens, CD147; EC 3.4.24.24 / Matrix Metalloproteinase 2
2.
Prayson RA, Fong J, Najm I:
Coexistent pathology in chronic epilepsy patients with neoplasms.
Mod Pathol
; 2010 Aug;23(8):1097-103
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Neoplasms are
a well
-established cause of medically intractable or chronic epilepsy.
Certain tumors, including gangliogliomas and dysembryoplastic neuroepithelial tumors, are
well
known to be associated with cortical dysplasia.
Tumor
diagnoses included ganglioglioma (n=29), dysembryoplastic neuroepithelial
tumor
(n=10), low-
grade
glial/glioneuronal
neoplasm
(n=5), low-
grade astrocytoma
(n=2), angiocentric
glioma
(n=1), low-
grade
mixed
glioma
(n=1), dysembryoplastic neuroepithelial
tumor
/ganglioglioma mixed
tumor
(n=1), and meningioangiomatosis (n=1).
Forty-
one
(82%) tumors represented
WHO
grade
-I neoplasms.
Hamartias were identified in 10 patients (20%), hippocampal sclerosis in four patients (8%), and nodular heterotopia in
one
patient (2%).
The true incidence of coexistent pathology (17.8% in this study) was likely underrepresented, given the limited extent of adjacent non-tumoral tissue sampling in cases of resected
tumor
.
Coexistent pathology may account for the incidence of recurrent or residual epilepsy in patients
who
undergo
tumor
resection.
[MeSH-major]
Brain Neoplasms / pathology. Epilepsy / pathology.
Glioma
/ pathology
[MeSH-minor]
Adolescent. Adult. Brain / abnormalities. Child. Child, Preschool. Chronic
Disease
. Comorbidity. Female. Humans. Infant. Male. Middle Aged. Ohio / epidemiology. Retrospective Studies. Temporal Lobe / pathology. Young Adult
Genetic Alliance.
consumer health - Epilepsy
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
MedlinePlus Health Information.
consumer health - Epilepsy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20495542.001).
[ISSN]
1530-0285
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
3.
Nejat F, El Khashab M, Rutka JT:
Initial management of childhood brain tumors: neurosurgical considerations.
J Child Neurol
; 2008 Oct;23(10):1136-48
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The infratentorial compartment will be the primary site for 60% to 70% of these tumors, including
astrocytomas
, medulloblastomas, and ependymomas.
We review current diagnostic and therapeutic approaches and outcome for children harboring the most common pediatric brain tumors:
astrocytomas
(low-
grade
and high-
grade
glioma
), ependymoma, medulloblastoma, and craniopharyngioma.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 1994 Aug;12(8):1607-15
[
8040673.001
]
[Cites]
J Neurooncol. 1994;18(1):69-81
[
8057137.001
]
[Cites]
Cancer. 1994 Oct 15;74(8):2352-60
[
7922986.001
]
[Cites]
N Engl J Med. 1994 Dec 1;331(22):1500-7
[
7969301.001
]
[Cites]
Am J Clin Oncol. 1994 Dec;17(6):475-9
[
7977163.001
]
[Cites]
J Clin Oncol. 1995 Jan;13(1):112-23
[
7799011.001
]
[Cites]
J Neurosurg. 1995 Apr;82(4):536-47
[
7897512.001
]
[Cites]
J Pediatr Oncol Nurs. 1995 Oct;12(4):181-7
[
7495523.001
]
[Cites]
Neurosurgery. 1996 Apr;38(4):696-701; discussion 701-2
[
8692387.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Jul;81(7):2734-7
[
8675604.001
]
[Cites]
J Neurosurg. 1996 Oct;85(4):618-24
[
8814165.001
]
[Cites]
J Neurooncol. 1996 Jul;29(1):45-54
[
8817415.001
]
[Cites]
Pediatr Neurosurg. 1996;24(1):9-23
[
8817611.001
]
[Cites]
Pediatr Neurosurg. 1996;24(2):98-102
[
8841080.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1996 Oct 1;36(3):549-56
[
8948338.001
]
[Cites]
Pediatr Neurosurg. 1996 Jul;25(1):45-53
[
9055335.001
]
[Cites]
Surg Neurol. 1997 Mar;47(3):291-9
[
9068702.001
]
[Cites]
J Neurosurg. 2007 Jul;107(1 Suppl):5-10
[
17644914.001
]
[Cites]
Lancet Neurol. 2007 Dec;6(12):1073-85
[
18031705.001
]
[Cites]
Childs Nerv Syst. 2000 Jan;16(1):15-20
[
10672424.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1999 May 1;44(2):255-63
[
10760417.001
]
[Cites]
Childs Nerv Syst. 2000 Jun;16(6):341-50
[
10933229.001
]
[Cites]
J Neurosurg. 1997 Aug;87(2):257-61
[
9254090.001
]
[Cites]
J Clin Oncol. 1997 Aug;15(8):2792-9
[
9256121.001
]
[Cites]
J Neurosurg. 1998 Jan;88(1):1-10
[
9420066.001
]
[Cites]
J Clin Oncol. 1998 Jan;16(1):210-21
[
9440745.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1998 Mar 1;40(4):845-50
[
9531369.001
]
[Cites]
Pediatr Neurol. 1998 Feb;18(2):103-15
[
9535295.001
]
[Cites]
J Neurosurg. 1998 Jul;89(1):52-9
[
9647172.001
]
[Cites]
Pediatr Neurosurg. 1998 Apr;28(4):215-22
[
9732252.001
]
[Cites]
Pediatr Neurosurg. 1998 May;28(5):273-8
[
9732262.001
]
[Cites]
Clin Neurosurg. 1997;44:559-70
[
10080027.001
]
[Cites]
J Neurooncol. 2004 Aug-Sep;69(1-3):139-50
[
15527086.001
]
[Cites]
Cancer. 2005 Jan 1;103(1):133-9
[
15565574.001
]
[Cites]
Neurosurg Focus. 2003 Feb 15;14(2):e1
[
15727422.001
]
[Cites]
Neurosurg Focus. 2002 Sep 15;13(3):e4
[
15844876.001
]
[Cites]
J Neurosurg. 2005 Apr;102(4):629-36
[
15871504.001
]
[Cites]
Neurosurg Focus. 2005 Jun 15;18(6A):E10
[
16048286.001
]
[Cites]
Lancet Oncol. 2005 Aug;6(8):573-80
[
16054568.001
]
[Cites]
Childs Nerv Syst. 2005 Aug;21(8-9):660-8
[
15959733.001
]
[Cites]
Childs Nerv Syst. 2005 Aug;21(8-9):604-5
[
16012874.001
]
[Cites]
Childs Nerv Syst. 2005 Aug;21(8-9):729-46
[
16044343.001
]
[Cites]
Childs Nerv Syst. 2005 Aug;21(8-9):808-16
[
16075214.001
]
[Cites]
Neurosurg Focus. 2006;20(1):E8
[
16459998.001
]
[Cites]
Cancer. 2004 Aug 15;101(4):817-24
[
15305415.001
]
[Cites]
J Pediatr. 1975 Feb;86(2):254-8
[
1111694.001
]
[Cites]
Cancer. 1976 Apr;37(4):1944-52
[
1260697.001
]
[Cites]
J Neurosurg. 1981 Aug;55(2):174-82
[
7252539.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1983 Aug;9(8):1231-4
[
6347998.001
]
[Cites]
J Neurosurg. 1984 Mar;60(3):495-9
[
6699693.001
]
[Cites]
Neurosurgery. 1986 May;18(5):568-75
[
3714005.001
]
[Cites]
J Neurosurg. 2006 Feb;104(2 Suppl):108-14
[
16506498.001
]
[Cites]
Childs Nerv Syst. 2006 Oct;22(10):1296-300
[
16761160.001
]
[Cites]
J Neurosurg. 2007 Jan;106(1 Suppl):1-2; discussion 2
[
17233304.001
]
[Cites]
Eur J Cancer. 2007 Apr;43(6):1037-44
[
17349783.001
]
[Cites]
Cancer. 2007 Jul 15;110(2):432-41
[
17559078.001
]
[Cites]
J Neurosurg. 2000 Oct;93(4):605-13
[
11014538.001
]
[Cites]
Am J Pathol. 2001 Apr;158(4):1525-32
[
11290570.001
]
[Cites]
Neuro Oncol. 1999 Jul;1(3):232-50
[
11550316.001
]
[Cites]
Childs Nerv Syst. 2001 Sep;17(9):538-42; discussion 543
[
11585328.001
]
[Cites]
N Engl J Med. 2002 Feb 7;346(6):420-7
[
11832530.001
]
[Cites]
Eur Radiol. 2002 Jun;12(6):1342-8
[
12042937.001
]
[Cites]
J Clin Oncol. 2003 Apr 15;21(8):1581-91
[
12697884.001
]
[Cites]
Med Pediatr Oncol. 2003 Aug;41(2):123-7
[
12825216.001
]
[Cites]
J Clin Oncol. 2003 Aug 1;21(15):2968-73
[
12885817.001
]
[Cites]
Mod Pathol. 2003 Oct;16(10):980-91
[
14559980.001
]
[Cites]
Childs Nerv Syst. 2004 Mar;20(3):143-53
[
14669023.001
]
[Cites]
Pediatr Blood Cancer. 2004 May;42(5):461-4
[
15049021.001
]
[Cites]
J Neurosurg. 1986 Dec;65(6):751-5
[
3772472.001
]
[Cites]
J Neurooncol. 1988 Dec;6(4):309-17
[
3221258.001
]
[Cites]
J Neurooncol. 1989 Jul;7(2):165-77
[
2550594.001
]
[Cites]
Neurosurgery. 1989 Dec;25(6):959-64
[
2513523.001
]
[Cites]
J Neurosurg. 1990 Mar;72(3):408-17
[
2303876.001
]
[Cites]
Neuropediatrics. 1991 Feb;22(1):36-42
[
2038426.001
]
[Cites]
Neurosurgery. 1991 May;28(5):659-64; discussion 664-5
[
1876243.001
]
[Cites]
Neurosurgery. 1991 May;28(5):666-71; discussion 671-2
[
1876244.001
]
[Cites]
J Neurosurg. 1991 Oct;75(4):575-82
[
1885975.001
]
[Cites]
J Neuroradiol. 1991;18(2):201-9
[
1919685.001
]
[Cites]
Pediatr Neurosurg. 1990-1991;16(2):57-65
[
2132926.001
]
[Cites]
J Neurooncol. 1992 Jul;13(3):283-90
[
1517804.001
]
[Cites]
J Neurosurg. 1992 Oct;77(4):545-50
[
1527612.001
]
[Cites]
Radiother Oncol. 1993 Jan;26(1):1-10
[
8438080.001
]
[Cites]
Childs Nerv Syst. 1993 Feb;9(1):7-9
[
8481945.001
]
[Cites]
J Neurooncol. 1993 Feb;15(2):125-31
[
8509817.001
]
[Cites]
Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30
[
8133987.001
]
[Cites]
Neurosurgery. 1994 Feb;34(2):350-2; discussion 352-3
[
8177398.001
]
(PMID = 18952580.001).
[ISSN]
1708-8283
[Journal-full-title]
Journal of child neurology
[ISO-abbreviation]
J. Child Neurol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / R13 NS040925; United States / NINDS NIH HHS / NS / 5R13NS040925-09
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Number-of-references]
92
[Other-IDs]
NLM/ NIHMS487102; NLM/ PMC3714852
Advertisement
4.
Valera ET, Lucio-Eterovic AK, Neder L, Scrideli CA, Machado HR, Carlotti-Junior CG, Queiroz RG, Motta FJ, Tone LG:
Quantitative PCR analysis of the expression profile of genes related to multiple drug resistance in tumors of the central nervous system.
J Neurooncol
; 2007 Oct;85(1):1-10
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Quantitative PCR analysis of the expression profile of genes related to multiple drug resistance in tumors of the
central nervous system
.
METHODS: Eighty microdissected brain
tumor
samples from 79 patients were analyzed by RQ-PCR for the genes MDR1, MRP1, MRP3, LRP and BCRP.
Histological diagnoses: 21
astrocytomas
I and II, 28
astrocytomas
III and glioblastomas, 17 medulloblastomas, 8 ependymomas, and 6 oligodendrogliomas.
Low-
grade
astrocytomas
expressed high MDR1 (P = 0.001), MRP3 (P = 0.01) and LRP (P = 0.02) levels.
The profile of gene expression of primary pilocytic
astrocytomas of
the hypothalamus and of the other locations was similar.
Increased expression of resistance genes, separately or jointly, was not correlated with shorter overall survival in patients with medulloblastomas/PNET and malignant
gliomas
.
CONCLUSIONS: Drug resistance genes do not explain the higher sensitivity
of gliomas
of the hypothalamus/pituitary/optic pathways to chemotherapy.
The increased expression of resistance genes had no impact on the overall survival of patients with medulloblastomas/PNET and high
grade
gliomas
.
High MDR1, MRP3 and LRP levels may be implicated in the primary resistance of pilocytic
astrocytomas
to chemotherapy.
[MeSH-major]
Central Nervous System
Neoplasms / genetics. Drug Resistance, Multiple / genetics. Drug Resistance,
Neoplasm
/ genetics. Gene Expression Regulation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / physiology. Reverse Transcriptase Polymerase Chain Reaction / methods
[MeSH-minor]
Adolescent. Adult. Aged. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Brain Neoplasms / mortality. Calibration. Child. Child, Preschool. DNA Primers. Female. Gene Expression Profiling.
Glioma
/ drug therapy.
Glioma
/ genetics.
Glioma
/ mortality. Humans. Immunohistochemistry. Infant. Male. Medulloblastoma / drug therapy. Medulloblastoma / genetics. Medulloblastoma / mortality. Middle Aged. RNA,
Neoplasm
/ biosynthesis. RNA,
Neoplasm
/ genetics. Survival Analysis
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nat Rev Drug Discov. 2006 Mar;5(3):219-34
[
16518375.001
]
[Cites]
Clin Neuropathol. 2004 Sep-Oct;23(5):223-31
[
15581025.001
]
[Cites]
Clin Neuropathol. 2004 Jan-Feb;23(1):21-7
[
14986930.001
]
[Cites]
Clin Chem. 2002 Jun;48(6 Pt 1):811-7
[
12028995.001
]
[Cites]
Pediatr Neurosurg. 1995;23(6):283-91; discussion 291-2
[
8743996.001
]
[Cites]
Blood. 1999 Aug 1;94(3):1086-99
[
10419902.001
]
[Cites]
Blood. 1998 Mar 15;91(6):2092-8
[
9490695.001
]
[Cites]
Int J Cancer. 2001 Nov 1;94(3):377-82
[
11745417.001
]
[Cites]
Nat Struct Mol Biol. 2004 Oct;11(10):918-26
[
15452563.001
]
[Cites]
Epilepsia. 2005 Jun;46(6):849-57
[
15946326.001
]
[Cites]
Annu Rev Biochem. 1993;62:385-427
[
8102521.001
]
[Cites]
Anticancer Drugs. 1999 Nov;10(10):861-72
[
10630353.001
]
[Cites]
Br J Cancer. 1996 Oct;74(8):1263-8
[
8883415.001
]
[Cites]
Acta Neuropathol. 1997 Dec;94(6):605-11
[
9444363.001
]
[Cites]
Int J Cancer. 2001 Jul 1;93(1):62-6
[
11391622.001
]
[Cites]
Br J Neurosurg. 1994;8(5):585-91
[
7857540.001
]
[Cites]
Virchows Arch. 1994;425(2):133-8
[
7952498.001
]
[Cites]
J Neurooncol. 2005 Sep;74(2):113-21
[
16193381.001
]
[Cites]
J Neurosurg. 1990 Jan;72(1):96-101
[
2294193.001
]
[Cites]
Biol Pharm Bull. 2002 Nov;25(11):1391-400
[
12419946.001
]
[Cites]
An Acad Bras Cienc. 2001 Mar;73(1):57-69
[
11246270.001
]
[Cites]
J Neurosurg. 1994 Nov;81(5):690-8
[
7931615.001
]
[Cites]
J Neurooncol. 1998 Oct;40(1):11-8
[
9874181.001
]
[Cites]
J Cell Sci. 1993 Sep;106 ( Pt 1):23-9
[
8270627.001
]
[Cites]
Pediatr Pathol Lab Med. 1996 Jul-Aug;16(4):551-61
[
9025853.001
]
[Cites]
Brain Tumor Pathol. 1999;16(1):23-7
[
10532420.001
]
[Cites]
Int J Cancer. 2002 Mar 10;98 (2):173-80
[
11857404.001
]
[Cites]
Cancer Res. 2005 Dec 15;65(24):11419-28
[
16357150.001
]
[Cites]
Curr Drug Deliv. 2004 Jan;1(1):27-42
[
16305368.001
]
(PMID = 17429576.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / RNA, Neoplasm
5.
De Falco G, Bellan C, D'Amuri A, Angeloni G, Leucci E, Giordano A, Leoncini L:
Cdk9 regulates neural differentiation and its expression correlates with the differentiation grade of neuroblastoma and PNET tumors.
Cancer Biol Ther
; 2005 Mar;4(3):277-81
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cdk9 regulates neural differentiation and its expression correlates with the differentiation
grade
of neuroblastoma and PNET tumors.
Cdk9 and Cyclin T1 expression levels were monitored during the differentiation program of neuroblastoma and
astrocytoma
cell lines.
Our results suggest that Cdk9/Cyclin T1 complex may be required for neuron differentiation induced by retinoic acid, because the expression level of the complex varies during differentiation, but no significant changes were observed in its expression in the
astrocytoma
cell line.
In addition, the expression of Cdk9 and Cyclin T1 was evaluated by immunohistochemistry in samples of neuroblastoma, PNET (Primary Neuroectodermal
Tumor
) and
astrocytoma
tumors of different grades, in order to assess whether there was a correlation between Cdk9 expression and
tumor
grading.
Our results show that in neuroblastoma and PNET
tumor
samples Cdk9 is more expressed the more
differentiated
the
tumor
is.
Conversely, no significant alteration of Cdk9 expression was observed in
astrocytoma
tumor
samples of different grades, thus confirming the results obtained for the cell lines.
[MeSH-minor]
Astrocytes / cytology. Astrocytes / drug effects. Astrocytes / pathology. Cell Differentiation. Cell Line,
Tumor
. Cyclin T. Cyclins / analysis. Cyclins / genetics. Cyclins / metabolism. Humans. Immunohistochemistry. RNA, Messenger / analysis. RNA, Messenger / metabolism. Tretinoin / pharmacology
Genetic Alliance.
consumer health - Neuroblastoma
.
MedlinePlus Health Information.
consumer health - Neuroblastoma
.
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15753651.001).
[ISSN]
1538-4047
[Journal-full-title]
Cancer biology & therapy
[ISO-abbreviation]
Cancer Biol. Ther.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CCNT1 protein, human; 0 / Cyclin T; 0 / Cyclins; 0 / RNA, Messenger; 5688UTC01R / Tretinoin; EC 2.7.11.22 / Cyclin-Dependent Kinase 9
6.
Huang H, Hara A, Homma T, Yonekawa Y, Ohgaki H:
Altered expression of immune defense genes in pilocytic astrocytomas.
J Neuropathol Exp Neurol
; 2005 Oct;64(10):891-901
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Altered expression of immune defense genes in pilocytic
astrocytomas
.
Pilocytic
astrocytoma
(
WHO
grade I
) is a circumscribed, slowly growing, benign
astrocytoma
that most frequently develops in the cerebellar hemispheres and in midline structures and occurs predominantly in childhood and adolescence.
In contrast to diffusely infiltrating
gliomas
in adults (e.g.
grade
II
astrocytomas
, oligodendrogliomas), survival of patients with pilocytic
astrocytoma
is excellent after surgical intervention.
To search for potential molecular mechanisms underlying its benign biologic behavior, we compared gene expression profiles of pilocytic
astrocytomas
(8 cases) with those of normal cerebellum (4 cases), low-
grade
astrocytomas
(
WHO
grade
II; 15 cases), and oligodendrogliomas (
WHO
grade
II; 17 cases) by cDNA array analysis.
A number of immune
system
-related genes such as HLA-DRalpha, HLA-DPB1, HLA-DQB1, IgG3, IgGK, FCER1G, A2M, FCRN, IFI-56K, and DAP12 were upregulated in pilocytic
astrocytomas
relative to normal cerebellum,
grade
II
astrocytomas
, and oligodendrogliomas.
Genes expressed at higher levels in pilocytic
astrocytomas
than in
grade
II
astrocytomas
and oligodendrogliomas include HLA-DRalpha, HLA-DPA1, HLA-DPB1, HLA-DQB1, A2M, TIMP1, TIMP2, CDKN1A, and SOCS3 and those expressed at lower levels include EGFR and PDGFRA.
Hierarchical clustering analysis using the entire set of 1176 genes distinguished pilocytic
astrocytomas
from
grade
II
astrocytomas
and oligodendrogliomas.
Clustering analysis using selected subgroups of genes based on their molecular functions revealed that immune
system
-related genes (75 genes) or cell adhesion, migration, and angiogenesis-related genes (69 genes) showed similar power to the entire gene set for separation of pilocytic
astrocytomas
from diffusely infiltrating low-
grade
gliomas
.
Immunohistochemistry revealed that HLA-DRalpha is expressed diffusely in neoplastic cells in pilocytic
astrocytomas
, whereas in oligodendrogliomas, expression was limited to scattered reactive astrocytes.
These results suggest that gene expression profiles of pilocytic
astrocytomas
differ significantly from those of diffusely infiltrating low-
grade
gliomas
and that their benign biologic behavior may be related to upregulation of immune defense-associated genes.
[MeSH-major]
Astrocytoma
/ genetics.
Astrocytoma
/ immunology. Brain Neoplasms / genetics. Brain Neoplasms / immunology. Gene Expression. Immunity / genetics
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16215461.001).
[ISSN]
0022-3069
[Journal-full-title]
Journal of neuropathology and experimental neurology
[ISO-abbreviation]
J. Neuropathol. Exp. Neurol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / HLA-DR Antigens; 0 / RNA, Messenger
7.
Tan G, Sun SQ, Yuan DL:
Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade.
Biochem Biophys Res Commun
; 2008 Mar 21;367(4):743-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression of Kir 4.1 in human
astrocytic
tumors: correlation with pathologic
grade
.
In this study, we investigated the expression of Kir 4.1 mRNA and protein in 80 cases of human
astrocytic
tumors by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry, respectively.
The correlation between Kir 4.1 expression and pathologic
grade
of astrocytic
tumors was further analyzed.
The results showed that the expression of Kir 4.1 mRNA and protein, as
well
as the Kir 4.1 immunoreactivity score (IRS), increased markedly with increasing pathologic
grade
.
Therefore, Kir 4.1 may be a new biomarker
for astrocytic
tumors.
It may also be an attractive therapy target for human
astrocytic
tumors.
[MeSH-major]
Astrocytoma
/ metabolism. Biomarkers,
Tumor
/ metabolism. Brain Neoplasms / metabolism.
Neoplasm
Proteins / metabolism. Potassium Channels, Inwardly Rectifying / metabolism
[MeSH-minor]
Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Statistics as Topic.
Tumor
Cells, Cultured
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18191638.001).
[ISSN]
1090-2104
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Kcnj10 (channel); 0 / Neoplasm Proteins; 0 / Potassium Channels, Inwardly Rectifying
8.
Sanli AM, Turkoglu E, Dolgun H, Sekerci Z:
Unusual manifestations of primary Glioblastoma Multiforme: A report of three cases.
Surg Neurol Int
; 2010;1:87
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
BACKGROUND: Brain tumors, especially high-
grade
gliomas
, can present with focal or generalized signs due to mass effect, parenchymal infiltration and destruction.
Microscopic total
tumor
excision was done and histopathological analysis revealed that these tumors were glioblastoma multiforme.
CONCLUSIONS: Physicians should keep brain tumors in mind in the case of patients
who
present with atypical symptoms such as those reported here.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Arch Neurol. 2003 Mar;60(3):437-40
[
12633158.001
]
[Cites]
Expert Rev Neurother. 2007 Apr;7(4):343-9
[
17425489.001
]
[Cites]
Acta Neuropathol. 2007 Aug;114(2):97-109
[
17618441.001
]
[Cites]
Neurology. 2010 Feb 16;74(7):610-2
[
20157165.001
]
[Cites]
Neurology. 1984 Jun;34(6):837-9
[
6539452.001
]
[Cites]
J Neurosurg. 1960 Jul;17:736-50
[
14439403.001
]
[Cites]
J Formos Med Assoc. 2003 Oct;102(10):737-40
[
14691602.001
]
[Cites]
JAMA. 2005 Feb 2;293(5):557-64
[
15687310.001
]
[Cites]
Mayo Clin Proc. 2007 Oct;82(10):1271-86
[
17908533.001
]
[Cites]
West J Med. 1995 Jul;163(1):19-25
[
7667978.001
]
[Cites]
Acta Neurol Scand. 1994 Sep;90(3):218-21
[
7847064.001
]
[Cites]
Neurology. 1993 Sep;43(9):1678-83
[
8414011.001
]
[Cites]
Am Fam Physician. 2008 May 15;77(10):1423-30
[
18533376.001
]
[Cites]
Neurosurgery. 1996 Aug;39(2):253-8; discussion 258-9
[
8832661.001
]
[Cites]
J Neurosurg. 1958 Sep;15(5):489-503
[
13576192.001
]
(PMID = 21206896.001).
[ISSN]
2152-7806
[Journal-full-title]
Surgical neurology international
[ISO-abbreviation]
Surg Neurol Int
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC3011111
[Keywords]
NOTNLM ; Astrocytoma / brain tumor / glioblastoma multiforme / presentation / symptom
9.
Zeng Y, Yang Z, Long XD, You C:
Inhibition of all-trans retinoic acid on MDM2 gene expression in astrocytoma cell line SHG-44.
Neurosci Bull
; 2008 Oct;24(5):297-304
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Inhibition of all-trans retinoic acid on MDM2 gene expression in
astrocytoma
cell line SHG-44.
OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in
astrocytoma
cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human
astrocytoma
.
The expressions of MDM2 protein in
WHO
grade
II and
grade
IV
astrocytomas
were determined by immunohistochemical streptavidin-peroxidase method.
Moreover, the percentages of MDM2-positive protein were 24.00% (6/25) and 56.52% (13/23) (chi(2) = 5.298, P = 0.021) in
WHO
grade
II and
grade
IV
astrocytomas
, respectively, suggesting that the expression of MDM2 protein may increase along with the elevation of
astrocytoma
malignancy.
CONCLUSION: ATRA can inhibit MDM2 gene expression in SHG-44 cells, and MDM2 is related to
astrocytoma
progression.
[MeSH-minor]
Astrocytoma
/ metabolism.
Astrocytoma
/ pathology. Cell Line,
Tumor
. Cell Proliferation / drug effects. Cell Size / drug effects. Humans. Oligonucleotide Array Sequence Analysis / methods. Time Factors
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9
[
11895036.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):731-6
[
15644444.001
]
[Cites]
Ai Zheng. 2006 Dec;25(12):1470-6
[
17166369.001
]
[Cites]
Gene. 2000 Jan 25;242(1-2):15-29
[
10721693.001
]
[Cites]
Mol Cancer Ther. 2006 Sep;5(9):2358-65
[
16985070.001
]
[Cites]
Neurosurgery. 2000 Feb;46(2):419-30
[
10690732.001
]
[Cites]
Cancer Res. 2005 Jul 1;65(13):5481-4
[
15994915.001
]
[Cites]
Cancer Res. 2005 Sep 15;65(18):8200-8
[
16166295.001
]
[Cites]
FEBS Lett. 2005 Jul 18;579(18):3965-9
[
15996664.001
]
[Cites]
Mol Cell Biol. 2006 Jan;26(1):192-8
[
16354690.001
]
[Cites]
Zhonghua Zhong Liu Za Zhi. 1984 Jul;6(4):241-3
[
6525937.001
]
[Cites]
Brain Res Mol Brain Res. 2001 Feb 19;87(1):100-8
[
11223164.001
]
[Cites]
Mol Cancer Res. 2003 Dec;1(14 ):993-1000
[
14707282.001
]
(PMID = 18839023.001).
[ISSN]
1673-7067
[Journal-full-title]
Neuroscience bulletin
[ISO-abbreviation]
Neurosci Bull
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Singapore
[Chemical-registry-number]
0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
10.
Walton NM, Snyder GE, Park D, Kobeissy F, Scheffler B, Steindler DA:
Gliotypic neural stem cells transiently adopt tumorigenic properties during normal differentiation.
Stem Cells
; 2009 Feb;27(2):280-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
An increasing body of evidence suggests that
astrocytic gliomas
of the
central nervous system
may be derived from gliotypic neural stem cells.
However, when induced to
differentiate
, neural stem cells give rise to intermediate progenitors that transiently exhibit multiple
glioma
characteristics, including aneuploidy, loss of growth-contact inhibition, alterations in cell cycle, and growth factor insensitivity.
Further examination of progenitor populations revealed a subset of cells defined by the aberrant expression of (the pathological
glioma
marker) class III beta-tubulin that exhibit intrinsic parental properties
of gliomas
, including multilineage differentiation and continued proliferation in the absence
of a
complex cellular regulatory environment.
MedlinePlus Health Information.
consumer health - Stem Cells
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18988710.001).
[ISSN]
1549-4918
[Journal-full-title]
Stem cells (Dayton, Ohio)
[ISO-abbreviation]
Stem Cells
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01 HL070143; United States / NICHD NIH HHS / HD / T32 HD043730; United States / NINDS NIH HHS / NS / NS055165; United States / NINDS NIH HHS / NS / NS37556; United States / NICHD NIH HHS / HD / T32HD043730; United States / NHLBI NIH HHS / HL / HL70143; United States / NINDS NIH HHS / NS / NS46384; United States / NINDS NIH HHS / NS / R01 NS037556; United States / NINDS NIH HHS / NS / R01 NS055165; United States / NINDS NIH HHS / NS / R21 NS046384
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Tubulin
[Other-IDs]
NLM/ NIHMS686089; NLM/ PMC4425277
11.
Grunwald I, Dillmann K, Roth C, Backens M, Reith W:
[Supratentorial tumors].
Radiologe
; 2007 Jun;47(6):471-85
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Magnetic resonance imaging is a routine diagnostic measure
for a
suspected intracerebral mass.
Further diagnostic procedures as
well
as the interpretation of the findings vary depending on the
tumor
location.
Supratentorial tumors include
astrocytoma
,
differentiated
by their circumscribed and diffuse growth, ganglioglioma, ependyoma, neurocytoma, primitive neuroectodermal tumors (PNET), oligodendroglioma, dysem-bryoplastic neuroepithelial tumors (DNET), meningoangiomatosis, pineal tumors, hamatoma, lymphoma, craniopharyngeoma and metastases.
The most common sub-forms, especially of
astrocytoma
, will also be presented.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Childs Nerv Syst. 2006 Jun;22(6):577-85
[
16555075.001
]
[Cites]
Cancer. 2004 Jul 1;101(1):146-55
[
15222000.001
]
[Cites]
Pediatr Dev Pathol. 1999 Nov-Dec;2(6):582-7
[
10508884.001
]
[Cites]
J Neurosurg Sci. 2005 Sep;49(3):73-6
[
16288189.001
]
[Cites]
Childs Nerv Syst. 2003 Jun;19(5-6):292-7
[
12750935.001
]
[Cites]
Neurology. 1996 Jun;46(6):1669-73
[
8649567.001
]
[Cites]
Childs Nerv Syst. 1998 Aug;14(8):357-61
[
9753400.001
]
[Cites]
Nat Clin Pract Neurol. 2007 Jan;3(1):24-35
[
17205072.001
]
[Cites]
Endocr Rev. 2006 Jun;27(4):371-97
[
16543382.001
]
[Cites]
J Neurooncol. 2001 Sep;54(3):251-61
[
11767291.001
]
[Cites]
AJNR Am J Neuroradiol. 1999 Nov-Dec;20(10):1839-41
[
10588106.001
]
[Cites]
AJNR Am J Neuroradiol. 2006 Jan;27(1):85-93
[
16418363.001
]
[Cites]
J Neurooncol. 1997 Aug;34(1):61-78
[
9210053.001
]
[Cites]
AJNR Am J Neuroradiol. 2001 Sep;22(8):1632
[
11559521.001
]
[Cites]
J Neurooncol. 1997 Aug;34(1):37-59
[
9210052.001
]
[Cites]
Childs Nerv Syst. 2005 Aug;21(8-9):635-9
[
16078078.001
]
[Cites]
J Neurooncol. 2004 Nov;70(2):161-81
[
15674476.001
]
[Cites]
Australas Radiol. 2005 Oct;49(5):433-7
[
16174188.001
]
[Cites]
Acta Neurochir (Wien). 2000;142(7):829-31
[
10955682.001
]
[Cites]
Mo Med. 1990 Dec;87(12):889-91
[
2270072.001
]
[Cites]
Neurocirugia (Astur). 2005 Dec;16(6):518-22
[
16378134.001
]
[Cites]
Childs Nerv Syst. 2003 Sep;19(9):650-4
[
12720031.001
]
[Cites]
J Neurol Neurosurg Psychiatry. 1994 Dec;57(12):1497-502
[
7798980.001
]
[Cites]
J Comput Assist Tomogr. 2004 May-Jun;28(3):407-13
[
15100549.001
]
[Cites]
Arq Neuropsiquiatr. 2006 Sep;64(3A):613-8
[
17119805.001
]
[Cites]
J Neuroimaging. 2006 Jan;16(1):52-8
[
16483277.001
]
[Cites]
Childs Nerv Syst. 2006 May;22(5):514-6
[
16369853.001
]
[Cites]
Cell Tissue Res. 2002 Dec;310(3):257-70
[
12457224.001
]
[Cites]
J Neurooncol. 1999;44(3):275-81
[
10720207.001
]
[Cites]
Neurology. 1998 Oct;51(4):1046-50
[
9781527.001
]
[Cites]
J Nippon Med Sch. 2000 Oct;67(5):388-91
[
11031374.001
]
[Cites]
Neurology. 2002 Sep 24;59(6):947-9
[
12297589.001
]
[Cites]
Neuroradiology. 1992;34(3):173-8
[
1630604.001
]
[Cites]
Semin Oncol. 2004 Oct;31(5):595-604
[
15497113.001
]
[Cites]
Radiology. 2003 Jul;228(1):193-9
[
12832582.001
]
[Cites]
Neuroradiology. 2006 Jan;48(1):1-7
[
16237548.001
]
[Cites]
AJR Am J Roentgenol. 1998 Mar;170(3):804-5
[
9490984.001
]
[Cites]
Cancer Imaging. 2006 Oct 31;6:S178-84
[
17114073.001
]
[Cites]
Radiographics. 2002 Sep-Oct;22(5):1177-89
[
12235346.001
]
[Cites]
Curr Neurol Neurosci Rep. 2003 May;3(3):193-9
[
12691623.001
]
[Cites]
Curr Opin Neurol. 1993 Dec;6(6):882-7
[
8293162.001
]
[Cites]
Semin Oncol. 2000 Jun;27(3 Suppl 6):1-10
[
10866344.001
]
[Cites]
Lancet. 2004 May 8;363(9420):1535-43
[
15135603.001
]
[Cites]
Arch Iran Med. 2007 Apr;10 (2):194-8
[
17367223.001
]
[Cites]
J Neurooncol. 2004 Nov;70(2):183-202
[
15674477.001
]
[Cites]
Am J Dis Child. 1988 May;142(5):486
[
3358385.001
]
[Cites]
Neurosurgery. 2005 Nov;57(5 Suppl):S10-23; discusssion S1-4
[
16237282.001
]
[Cites]
Eur Radiol. 2002 Jul;12 (7):1829-36
[
12111075.001
]
[Cites]
Expert Rev Neurother. 2006 Apr;6(4):519-32
[
16623651.001
]
[Cites]
Clin Radiol. 2006 Apr;61(4):348-57
[
16546465.001
]
[Cites]
Australas Radiol. 2000 Nov;44(4):460-3
[
11103549.001
]
[Cites]
Surg Neurol. 1998 Feb;49(2):197-204
[
9457271.001
]
[Cites]
J Neurooncol. 2006 May;78(1):59-62
[
16314940.001
]
[Cites]
Curr Opin Investig Drugs. 2005 Dec;6(12 ):1200-14
[
16370386.001
]
[Cites]
AJNR Am J Neuroradiol. 2000 Sep;21(8):1470-7
[
11003281.001
]
[Cites]
J Neurooncol. 1996 Jul;29(1):1-7
[
8817411.001
]
[Cites]
Cancer J. 2006 Jan-Feb;12(1):1-13
[
16613654.001
]
[Cites]
Neurosurg Focus. 2005 Jun 15;18(6A):E7
[
16048293.001
]
[Cites]
Clin Neurol Neurosurg. 2006 Jun;108(4):363-8
[
15893874.001
]
[Cites]
J Belge Radiol. 1994 Oct;77(5):221
[
7961378.001
]
(PMID = 17541538.001).
[ISSN]
0033-832X
[Journal-full-title]
Der Radiologe
[ISO-abbreviation]
Radiologe
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
30
12.
Nakase H, Tamura K, Kim YJ, Hirabayashi H, Sakaki T, Hoshida T:
Long-term follow-up outcome after surgical treatment for lesional temporal lobe epilepsy.
Neurol Res
; 2007 Sep;29(6):588-93
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Neuropathologic diagnoses were cavernoma in three cases,
astrocytoma
(
grade
2) in two cases, arteriovenous malformation in two cases, gliosis in two cases and ganglioglioma in
one
case.
Patients
who
had post-operative seizures may also achieve long-term seizure decrease or freedom in three cases: case 5 (E4-E2), case 6 (E4-E2) and case 7 (E3-E1).
Genetic Alliance.
consumer health - Epilepsy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17535567.001).
[ISSN]
0161-6412
[Journal-full-title]
Neurological research
[ISO-abbreviation]
Neurol. Res.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
England
13.
Lichy MP, Bachert P, Hamprecht F, Weber MA, Debus J, Schulz-Ertner D, Schlemmer HP, Kauczor HU:
[Application of (1)H MR spectroscopic imaging in radiation oncology: choline as a marker for determining the relative probability of tumor progression after radiation of glial brain tumors].
Rofo
; 2006 Jun;178(6):627-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Application of (1)H MR spectroscopic imaging in radiation
oncology
: choline as a marker for determining the relative probability
of tumor
progression after radiation of glial brain tumors].
PURPOSE: To determine the relative signal intensity ratios of choline (Cho), phosphocreatine (CR) and N-acetyl-aspartate (NAA) in MR spectroscopic imaging (proton-MRSI)
for differentiating
progressive tumors (PT) from non-progressive tumors (nPT) in follow-up and treatment planning
of gliomas
.
Threshold values to indicate the probability
of a
progressive
tumor
were also calculated.
MATERIAL AND METHODS: Thirty-four patients with histologically proven
gliomas
showing a suspicious brain lesion in MRI after stereotactic radiotherapy were evaluated on
a 1
.5 Tesla unit (Magnetom Vision, Siemens, Erlangen, Germany) using 2D proton MRSI (repetition time/echo time = 1500/135 msec, PRESS; voxel size 9 x 9 x 15 mm (3)).
PT and nPT were
differentiated
between on the basis of clinical course and follow-up by MRI, CT and positron emission tomography.
RESULTS: The Cho parameter and the relative signal intensity ratios of Cr and NAA were most effective in
differentiating
between PT and nPT.
CONCLUSION: (1)H-MRSI has a high sensitivity and specificity
for differentiating
between therapy-related effects and the relapse of irradiated
gliomas
.
[MeSH-major]
Aspartic Acid / analogs & derivatives.
Astrocytoma
/ diagnosis.
Astrocytoma
/ radiotherapy. Brain / radiation effects. Brain Neoplasms / diagnosis. Brain Neoplasms / radiotherapy. Choline / metabolism. Cranial Irradiation. Glioblastoma / diagnosis. Glioblastoma / radiotherapy. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy.
Neoplasm
Recurrence, Local / diagnosis. Oligodendroglioma / diagnosis. Oligodendroglioma / radiotherapy. Phosphocreatine / metabolism. Stereotaxic Techniques
[MeSH-minor]
Adult. Chemotherapy, Adjuvant. Combined Modality Therapy. Contrast Media. Diagnosis, Differential.
Disease
Progression. Female. Follow-Up Studies. Gadolinium DTPA. Humans. Male. Middle Aged. Neoadjuvant Therapy. Predictive
Value of
Tests. Radiotherapy Planning, Computer-Assisted. Radiotherapy, Adjuvant. Reference Values
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
Hazardous Substances Data Bank.
(L)-ASPARTIC ACID
.
Hazardous Substances Data Bank.
CHOLINE CHLORIDE
.
Hazardous Substances Data Bank.
GADOPENTETATE DIMEGLUMINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16703499.001).
[ISSN]
1438-9029
[Journal-full-title]
RöFo : Fortschritte auf dem Gebiete der Röntgenstrahlen und der Nuklearmedizin
[ISO-abbreviation]
Rofo
[Language]
ger
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Contrast Media; 020IUV4N33 / Phosphocreatine; 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; K2I13DR72L / Gadolinium DTPA; N91BDP6H0X / Choline
14.
Balss J, Meyer J, Mueller W, Korshunov A, Hartmann C, von Deimling A:
Analysis of the IDH1 codon 132 mutation in brain tumors.
Acta Neuropathol
; 2008 Dec;116(6):597-602
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
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%).
The very high frequency of IDH1 mutations in
WHO
grade
II
astrocytic
and oligodendroglial
gliomas
suggests a role in early
tumor
development.
[MeSH-minor]
Astrocytoma
/ genetics.
Astrocytoma
/ pathology. Base Sequence. DNA Mutational Analysis.
Disease
Progression. Gene Frequency. Glioblastoma / genetics. Glioblastoma / pathology.
Glioma
/ etiology.
Glioma
/ pathology. Humans. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Polymerase Chain Reaction
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18985363.001).
[ISSN]
1432-0533
[Journal-full-title]
Acta neuropathologica
[ISO-abbreviation]
Acta Neuropathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
EC 1.1.1.41 / Isocitrate Dehydrogenase
15.
Tepel M, Roerig P, Wolter M, Gutmann DH, Perry A, Reifenberger G, Riemenschneider MJ:
Frequent promoter hypermethylation and transcriptional downregulation of the NDRG2 gene at 14q11.2 in primary glioblastoma.
Int J Cancer
; 2008 Nov 1;123(9):2080-6
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
To further address the role of NDRG2 as a candidate
tumor
suppressor in human
gliomas
, we analyzed 67
astrocytic
tumors (10 diffuse
astrocytomas
, 11 anaplastic
astrocytomas
, 34 primary glioblastomas and 12 secondary glioblastomas) for NDRG2 gene mutation, promoter methylation and expression at the mRNA and protein levels.
Using real-time reverse transcription PCR analysis, we found decreased NDRG2 mRNA levels in primary glioblastomas as compared to diffuse and anaplastic
astrocytomas
.
Mutational analysis of the entire NDRG2 coding sequence did not reveal any
tumor
-associated DNA sequence alterations.
In contrast to primary glioblastomas, NDRG2 promoter hypermethylation was detected in only
1 of
11 anaplastic
astrocytomas
(9%) and was absent in 10 diffuse
astrocytomas
and 12 secondary glioblastomas.
Taken together, our data support NDRG2 as a candidate
tumor
suppressor gene that is epigenetically silenced in the majority of primary glioblastomas, but not in lower
grade
astrocytomas
and secondary glioblastomas.
[MeSH-major]
Brain Neoplasms / genetics. Chromosomes, Human, Pair 14. DNA Methylation. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Promoter Regions, Genetic.
Tumor
Suppressor Proteins / genetics
[MeSH-minor]
Down-Regulation. Gene Silencing. Genes,
Tumor
Suppressor. Humans. Immunohistochemistry. RNA, Messenger / analysis
Genetic Alliance.
consumer health - Glioblastoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 18709645.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / NDRG2 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
16.
Zarghooni M, Bartels U, Lee E, Buczkowicz P, Morrison A, Huang A, Bouffet E, Hawkins C:
Whole-genome profiling of pediatric diffuse intrinsic pontine gliomas highlights platelet-derived growth factor receptor alpha and poly (ADP-ribose) polymerase as potential therapeutic targets.
J Clin Oncol
; 2010 Mar 10;28(8):1337-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Whole-genome profiling of pediatric diffuse intrinsic pontine
gliomas
highlights platelet-derived growth factor receptor alpha and poly (ADP-ribose) polymerase as potential therapeutic targets.
PURPOSE: Diffuse intrinsic pontine
glioma
(DIPG) is
one of
the most devastating of pediatric malignancies and
one for
which no effective therapy exists.
A major contributor to the failure of therapeutic trials is the assumption that biologic properties of brainstem tumors in children are identical to cerebral high-
grade
gliomas of
adults.
A better understanding of the biology of DIPG itself is needed in order to develop agents targeted more specifically to these children's
disease
.
Herein, we address this lack of knowledge by performing the first high-resolution single nucleotide polymorphism (SNP) -based DNA microarray analysis
of a
series of DIPGs.
RESULTS: Analysis of DIPG copy number alterations showed recurrent changes distinct from those of pediatric supratentorial high-
grade
astrocytomas
.
Our findings of recurrent involvement of the PDGFR pathway as
well
as defects in DNA repair pathways coupled with gain of PARP-1 highlight two potential, biologically based, therapeutic targets directed specifically at this devastating
disease
.
[MeSH-major]
Brain Stem Neoplasms / genetics.
Glioma
/ genetics. Poly(ADP-ribose) Polymerases / genetics. Polymorphism, Single Nucleotide. Receptor, Platelet-Derived Growth Factor alpha / genetics
[MeSH-minor]
Autopsy. Case-Control Studies. Child. Child, Preschool. DNA Repair / genetics. DNA,
Neoplasm
/ analysis. Female. Gene Dosage. Humans. Infant. Infant, Newborn. Loss of Heterozygosity. Male. Oligonucleotide Array Sequence Analysis
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20142589.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
Canada / Canadian Institutes of Health Research / / MOP 82727
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
17.
Opstad KS, Bell BA, Griffiths JR, Howe FA:
An assessment of the effects of sample ischaemia and spinning time on the metabolic profile of brain tumour biopsy specimens as determined by high-resolution magic angle spinning (1)H NMR.
NMR Biomed
; 2008 Nov;21(10):1138-47
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
High-resolution magic angle spinning (HRMAS) (1)H NMR of biopsy tissue provides a biochemical profile that has potential diagnostic and prognostic
value
, and can aid interpretation of the lower-resolution (1)H-NMR spectra obtained in vivo.
In addition, we have compared biochemical changes that occur in normal rat brain during HRMAS (spun continuously at 5 kHz for 4 h at 4 degrees C as could be required
for a
two-dimensional acquisition) with those that occur in biopsy samples from low-
grade
and high-
grade
adult human
astrocytomas
, during the same HRMAS procedure.
In particular, the 18% total creatine increase observed is unlikely to be
de
novo synthesis of creatine.
[MeSH-major]
Biomarkers,
Tumor
/ analysis. Brain Ischemia / metabolism. Brain Ischemia / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Magnetic Resonance Spectroscopy / methods. Specimen Handling / methods
[MeSH-minor]
Animals. Biopsy / methods. Cell Line,
Tumor
. Female.
Glioma
/ metabolism.
Glioma
/ pathology. Humans. Protons. Rats. Rats, Wistar. Reproducibility of Results. Sensitivity and Specificity. Spin Labels
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2008 John Wiley & Sons, Ltd.
(PMID = 18666093.001).
[ISSN]
0952-3480
[Journal-full-title]
NMR in biomedicine
[ISO-abbreviation]
NMR Biomed
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / C1459/A2592
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Protons; 0 / Spin Labels
18.
Lacoste-Collin L, d'Aure D, Aziza J, Quintyn ML, Uro-Coste E, Courtade-Saïdi M:
Cerebrospinal fluid cytologic findings of a pleomorphic xanthoastrocytoma: a case report.
Acta Cytol
; 2010 Sep-Oct;54(5 Suppl):871-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cerebrospinal fluid cytologic findings
of a
pleomorphic xanthoastrocytoma: a case report.
BACKGROUND: Pleomorphic xanthoastrocytoma (PXA) is a rare
astrocytic neoplasm
with a relatively favorable prognosis.
Characteristic histologic features include pleomorphic
tumor
cells and lipidized cells expressing glial fibrillary acidic protein (GFAP), corresponding to
a World Health Organization
grade
2
tumor
.
Computed tomography of the
central nervous system
revealed a supracallous periventricular
tumor
mass suggestive of either a lymphoma or a metastatic carcinoma.
CSF revealed 18 cells/mm3 and contained numerous
tumor
cells highly pleomorphic in size and shape.
Some atypical cells of moderate size were closely packed with
well
-defined cytoplasmic limits and a vacuolated appearance, suggesting an epithelial proliferation.
A primitive glial proliferation was found, and paraffin-embedded
tumor
tissue obtained by biopsy confirmed the diagnosis of anaplastic PXA.
[MeSH-major]
Astrocytoma
/ cerebrospinal fluid.
Astrocytoma
/ pathology. Brain Neoplasms / cerebrospinal fluid. Brain Neoplasms / pathology
Genetic Alliance.
consumer health - Pleomorphic xanthoastrocytoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21053559.001).
[ISSN]
0001-5547
[Journal-full-title]
Acta cytologica
[ISO-abbreviation]
Acta Cytol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
19.
Matsuda K, Sakurada K, Mouri W, Saino M, Sato S, Saito S, Kayama T, Nakazato Y:
[Operative case of isomorphic astrocytoma].
Brain Nerve
; 2007 Aug;59(8):881-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Operative case of isomorphic
astrocytoma
].
Diffuse
astrocytomas
are classified as
WHO
Grade
II tumors.
Recently,
a subtype
presenting with better prognosis has been proposed, and it is known as "isomorphic
astrocytoma
."
A clinical case that we encountered was believed to be categorized as this
subtype
; it has been presented in this report.
The
tumor
was resected under awake surgery.
The pathological diagnosis was diffuse
astrocytoma
, but this
tumor
was considered to be the isomorphic
subtype
.
Some parts of the
tumor
showed a relatively high MIB-1 labeling index (LI) of 9.2%, and additional 50-Gy radiotherapy was performed.
Isomorphic
astrocytoma
is characterized by prolonged epileptic seizures, a low MIB-1 LI, and better prognosis.
In our case, since the MIB-1 LI was higher in some parts of the
tumor
, the appropriate therapy
for WHO
Grade
II tumors was performed.
However, this case was considered representative of isomorphic
astrocytoma
.
No reports of this
tumor subtype
have been previously described in Japan.
Therefore, this report is the first case of isomorphic
astrocytoma
reported to Japanese literature.
[MeSH-major]
Astrocytoma
/ surgery. Brain Neoplasms / surgery
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17713125.001).
[ISSN]
1881-6096
[Journal-full-title]
Brain and nerve = Shinkei kenkyū no shinpo
[ISO-abbreviation]
Brain Nerve
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
20.
Watanabe T, Katayama Y, Yoshino A, Yachi K, Ohta T, Ogino A, Komine C, Fukushima T:
Aberrant hypermethylation of p14ARF and O6-methylguanine-DNA methyltransferase genes in astrocytoma progression.
Brain Pathol
; 2007 Jan;17(1):5-10
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Aberrant hypermethylation of p14ARF and O6-methylguanine-DNA methyltransferase genes in
astrocytoma
progression.
The aim of the present study was to elucidate genetic alterations that are critically involved in
astrocytoma
progression.
We characterized 27
World Health Organization
grade
II fibrillary
astrocytomas
which later underwent recurrence or progression, paying specific attention to the CpG island methylation status of critical growth regulatory genes. p14(ARF) and O(6)-methylguanine-DNA methyltransferase (MGMT) hypermethylation represented frequent events (26% and 63%, respectively), which were mutually exclusive except in
one
case, with alternate or simultaneous methylation of these two genes occurring in 85% of our
tumor
series.
Methylation of the p21(Waf1/Cip1), p27(Kip1) and p73 genes and homozygous deletion of the p16(INK4a), p15(INK4b) and p14(ARF) genes were not detected in any of the primary low-
grade
tumors.
On analysis of their respective recurrent tumors, five of six patients whose primary low-
grade
tumors carried p14(ARF) methylation exhibited homozygous co-deletions of the p14(ARF), p15(INK4b) and p16(INK4a) genes, which were restricted to glioblastoma as the most malignant end point.
Our findings suggest that p14(ARF) hypermethylation and MGMT hypermethylation constitute distinct molecular pathways of
astrocytoma
progression, which could differ in biological behavior and clinical outcome.
[MeSH-major]
Astrocytoma
/ metabolism. Brain Neoplasms / metabolism. CpG Islands / physiology.
Neoplasm
Recurrence, Local / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism.
Tumor
Suppressor Protein p14ARF / metabolism
[MeSH-minor]
Adult. Aged. Female. Humans. Male. Methylation. Middle Aged. Mutation / genetics. Promoter Regions, Genetic / physiology. Survival Analysis.
Tumor
Suppressor Protein p53 / genetics
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17493032.001).
[ISSN]
1015-6305
[Journal-full-title]
Brain pathology (Zurich, Switzerland)
[ISO-abbreviation]
Brain Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
21.
Quick Q, Skalli O:
Alpha-actinin 1 and alpha-actinin 4: contrasting roles in the survival, motility, and RhoA signaling of astrocytoma cells.
Exp Cell Res
; 2010 Apr 15;316(7):1137-47
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Alpha-actinin 1 and alpha-actinin 4: contrasting roles in the survival, motility, and RhoA signaling of
astrocytoma
cells.
Here, we have examined whether the two highly homologous non-muscle alpha-actinin isoforms 1 and 4 exhibit functional differences in
astrocytoma
cells.
The protein levels of these isoforms were differentially regulated during the development and progression
of astrocytomas
, as alpha-actinin 1 was higher in
astrocytomas
compared to normal brains whereas alpha-actinin 4 was elevated in high-
grade
astrocytomas
compared to normal brains and low
grade
astrocytomas
.
RNAi demonstrated contrasted contributions of alpha-actinin 1 and 4 to the malignant behavior of U-373, U-87 and A172
astrocytoma
cells.
While alpha-actinin 1 appeared to favor the expansion of U-373, U-87 and A172
astrocytoma
cell populations, alpha-actinin 4 played this role only for U-373 cells.
Finally, in the three
astrocytoma
cell lines examined, alpha-actinin 1 and 4 had contrasted biochemical properties as alpha-actinin 4 was significantly more abundant in the actin cytoskeleton than alpha-actinin 1.
Collectively, these findings suggest that alpha-actinin 1 and 4 are differentially regulated during the development and progression
of astrocytomas
because each of these isoforms uniquely contributes to distinct malignant properties of
astrocytoma
cells.
[MeSH-major]
Actinin / physiology.
Astrocytoma
/ pathology. Brain Neoplasms / pathology. Cell Movement / genetics. rhoA GTP-Binding Protein / physiology
[MeSH-minor]
Brain / metabolism. Cell Proliferation. Cell Survival / genetics.
Disease
Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Signal Transduction / genetics. Signal Transduction / physiology. Time Factors.
Tumor
Cells, Cultured
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
antibodies-online.
View related products from antibodies-online.com
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Published by Elsevier Inc.
(PMID = 20156433.001).
[ISSN]
1090-2422
[Journal-full-title]
Experimental cell research
[ISO-abbreviation]
Exp. Cell Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ACTN1 protein, human; 0 / ACTN4 protein, human; 11003-00-2 / Actinin; EC 3.6.5.2 / rhoA GTP-Binding Protein
22.
Yao Y, Wang X, Jin K, Zhu J, Wang Y, Xiong S, Mao Y, Zhou L:
B7-H4 is preferentially expressed in non-dividing brain tumor cells and in a subset of brain tumor stem-like cells.
J Neurooncol
; 2008 Sep;89(2):121-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
B7-H4 is preferentially expressed in non-dividing brain
tumor
cells and in a subset of brain
tumor
stem-like cells.
B7-H4, a newly discovered member of B7 family that negatively regulates T cell-mediated immunity, may facilitate
tumor
progression by undermining host immunity.
Recent studies show that brain
tumor
stem-like cells (TSCs) contribute to tumorigenesis.
In this study, we found that B7-H4 was expressed in cultured
tumor
cells from human
gliomas
(n = 5) and medulloblastomas (n = 3).
Double immunostaining indicated that B7-H4 was primarily restricted to non-dividing (Ki67(-)) cultured
tumor
cells.
Tumor
cells cultured under medium conditions favoring the growth of neural stem cells were able to form primary and secondary spheres, along with expression of neural stem/progenitor cell markers.
These cells
differentiated
into different neural lineages when cultured in differentiation medium, indicating that these cells have TSCs characteristics.
Secondary
glioma
cells derived from CD133(+) or CD133(-) cell xenografts expressed B7-H4 as
well
.
Our data suggest B7-H4 is preferentially expressed in non-dividing brain
tumor
cells and in a subpopulation of brain TSCs, and CD133(-)
tumor
cells also have the capacity to initiate brain formation in vivo.
[MeSH-major]
Antigens, CD80 / metabolism.
Astrocytoma
/ pathology. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Medulloblastoma / pathology. Neoplastic Stem Cells / metabolism
[MeSH-minor]
Adolescent. Aged. Animals. Antigens, CD / metabolism. Child. Female. Flow Cytometry. Humans. Ki-67 Antigen / metabolism. Male. Mice. Mice, SCID. Middle Aged.
Neoplasm
Metastasis. Nerve Tissue Proteins / metabolism.
Tumor
Cells, Cultured. V-Set Domain-Containing T-Cell Activation Inhibitor 1
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Physiol Cell Physiol. 2005 Apr;288(4):C805-12
[
15601754.001
]
[Cites]
J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9
[
11895036.001
]
[Cites]
Brain Res Brain Res Rev. 2003 May;42(2):97-122
[
12738053.001
]
[Cites]
Exp Cell Res. 2005 May 15;306(1):128-41
[
15878339.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10388-92
[
12920180.001
]
[Cites]
Clin Neuropathol. 2002 Nov-Dec;21(6):252-7
[
12489673.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83
[
14645703.001
]
[Cites]
Eur J Cancer. 2007 Jul;43(10 ):1502-7
[
17524637.001
]
[Cites]
Lung Cancer. 2006 Aug;53(2):143-51
[
16782226.001
]
[Cites]
Front Biosci. 2007 Jan 01;12:2252-9
[
17127461.001
]
[Cites]
J Immunol. 2003 Nov 1;171(9):4650-4
[
14568939.001
]
[Cites]
J Immunother. 2007 Apr;30(3):251-60
[
17414316.001
]
[Cites]
J Exp Med. 2006 Apr 17;203(4):871-81
[
16606666.001
]
[Cites]
J Immunol. 1984 Oct;133(4):1710-5
[
6206131.001
]
[Cites]
Cancer Res. 2003 Sep 15;63(18):5821-8
[
14522905.001
]
[Cites]
Immunity. 2003 Jun;18(6):849-61
[
12818165.001
]
[Cites]
Leukemia. 2003 Oct;17 (10 ):2049-51
[
14513057.001
]
[Cites]
Mol Cancer. 2006 Dec 02;5:67
[
17140455.001
]
[Cites]
Nature. 2001 Nov 1;414(6859):105-11
[
11689955.001
]
[Cites]
Immunity. 2003 Jun;18(6):863-73
[
12818166.001
]
[Cites]
Cancer Res. 2007 May 1;67(9):4010-5
[
17483311.001
]
[Cites]
Nature. 2006 Dec 7;444(7120):756-60
[
17051156.001
]
[Cites]
Neurosurgery. 2002 Jun;50(6):1238-44; discussion 1244-5
[
12015841.001
]
[Cites]
Cancer. 1996 Jan 15;77(2):373-80
[
8625247.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10391-6
[
16798883.001
]
(PMID = 18478183.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD80; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / VTCN1 protein, human
23.
Daumas-Duport C, Koziak M, Miquel C, Nataf F, Jouvet A, Varlet P:
[Reappraisal of the Sainte-Anne Hospital classification of oligodendrogliomas in view of retrospective studies].
Neurochirurgie
; 2005 Sep;51(3-4 Pt 2):247-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Reappraisal of the Sainte-Anne Hospital
classification of
oligodendrogliomas in view of retrospective studies].
[Transliterated title]
Classification
des oligodendrogliomes
de
l'hôpital Sainte-Anne. Mise au point à l'usage des études rétrospectives.
PURPOSE: Definition of homogeneous
tumor
groups of oligodendrogliomas or oligo-
astrocytomas
is a basic condition for an adequate evaluation and comparison of the results of treatments in patients from various institutions.
The main goal of this study is to assess whether, for retrospective studies, MRI data may serve as a common basis for encompassing asymmetry in diagnosis established according to the
WHO
or Ste-Anne (SA)
classification
.
PATIENTS AND METHODS: This study included 251 adult patients in whom a SA
grade
A or B oligodendroglioma or oligo-
astrocytoma
was newly diagnosed at our institution from 1984 to 2003.
Routine histological preparations and post-contrast preoperative MRI/CT-scan were simultaneously reviewed in order to assess the impact on survival of the following features: presence or absence
of a
polymorphous or gemistocytic
astrocytic
component, of necrosis and of contrast enhancement (CH); endothelial hyperplasia (EH) assessed as absent, present minor (HE+) or (HE++) when conform to the threshold of HE defined in the SA grading
system of
oligodendrogliomas.
RESULTS: 70.1% of the tumors were classified as "pure" oligodendroglioma, 19.5% as "polymorphous oligo-astroastrocytoma" and 10.3% as "gemistocytic oligo-
astrocytoma
".
In
grade
A, or B tumors, the presence
of a
polymorphous or a gemistocytic component had no significant influence on survival; however respectively 53% and 65% of these tumours versus 32% of "pure" oligodendrogliomas were
grade
B at the time of diagnosis.
After regrouping of the histological subtypes and of the tumors with HE+ or absent, the series included 153 oligodendrogliomas
grade
A and 98
grade
B.
Survival in patients with
grade
A versus
grade
B tumors was respectively 142 versus 52 months (p<0.0001).
In
grade
B tumors, necrosis had no significant influence on survival.
On post contrast MRI done in 235 patients, only 7 tumors (3%) were
grade
A/B (EH++ but no CH).
CONCLUSIONS: From these results and our previous observation that, according to the SA
classification of gliomas
, only oligodendrogliomas or oligo-
astrocytomas
may not show CE, we propose that for retrospective studies:.
1) tumors diagnosed according to the Ste-Anne
classification
as oligodendroglioma or oligo-
astrocytoma
be regrouped in a unique category, 2) independent of their histological type and
grade
according to the
WHO
,
gliomas
that do not show CE be regrouped with SA oligodendrogliomas
grade
A, 3) concerning
gliomas
that show CE on MRI: oligodendrogliomas or oligo-
astrocytomas WHO
grade
II or III, as
well
as
WHO
secondary glioblastomas or glioblastomas with an oligodendroglial component, be regrouped with SA oligodendrogliomas
grade
B; however tumors that show ring-like CE surrounding large foci of necrosis and finger-like "peritumoral" edema should be excluded or analysed separately.
[MeSH-major]
Brain / pathology. Brain / radiography. Brain Neoplasms /
classification
.
Glioma
/
classification
. Oligodendroglioma /
classification
[MeSH-minor]
Adult. France. Hospitals. Humans. Magnetic Resonance Imaging.
Neoplasm
Staging. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16292168.001).
[ISSN]
0028-3770
[Journal-full-title]
Neuro-Chirurgie
[ISO-abbreviation]
Neurochirurgie
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
24.
Gururangan S, Fisher MJ, Allen JC, Herndon JE 2nd, Quinn JA, Reardon DA, Vredenburgh JJ, Desjardins A, Phillips PC, Watral MA, Krauser JM, Friedman AH, Friedman HS:
Temozolomide in children with progressive low-grade glioma.
Neuro Oncol
; 2007 Apr;9(2):161-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Temozolomide in children with progressive low-
grade
glioma
.
We conducted a phase II study to assess the efficacy of oral temozolomide (TMZ) in children with progressive low-
grade
glioma
.
Best responses in the 26 patients (86%) with optic pathway
glioma
(OPG)/pilocytic
astrocytoma
(PA) included partial response in 3 patients (11%), minor response in 1 (4%), stable
disease
in 10 (38%), and progressive
disease
in 12 (46%).
Only
one of
four patients with fibrillary
astrocytoma
had stable
disease for
29 months after TMZ.
The overall
disease
stabilization rate in patients with OPG/PA was 54%, and
disease
control was maintained
for a
median interval of 34 months.
Seventeen of 26 patients had progressive
disease
either on or off therapy, and three have died
of disease
.
Worst toxicity related to TMZ in all 30 patients included
grade
2-4 thrombocytopenia in seven patients,
grade
2-4 neutropenia in seven,
grade
2 skin rash in
one
, and intratumor hemorrhage in
one
.
TMZ given in this schedule was successful in stabilizing
disease
in a significant proportion of the patients with OPG/PA, with manageable toxicity.
[MeSH-major]
Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives.
Glioma
/ drug therapy
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DACARBAZINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Cancer. 1999 Nov;81(6):1022-30
[
10576660.001
]
[Cites]
Neuro Oncol. 2006 Jan;8(1):79-82
[
16443951.001
]
[Cites]
Semin Radiat Oncol. 2001 Apr;11(2):152-62
[
11285553.001
]
[Cites]
J Clin Oncol. 2002 May 1;20(9):2388-99
[
11981013.001
]
[Cites]
J Clin Oncol. 2002 Jul 1;20(13):2951-8
[
12089224.001
]
[Cites]
Mol Cancer Ther. 2002 Sep;1(11):943-8
[
12481416.001
]
[Cites]
J Clin Oncol. 2003 Feb 15;21(4):646-51
[
12586801.001
]
[Cites]
Br J Cancer. 2003 Apr 7;88(7):1004-11
[
12671695.001
]
[Cites]
J Pediatr Hematol Oncol. 2003 May;25(5):372-8
[
12759623.001
]
[Cites]
Ann Oncol. 2003 Dec;14(12):1715-21
[
14630674.001
]
[Cites]
Ann Oncol. 2003 Dec;14(12):1722-6
[
14630675.001
]
[Cites]
Clin Cancer Res. 2004 Jun 1;10(11):3728-36
[
15173079.001
]
[Cites]
J Clin Oncol. 2004 Aug 1;22(15):3133-8
[
15284265.001
]
[Cites]
Neurol Clin. 1991 May;9(2):479-95
[
1944111.001
]
[Cites]
J Neurooncol. 1997 May;32(3):235-41
[
9049885.001
]
[Cites]
J Neurosurg. 1997 May;86(5):747-54
[
9126887.001
]
[Cites]
J Clin Oncol. 1998 Sep;16(9):3037-43
[
9738573.001
]
[Cites]
Ann Neurol. 1999 Mar;45(3):393-6
[
10072056.001
]
[Cites]
Clin Cancer Res. 2005 Apr 1;11(7):2747-55
[
15814657.001
]
[Cites]
Ann Hematol. 2005 Oct;84(11):760-2
[
16044311.001
]
[Cites]
J Clin Oncol. 2005 Oct 20;23(30):7646-53
[
16234526.001
]
[Cites]
J Neurooncol. 2005 Dec;75(3):301-7
[
16195800.001
]
[Cites]
Clin Cancer Res. 2000 Jul;6(7):2585-97
[
10914698.001
]
(PMID = 17347491.001).
[ISSN]
1522-8517
[Journal-full-title]
Neuro-oncology
[ISO-abbreviation]
Neuro-oncology
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
[Other-IDs]
NLM/ PMC1871667
25.
Kikuchi T:
[Novel immunotherapeutic approach].
Gan To Kagaku Ryoho
; 2005 Apr;32(4):453-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Malignant
astrocytoma
is the most common primary brain
tumor
in adults.
The median survival time of patients with high-
grade
malignant
astrocytoma
is about 1 year, despite aggressive treatment with surgical resection, radiotherapy, and cytotoxic chemotherapy.
Immunotherapy is
one
such novel approach that has been investigated for application with different types of tumors, including brain tumors.
The author reviews immunotherapeutic approaches for malignant
gliomas
and the relevance of recent clinical trials and their outcomes.
A number of potentially targetable antigens have been identified in
gliomas
.
DCs have been investigated in several clinical trials in patients with malignant tumors including malignant
gliomas
.
So far, seven papers concerning immunotherapy with DCs against malignant
gliomas
have been published.
These reports demonstrate that immunotherapy with DCs induces immune responses and clinically antitumor effects in some patients with malignant
glioma
.
[MeSH-major]
Astrocytoma
/ therapy. Brain Neoplasms / therapy.
Glioma
/ therapy. Immunotherapy
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15853209.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Immunotoxins; 0 / Interleukin-13; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
[Number-of-references]
23
26.
Yoshida T, Niwa F, Kimura S, Nakagawa M:
Anaplastic astrocytoma presenting as reversible posterior leukoencephalopathy syndrome.
Neurologist
; 2006 Nov;12(6):311-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Anaplastic
astrocytoma
presenting as reversible posterior leukoencephalopathy syndrome.
We report a 60-year-old man with
grade
III
astrocytoma
,
who
presented with status epilepticus.
The initial MRI did not demonstrate typical findings of an
astrocytoma
but rather showed reversible posterior leukoencephalopathy syndrome (RPLS).
A brain
tumor
should be considered and the patient carefully followed by MRI, even if the MRI white matter lesion pattern suggests RPLS.
[MeSH-major]
Astrocytoma
/ diagnosis. Brain
Diseases
/ diagnosis. Occipital Lobe / pathology
Genetic Alliance.
consumer health - Anaplastic Astrocytoma
.
MedlinePlus Health Information.
consumer health - Brain Diseases
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17122727.001).
[ISSN]
1074-7931
[Journal-full-title]
The neurologist
[ISO-abbreviation]
Neurologist
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
27.
Shannon P, Sabha N, Lau N, Kamnasaran D, Gutmann DH, Guha A:
Pathological and molecular progression of astrocytomas in a GFAP:12 V-Ha-Ras mouse astrocytoma model.
Am J Pathol
; 2005 Sep;167(3):859-67
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Pathological and molecular progression
of astrocytomas
in a GFAP:12 V-Ha-Ras mouse
astrocytoma
model.
We previously characterized a genetically engineered mouse
astrocytoma
model with embryonic astrocyte-specific, activated (12)V-Ha-RAS (GFAP-RAS) transgenesis.
The GFAP-RAS line Ras-B8 appears normal at birth, but 50% of mice die by 4 months from low- and high-
grade
astrocytomas
.
We examined the development and progression
of astrocytomas
in the Ras-B8 genetically engineered mouse.
From 3 to 8 weeks the incidence of low-
grade
astrocytomas
progressively increased with 85% of 12-week-old mice harboring low- or high-
grade
astrocytomas
, the latter characterized by increased proliferation, nuclear atypia, and angiogenesis.
Tp 53 mutations were detected in both
astrocytoma
grades, with high-
grade
astrocytomas
expressing elevated levels of epidermal growth factor receptor and vascular endothelial growth factor, plus decreased levels of PTEN and p16, similar to human
astrocytomas
.
Of interest, many of these acquired alterations occur in human
astrocytomas
, further validating GFAP-RAS as a useful model for studying
astrocytoma
development and progression.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2001 May 1;61(9):3826-36
[
11325859.001
]
[Cites]
Exp Neurol. 1999 Jun;157(2):327-37
[
10364444.001
]
[Cites]
J Neurooncol. 2001 Jul;53(3):289-96
[
11718261.001
]
[Cites]
Glia. 2002 Sep;39(3):193-206
[
12203386.001
]
[Cites]
Oncogene. 2002 Oct 24;21(49):7453-63
[
12386807.001
]
[Cites]
Carcinogenesis. 2003 Feb;24(2):335-42
[
12584185.001
]
[Cites]
Cancer Res. 2003 Mar 1;63(5):1106-13
[
12615729.001
]
[Cites]
Acta Neuropathol. 1978 Jan 19;41(1):27-31
[
636834.001
]
[Cites]
Acta Neuropathol. 1979 Mar 15;45(3):167-75
[
442982.001
]
[Cites]
Oncogene. 1999 Dec 9;18(52):7514-26
[
10602510.001
]
[Cites]
Oncogene. 2000 Aug 10;19(34):3948-54
[
10951588.001
]
[Cites]
Brain Res. 2000 Nov 10;883(1):87-97
[
11063991.001
]
[Cites]
Neuro Oncol. 2001 Jan;3(1):1-10
[
11305411.001
]
[Cites]
J Cell Biol. 1980 Jun;85(3):890-902
[
6248568.001
]
[Cites]
Cancer Res. 1986 Nov;46(11):5836-41
[
3756925.001
]
[Cites]
Cancer Res. 1991 Nov 15;51(22):6202-5
[
1933879.001
]
[Cites]
Cancer Res. 1992 Apr 1;52(7):1974-80
[
1551126.001
]
[Cites]
Cancer Res. 1992 Oct 1;52(19):5334-41
[
1382841.001
]
[Cites]
Cancer Res. 1993 Jun 1;53(11):2614-7
[
8495424.001
]
[Cites]
J Clin Endocrinol Metab. 1993 Oct;77(4):1054-8
[
8408453.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 May 24;91(11):5124-8
[
8197195.001
]
[Cites]
Gynecol Oncol. 1995 Dec;59(3):423-6
[
8522268.001
]
[Cites]
Br J Cancer. 1996 Jul;74(2):165-71
[
8688317.001
]
[Cites]
Cancer Res. 1996 Nov 15;56(22):5141-5
[
8912848.001
]
[Cites]
Neurosurgery. 1997 May;40(5):1016-26
[
9149260.001
]
[Cites]
Oncogene. 1997 Dec 4;15(23):2755-65
[
9419966.001
]
[Cites]
Int J Cancer. 1999 Mar 31;81(1):118-24
[
10077162.001
]
[Cites]
Cancer Res. 2001 Jun 1;61(11):4425-31
[
11389071.001
]
(PMID = 16127163.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / R01 NS041097; United States / NINDS NIH HHS / NS / NS41097
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Glial Fibrillary Acidic Protein; 0 / Growth Substances; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53
[Other-IDs]
NLM/ PMC1698742
28.
Sun J, Wang Z, Li Z, Liu B:
Microsurgical treatment and functional outcomes of multi-segment intramedullary spinal cord tumors.
J Clin Neurosci
; 2009 May;16(5):666-71
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
We aimed to prospectively analyze correlations between clinical features and histological
classification of
multi-segment intramedullary spinal cord tumors (MSICTs), and the extent of microsurgical resection and functional outcomes.
Fifty-six patients with MSICTs underwent microsurgery
for tumor
removal using a posterior approach.
The
tumor
was exposed through a dorsal myelotomy.
Pre-operative and post-operative
nervous
function was scored using the Improved Japanese Orthopaedic Association (IJOA) grading
system
.
Correlation analyses were performed between functional outcome (IJOA score) and histological features, age,
tumor
location, and the longitudinal extent of spinal cord involvement.
Ependymoma was the most frequent MSICT type, seen in 22 of 56 patients (39%), followed by low
grade astrocytoma
(17 patients, 30%) and glioblastoma multiforme (3 patients, 5%).
Gross total
tumor
removal was achieved in 33 cases (58%), subtotal resection in 4 (7%), and partial resection in 16 (28%).
The histological
classification of
the
tumor
was the most important factor influencing the extent of surgical removal (chi2=22.17, p=0.00).
Thus, MSICTs were most commonly seen in the medullo cervical and cervicothoracic regions, with ependymoma and low
grade astrocytoma
the most common tumour types.
[MeSH-minor]
Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neurologic Examination / methods. Outcome Assessment (
Health
Care). Prospective Studies. Spinal Cord / pathology. Spinal Cord / surgery. Young Adult
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19303302.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Scotland
29.
Gibson SE, Zeng WF, Weil RJ, Prayson RA:
Aurora B kinase expression in ependymal neoplasms.
Appl Immunohistochem Mol Morphol
; 2008 May;16(3):274-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Overexpression of Aurora B kinase, which regulates cell progression through mitosis and cytokinesis, has been shown to be associated with higher-
grade
tumors and shortened survival in
astrocytomas
.
The association between Aurora B expression and
World Health Organization
grade
II/III tumors was statistically significant (P<0.0001).
Aurora B expression was not associated with patient age, sex,
tumor
location,
tumor
recurrence, or death from
tumor
.
In contrast to
astrocytomas
, elevated Aurora B expression in higher-
grade
ependymomas does not seem to correlate with clinical course, although it may be a potential target of Aurora kinase inhibitors.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18301241.001).
[ISSN]
1533-4058
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
30.
Shuangshoti S, Thorner PS, Ruangvejvorachai P, Saha B, Groshen S, Taylor CR, Malhotra S, Imam SA:
J1-31 protein expression in astrocytes and astrocytomas.
Neuropathology
; 2009 Oct;29(5):521-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
J1-31 protein expression in astrocytes and
astrocytomas
.
J1-31 is
one of
the
astrocytic
proteins, the expression of which has not been evaluated in
astrocytomas
.
In the present study, we studied the expression of J1-31 protein in astrocytes and
astrocytomas
in comparison with GFAP, p53 and Ki-67.
Materials consisted of formalin-fixed paraffin-embedded tissue specimens that included five cases of normal brain, 17 of gliosis, 15 of pilocytic
astrocytoma
(
WHO
grade I
), 26 of low-
grade
diffuse
astrocytoma
(
WHO
grade
II), four of anaplastic
astrocytoma
(
WHO
grade
III), and eight of glioblastoma (
WHO
grade
IV).
The antibody showed reactivity with
tumor
cells in 12/15 (80%) cases of pilocytic
astrocytoma
, although intensity of staining was generally weaker and more focal than observed in reactive gliosis.
J1-31-positive
tumor
cells were detected in only 9/26 (35%) cases of the low-
grade
diffuse
astrocytoma
and none of the cases of anaplastic
astrocytoma
and glioblastoma.
Increasing Ki-67 indices paralleled advancing
tumor
grades. p53 protein was expressed more commonly in infiltrating
astrocytomas
compared to pilocytic
astrocytoma
.
In conclusion, down-regulation of J1-31 expression correlates with advancing
grade
of astrocytomas
.
The anti-J1-31 antibody may help further our understanding of astrocytes in
disease
and may be useful as an aid in the pathologic diagnosis
of astrocytic
lesions.
[MeSH-major]
Astrocytes / metabolism.
Astrocytoma
/ metabolism. Nerve Tissue Proteins / metabolism
[MeSH-minor]
Cytoplasm / metabolism. Down-Regulation. Glial Fibrillary Acidic Protein / metabolism. Glioblastoma / metabolism. Gliosis / metabolism. Humans. Ki-67 Antigen / metabolism.
Neoplasm
Staging.
Tumor
Suppressor Protein p53 / metabolism
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19019178.001).
[ISSN]
1440-1789
[Journal-full-title]
Neuropathology : official journal of the Japanese Society of Neuropathology
[ISO-abbreviation]
Neuropathology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Australia
[Chemical-registry-number]
0 / Glial Fibrillary Acidic Protein; 0 / J1-31 protein, human; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53
31.
Kubicek GJ, Werner-Wasik M, Machtay M, Mallon G, Myers T, Ramirez M, Andrews D, Curran WJ Jr, Dicker AP:
Phase I trial using proteasome inhibitor bortezomib and concurrent temozolomide and radiotherapy for central nervous system malignancies.
Int J Radiat Oncol Biol Phys
; 2009 Jun 1;74(2):433-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Phase I trial using proteasome inhibitor bortezomib and concurrent temozolomide and radiotherapy
for central nervous system
malignancies.
PURPOSE: To evaluate the toxicity and response rate of bortezomib with concurrent radiotherapy and temozolomide in the treatment of patients with
central nervous system
malignancies.
PATIENTS AND METHODS: This open-label, dose-escalation, Phase I clinical study evaluated the safety of three dose levels of intravenously administered bortezomib (0.7, 1.0, and 1.3 mg/m(2)/dose) on Days 1, 4, 8, and 11
of a
21-day cycle, in addition to concurrent radiotherapy and temozolomide at a daily dose of 75 mg/m(2) starting on Day 1.
The primary endpoint was dose-limiting toxicity, defined as any
Grade
4-5 toxicity or
Grade
3 toxicity directly attributable to protocol treatment, requiring hospitalization and/or radiotherapy interruption.
RESULTS: A total of 27 patients were enrolled, 23 of whom had high-
grade
glioma
(10 recurrent and 13 newly diagnosed).
The most frequent toxicities were
Grade
1 and 2 stomatitis, erythema, and alopecia.
At a median follow-up of 15.0 months, 9 patients were still alive, with a median survival of 17.4 months for all patients and 15.0 months for patients with high-
grade
glioma
.
CONCLUSION: Bortezomib administered at its typical "systemic" dose (1.3 mg/m(2)) is
well
tolerated and safe combined with temozolomide and radiotherapy when used in the treatment
of central nervous system
malignancies.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
Hazardous Substances Data Bank.
DACARBAZINE
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 2006 Nov 1;24(31):5025-33
[
17075122.001
]
[Cites]
J Clin Oncol. 2006 Oct 20;24(30):4867-74
[
17001068.001
]
[Cites]
Anticancer Res. 2006 Nov-Dec;26(6B):4499-503
[
17201170.001
]
[Cites]
Clin Cancer Res. 2007 Feb 15;13(4):1208-15
[
17317831.001
]
[Cites]
J Thorac Oncol. 2006 Feb;1(2):126-34
[
17409841.001
]
[Cites]
J Thorac Oncol. 2006 Nov;1(9):996-1001
[
17409985.001
]
[Cites]
Clin Cancer Res. 2007 Jun 1;13(11):3403-12
[
17545549.001
]
[Cites]
J Clin Oncol. 2007 Jun 20;25(18):2601-6
[
17577040.001
]
[Cites]
N Engl J Med. 2001 Jan 11;344(2):114-23
[
11150363.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):509-18
[
11208845.001
]
[Cites]
Cancer Res. 2004 Jul 15;64(14):4912-8
[
15256463.001
]
[Cites]
Lab Invest. 2004 Aug;84(8):941-51
[
15184909.001
]
[Cites]
Clin Cancer Res. 2004 Aug 15;10(16):5595-603
[
15328202.001
]
[Cites]
J Neurosurg. 1978 Sep;49(3):333-43
[
355604.001
]
[Cites]
Cancer Treat Rep. 1983 Feb;67(2):121-32
[
6337710.001
]
[Cites]
Cancer. 1983 Sep 15;52(6):997-1007
[
6349785.001
]
[Cites]
J Neurosurg. 1989 Jul;71(1):1-9
[
2661738.001
]
[Cites]
N Engl J Med. 2005 Mar 10;352(10):987-96
[
15758009.001
]
[Cites]
N Engl J Med. 2005 Jun 16;352(24):2487-98
[
15958804.001
]
[Cites]
Ann Oncol. 2006 May;17(5):813-7
[
16403809.001
]
[Cites]
J Clin Oncol. 2006 Jun 1;24(16):2563-9
[
16735709.001
]
[Cites]
Ann Oncol. 2006 Jun;17 Suppl 7:vii115-23
[
16760273.001
]
[Cites]
Cancer. 2006 Dec 1;107(11):2688-97
[
17075878.001
]
(PMID = 19084346.001).
[ISSN]
1879-355X
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA056036-08; United States / NCI NIH HHS / CA / P30 CA056036-08
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
[Other-IDs]
NLM/ NIHMS117014; NLM/ PMC2697394
32.
Blauwblomme T, Varlet P, Goodden JR, Cuny ML, Piana H, Roujeau T, Dirocco F, Grill J, Kieffer V, Boddaert N, Sainte-Rose C, Puget S:
Forniceal glioma in children. Clinical article.
J Neurosurg Pediatr
; 2009 Sep;4(3):249-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Forniceal
glioma
in children. Clinical article.
The aim of this study was to review the clinical, radiological, and histopathological features as
well
as the feasibility of surgical excision and the outcomes in these patients.
METHODS: From a retrospective analysis of 250 cases of supratentorial pediatric
glioma
, the records of 8 children presenting with forniceal lesions were selected and reviewed.
On histological review, the tumors were confirmed as pilocytic
astrocytoma
(4 lesions),
WHO
Grade
II
astrocytoma
(3), and ganglioglioma (1).
Additional treatment was required for 5 patients
for tumor
progression, with a median interval of 19 months from surgery.
At a median follow-up duration of 4.9 years, all patients had stable
disease
.
CONCLUSIONS: In this series, forniceal
gliomas
were found to be low-
grade
gliomas
.
Due to the high rate of progression of residual
disease
, adjuvant therapy is recommended for infiltrative tumors, and it yielded excellent results.
[MeSH-major]
Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Fornix, Brain.
Glioma
/ diagnosis.
Glioma
/ surgery
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19772409.001).
[ISSN]
1933-0707
[Journal-full-title]
Journal of neurosurgery. Pediatrics
[ISO-abbreviation]
J Neurosurg Pediatr
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
33.
Heimberger AB, Abou-Ghazal M, Reina-Ortiz C, Yang DS, Sun W, Qiao W, Hiraoka N, Fuller GN:
Incidence and prognostic impact of FoxP3+ regulatory T cells in human gliomas.
Clin Cancer Res
; 2008 Aug 15;14(16):5166-72
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Incidence and prognostic impact of FoxP3+ regulatory T cells in human
gliomas
.
PURPOSE: The incidence of regulatory T cells (Treg) in intrinsic
central nervous system
malignancies is unknown.
Immunotherapeutic approaches that inhibit the Treg population may be limited to a subset of patients with
gliomas
.
Our hypothesis is that only the most malignant
gliomas
have a prominent
glioma
-infiltrating Treg population that contributes to the immunosuppressive biology and that the presence of Tregs is a negative prognostic variable.
EXPERIMENTAL DESIGN: We measured the incidence of Tregs in 135 glial tumors (including all pathologic types) in
a glioma
microarray using immunohistochemical analysis.
RESULTS: Tregs were not present in normal brain tissue and were very rarely found in low-
grade
gliomas
and oligodendrogliomas.
We observed significant differences in the prevalence of Tregs between
astrocytic
and oligodendroglial tumors, between tumors of different grades, and between different pathologic types of tumors.
We identified Tregs most frequently in glioblastoma multiforme (GBM) but very rarely in low-
grade
astrocytomas
.
CONCLUSIONS: Treg infiltration differed significantly in the tumors according to lineage, pathology, and
grade
.
Tregs seemed to have the highest predilection for tumors of the
astrocytic
lineage and specifically in the high-
grade
gliomas
, such as GBM.
[MeSH-major]
Biomarkers,
Tumor
/ immunology. Brain Neoplasms / immunology. Forkhead Transcription Factors / metabolism.
Glioma
/ immunology. Lymphocytes,
Tumor
-Infiltrating / immunology. T-Lymphocytes, Regulatory / immunology
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18698034.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA120813-01A1
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
34.
Robert M, Wastie M:
Glioblastoma multiforme: a rare manifestation of extensive liver and bone metastases.
Biomed Imaging Interv J
; 2008 Jan;4(1):e3
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Glioblastoma multiforme (GBM) is the most aggressive form of primary brain tumours known collectively as
gliomas
.
Gliomas
are graded by their microscopic appearance.
As a rule, their behaviour can be predicted from histology:
Grade I
(pilocytic
astrocytomas
) and
Grade
II (benign
astrocytomas
) tumours are of low
grade
and grow slowly over many years.
Grade
IV tumours (GBM) are the most aggressive and, unfortunately, also the most common in humans, growing rapidly, invading and altering brain function.
Most patients with GBM die of their
disease
in less than a year and none have long term survival.Extracranial metastases from GBM are extremely rare, with a reported frequency of only 0.44% because of the absence of lymphatics in the brain and the difficulty of tumours to penetrate blood vessels.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 1995 Nov 1;55(21):4833-6
[
7585516.001
]
[Cites]
Cancer. 1980 Jan 1;45(1):112-25
[
6985826.001
]
[Cites]
J Neurosurg. 1970 Jul;33(1):88-94
[
4316740.001
]
[Cites]
Cancer. 1992 Apr 15;69(8):2149-53
[
1311985.001
]
[Cites]
J Neurosurg. 2000 Nov;93(5):887-90
[
11059674.001
]
[Cites]
Clin Imaging. 1994 Oct-Dec;18(4):386-9
[
8000959.001
]
(PMID = 21614314.001).
[ISSN]
1823-5530
[Journal-full-title]
Biomedical imaging and intervention journal
[ISO-abbreviation]
Biomed Imaging Interv J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Malaysia
[Other-IDs]
NLM/ PMC3097703
[Keywords]
NOTNLM ; GBM / Glioblastoma multiforme / extracranial metastases / glioma
35.
de Groot JF, Piao Y, Lu L, Fuller GN, Yung WK:
Knockdown of GluR1 expression by RNA interference inhibits glioma proliferation.
J Neurooncol
; 2008 Jun;88(2):121-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Knockdown of GluR1 expression by RNA interference inhibits
glioma
proliferation.
High-
grade
gliomas
release excitotoxic concentrations of glutamate which contributes to their malignant phenotype.
To improve our understanding of the mechanisms by which glutamate enhances
tumor
growth and invasion, we examined alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-mediated signaling in
glioma
cell lines. shRNA was used to stably knockdown GluR1, the most abundant AMPA receptor subunit in
glioma
, to evaluate its role in
tumor
signaling, proliferation and tumorigenicity.
In a tissue array, there was a statistically significant increase in GluR1 expression in glioblastoma samples compared to anaplastic
astrocytoma
and low-
grade
tumors.
Retroviral delivery of GluR1 shRNA in U251 and U87
glioma
cells reduced GluR1 protein expression, inhibited AMPA-mediated increases in MAPK phosphorylation, and decreased
glioma
proliferation in vitro.
These results suggest that AMPA receptors are abundantly expressed in high-
grade
gliomas
and gene silencing of the GluR1 AMPA receptor subunit results in abrogation of AMPA-mediated signaling and
tumor
growth.
[MeSH-major]
Brain Neoplasms / metabolism. Gene Expression Regulation / drug effects.
Glioma
/ prevention & control. RNA Interference / physiology. RNA, Small Interfering / therapeutic use. Receptors, AMPA / metabolism
[MeSH-minor]
Animals. Carcinogenicity Tests. Cell Cycle / drug effects. Cell Line,
Tumor
. Cell Proliferation / drug effects. Down-Regulation / drug effects. Down-Regulation / genetics. Humans. Ki-67 Antigen / metabolism. Mice. Mice, Nude. Microarray Analysis / methods. RNA, Double-Stranded / pharmacology. Signal Transduction / drug effects
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Neurosci. 1999 Dec 15;19(24):10767-77
[
10594060.001
]
[Cites]
Nucleic Acids Res. 2003 Nov 1;31(21):e127
[
14576327.001
]
[Cites]
Pharmacol Rev. 1999 Mar;51(1):7-61
[
10049997.001
]
[Cites]
Expert Rev Anticancer Ther. 2003 Oct;3(5):595-614
[
14599084.001
]
[Cites]
J Neurosci. 1993 Sep;13(9):3904-15
[
8103555.001
]
[Cites]
Neuron. 2000 Jun;26(3):603-17
[
10896157.001
]
[Cites]
Annu Rev Cell Biol. 1991;7:601-32
[
1667084.001
]
[Cites]
Neuron. 1994 Jun;12 (6):1207-21
[
8011335.001
]
[Cites]
J Biol Chem. 1994 Mar 4;269(9):7030-5
[
8120067.001
]
[Cites]
Cancer Metastasis Rev. 2003 Dec;22(4):395-403
[
12884914.001
]
[Cites]
J Neurosci. 2005 Aug 3;25(31):7101-10
[
16079392.001
]
[Cites]
Mol Cell. 2003 Oct;12(4):889-901
[
14580340.001
]
[Cites]
Nat Med. 2002 Sep;8(9):971-8
[
12172541.001
]
[Cites]
J Neurooncol. 2001 Feb;51(3):245-64
[
11407596.001
]
[Cites]
Brain Pathol. 2002 Jan;12(1):95-107
[
11770905.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14687-92
[
11717408.001
]
[Cites]
Trends Neurosci. 2003 Oct;26(10):543-9
[
14522147.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7058-61
[
11416187.001
]
[Cites]
J Neurosci. 2007 Jul 25;27(30):7987-8001
[
17652589.001
]
[Cites]
Nat Methods. 2004 Nov;1(2):163-7
[
16144086.001
]
[Cites]
J Neurooncol. 2003 Jan;61(2):151-60
[
12622454.001
]
[Cites]
J Cereb Blood Flow Metab. 2007 Aug;27(8):1431-43
[
17245419.001
]
[Cites]
J Biol Chem. 1993 Feb 15;268(5):3715-9
[
8429046.001
]
[Cites]
Neuron. 1999 Mar;22(3):511-24
[
10197531.001
]
[Cites]
Genes Dev. 1995 Sep 15;9(18):2279-91
[
7557381.001
]
[Cites]
J Med Chem. 1998 Jul 2;41(14):2513-23
[
9651156.001
]
[Cites]
J Neurochem. 2003 Mar;84(6):1288-95
[
12614329.001
]
[Cites]
Nature. 1998 Dec 10;396(6711):584-7
[
9859994.001
]
[Cites]
Nature. 1999 Jan 7;397(6714):72-6
[
9892356.001
]
[Cites]
Biochem Pharmacol. 2002 Oct 15;64(8):1195-200
[
12234599.001
]
[Cites]
J Neurosci Res. 1998 Dec 15;54(6):814-9
[
9856865.001
]
[Cites]
J Neurooncol. 2000 Mar;47(1):11-22
[
10930095.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 May 22;98(11):6372-7
[
11331750.001
]
[Cites]
Nat Med. 2001 Sep;7(9):1010-5
[
11533703.001
]
[Cites]
J Neurosci. 2005 Feb 16;25(7):1654-63
[
15716401.001
]
[Cites]
Cancer Res. 2005 Mar 1;65(5):1934-40
[
15753393.001
]
[Cites]
Cancer Res. 1999 Sep 1;59(17):4383-91
[
10485487.001
]
[Cites]
J Cereb Blood Flow Metab. 1998 Apr;18(4):396-406
[
9538905.001
]
[Cites]
Cancer Res. 2003 Aug 1;63(15):4315-21
[
12907597.001
]
[Cites]
Nat Rev Neurosci. 2004 Oct;5(10):771-81
[
15378037.001
]
[Cites]
J Biol Chem. 1995 Sep 29;270(39):22783-7
[
7559406.001
]
[Cites]
Cancer. 2004 Mar 15;100(6):1110-22
[
15022276.001
]
(PMID = 18317690.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / RNA, Double-Stranded; 0 / RNA, Small Interfering; 0 / Receptors, AMPA; 0 / glutamate receptor ionotropic, AMPA 1
36.
Ladha J, Donakonda S, Agrawal S, Thota B, Srividya MR, Sridevi S, Arivazhagan A, Thennarasu K, Balasubramaniam A, Chandramouli BA, Hegde AS, Kondaiah P, Somasundaram K, Santosh V, Rao SM:
Glioblastoma-specific protein interaction network identifies PP1A and CSK21 as connecting molecules between cell cycle-associated genes.
Cancer Res
; 2010 Aug 15;70(16):6437-47
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Glioblastoma (GBM;
grade
IV
astrocytoma
) is a very aggressive form of brain cancer with a poor survival and few qualified predictive markers.
A system
level analysis was used to construct GBM-specific network.
Computation of topological parameters of networks showed scale-free pattern and hierarchical
organization
.
Real-time quantitative reverse transcription-PCR analysis revealed CSK21 to be moderately upregulated and PP1A to be overexpressed by 20-fold in GBM
tumor
samples.
Genetic Alliance.
consumer health - Glioblastoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c)2010 AACR.
(PMID = 20663907.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / Casein Kinase II; EC 3.1.3.16 / Protein Phosphatase 1
37.
Palani M, Arunkumar R, Janardhanam VA:
Biochemical and cytogenetic analysis of brain tissues in different grades of glioma patients.
Ann Neurosci
; 2010 Jul;17(3):120-5
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Biochemical and cytogenetic analysis of brain tissues in different grades
of glioma
patients.
BACKGROUND:
Glioma
,
a neoplasm
of neuroglial cells, is the most common type of brain
tumor
, constituting more than 50% of all brain tumors.
PURPOSE: This report summarizes the current knowledge regarding the clinical utility of biochemical enzyme markers for both diagnostic and therapeutic purposes in different grades
of glioma
.
METHODS: Sixty patients with different grades
of glioma
include glioblastoma multiforme (n=20), Anaplastic
astrocytoma
(n=10).
Ependymoma (n=10), Pilocytic
astrocytoma
(n=10) and patients with benign lesions (n=5) served as controls.
CK, Na-K(+) ATPases, 5'-Nucleotidases showed marked increase in
grade
IV.
Similarly, Mg2-ATPase, Ca2+ATPases showed significant increase in
grade
III.
CONCLUSION: The clinical importance
for classification
and treatment
of glioma
is governed by biochemical enzyme markers.
The study of enzymes supported by related chromosomal changes is anticipated to provide better appreciation of biological properties in different grades
of glioma
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 25205887.001).
[ISSN]
0972-7531
[Journal-full-title]
Annals of neurosciences
[ISO-abbreviation]
Ann Neurosci
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC4116979
[Keywords]
NOTNLM ; Antioxidants / Biochemical profile in glioma / Chromosomal aberrations / Enzymes / Glioma
38.
Abel TJ, Chowdhary A, Thapa M, Rutledge JC, Geyer JR, Ojemann J, Avellino AM:
Spinal cord pilocytic astrocytoma with leptomeningeal dissemination to the brain. Case report and review of the literature.
J Neurosurg
; 2006 Dec;105(6 Suppl):508-14
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Spinal cord pilocytic
astrocytoma
with leptomeningeal dissemination to the brain. Case report and review of the literature.
Leptomeningeal dissemination of low-
grade
spinal cord
gliomas
is an uncommon event.
The authors report a unique case of leptomeningeal dissemination
of a
spinal cord pilocytic
astrocytoma
(PCA) to the intracranial cerebral subarachnoid spaces in a child.
An intradural intramedullary spinal cord
tumor
was identified, and the lesion was subtotally resected and diagnosed by the pathology department to be a PCA.
Subsequently, the patient had recurrences of the intradural intramedullary
tumor
at 6 months and 2 years after his original presentation.
He underwent a repeated resection of the recurrent
tumor
and fenestration of an associated syrinx on both occasions.
The pathological characteristics of the reresected
tumor
remained consistent with those
of a
PCA.
Postoperative imaging after his last surgery revealed diffuse intracranial leptomeningeal dissemination into the cisternal space surrounding the midbrain, the suprasellar region, and the internal auditory canal, as
well
as nodular subarachnoid
disease
in the upper cervical region.
The patient then underwent chemotherapy, and total spine magnetic resonance (MR) imaging 2 months later demonstrated stability in the size of the spinal cord
tumor
and a decrease in the associated syrinx.
However, an MR image of the head demonstrated two new areas of supratentorial subarachnoid leptomeningeal spread of the primary spinal cord
tumor
at the 2-month follow-up examination.
At the 6-month follow-up examination, MR imaging of the head and spine demonstrated stable metastatic
disease
.
[MeSH-major]
Astrocytoma
/ secondary. Brain Neoplasms / secondary. Meningeal Neoplasms / secondary. Spinal Cord Neoplasms / pathology
[MeSH-minor]
Child, Preschool. Humans. Magnetic Resonance Imaging. Male.
Neoplasm
Recurrence, Local / pathology.
Neoplasm
Recurrence, Local / surgery
Genetic Alliance.
consumer health - Pilocytic astrocytoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17184088.001).
[ISSN]
0022-3085
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
45
39.
Katoh N, Shirato H, Aoyama H, Onimaru R, Suzuki K, Hida K, Miyasaka K, Iwasaki Y:
Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.
J Neurooncol
; 2006 May;78(1):63-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-
grade
spinal cord
astrocytic tumor
.
PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord
glioma
with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-
grade
spinal cord
astrocytic
tumors.
MATERIALS AND METHODS: Forty-
one
patients with spinal cord
glioma
received post-operative radiotherapy between 1979 and 2003.
There were 12 low-
grade
astrocytic
tumors, 11 high-
grade
astrocytic
tumors, 16 low-
grade
ependymal tumors and 2 high-
grade
ependymal tumors.
Among 11 patients with high-
grade
astrocytic
tumors, 5 with anaplastic
astrocytoma
and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.
RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the
astrocytic
tumors and 84% for the ependymal tumors, respectively (P=0.009).
Among 11 patients with high-
grade
astrocytic
tumors, the actuarial survival rate at 10 years was 35%.
The actuarial survival rates at 10 years were 67% for those
who
received hypofractionated radiotherapy boost for dose escalation, and 20% for those
who
did not (P=0.47).
DISCUSSION: The results for ependymal tumors and low-
grade
astrocytic
tumors were comparable to those reported in the literature.
Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-
grade
astrocytic
tumors.
[MeSH-major]
Dose Fractionation.
Glioma
/ radiotherapy. Spinal Cord Neoplasms / radiotherapy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 1992 Sep;10(9):1379-85
[
1325539.001
]
[Cites]
J Clin Neurosci. 2002 Mar;9(2):211-6
[
11922720.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1993 Sep 30;27(2):223-9
[
8407395.001
]
[Cites]
Br J Neurosurg. 2000 Aug;14(4):331-6
[
11045198.001
]
[Cites]
Am J Clin Oncol. 1999 Aug;22(4):344-51
[
10440187.001
]
[Cites]
J Neurooncol. 2001 Mar;52(1):85-94
[
11451207.001
]
[Cites]
Radiology. 1980 May;135(2):473-9
[
7367644.001
]
[Cites]
J Neurosurg. 1995 Oct;83(4):590-5
[
7674006.001
]
[Cites]
J Neurooncol. 1997 Jul;33(3):205-11
[
9195492.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1997 Jul 1;38(4):805-11
[
9240650.001
]
[Cites]
Radiat Oncol Investig. 1998;6(6):276-80
[
9885944.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1998 Dec 1;42(5):953-8
[
9869215.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2000 Sep 1;48(2):421-6
[
10974456.001
]
[Cites]
Childs Nerv Syst. 1997 Jul;13(7):375-82
[
9298273.001
]
[Cites]
Neurosurgery. 1999 Feb;44(2):264-9
[
9932879.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1397-403
[
2542194.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2000 Oct 1;48(3):837-42
[
11020582.001
]
[Cites]
J Clin Oncol. 1995 Jul;13(7):1642-8
[
7602353.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):323-8
[
7673019.001
]
[Cites]
Oncol Rep. 2003 Nov-Dec;10(6):2079-82
[
14534747.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2003 Jan 1;55(1):162-7
[
12504049.001
]
[Cites]
J Neurosurg. 1998 Feb;88(2):215-20
[
9452226.001
]
[Cites]
J Neurosurg. 1989 Jan;70(1):50-4
[
2909688.001
]
(PMID = 16314938.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
40.
Tay A, Scheithauer BW, Cameron JD, Myhre MJ, Boerner MJ:
Retinal ependymoma: an immunohistologic and ultrastructural study.
Hum Pathol
; 2009 Apr;40(4):578-83
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Most are syndrome associated and include pilocytic
astrocytoma
in neurofibromatosis type 1 and subependymal giant cell
astrocytoma
in tuberous sclerosis complex.
Acquired, more conventional, diffuse
astrocytomas
are less frequent.
The
tumor
was sporadic in occurrence and unilateral, low
grade
, and of cellular type.
The literature regarding retinal glial neoplasia including ependymoma as
well
as the so-called massive retinal gliosis is discussed.
Genetic Alliance.
consumer health - Ependymoma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18835620.001).
[ISSN]
1532-8392
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
41.
Kurian KM, Summers DM, Statham PF, Smith C, Bell JE, Ironside JW:
Third ventricular chordoid glioma: clinicopathological study of two cases with evidence for a poor clinical outcome despite low grade histological features.
Neuropathol Appl Neurobiol
; 2005 Aug;31(4):354-61
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Third ventricular chordoid
glioma
: clinicopathological study of two cases with evidence
for a
poor clinical outcome despite low
grade
histological features.
Chordoid
glioma of
the third ventricle is a rare glial tumour whose precise histogenesis remains uncertain.
The
neoplasm
tends to occur in women and its clinical presentation is variable, resulting from acute hydrocephalus or impingement upon local structures.
The main differentials for histological diagnosis include chordoid meningiomas, pilocytic
astrocytomas
and ependymomas.
[MeSH-major]
Choroid Plexus Neoplasms / pathology. Choroid Plexus Neoplasms / physiopathology.
Glioma
/ pathology.
Glioma
/ physiopathology. Third Ventricle / pathology
Genetic Alliance.
consumer health - Glioma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16008819.001).
[ISSN]
0305-1846
[Journal-full-title]
Neuropathology and applied neurobiology
[ISO-abbreviation]
Neuropathol. Appl. Neurobiol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
42.
Zhang JG, Kruse CA, Driggers L, Hoa N, Wisoff J, Allen JC, Zagzag D, Newcomb EW, Jadus MR:
Tumor antigen precursor protein profiles of adult and pediatric brain tumors identify potential targets for immunotherapy.
J Neurooncol
; 2008 May;88(1):65-76
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Tumor
antigen precursor protein profiles of adult and pediatric brain tumors identify potential targets for immunotherapy.
OBJECTIVES: We evaluated and compared
tumor
antigen precursor protein (TAPP) profiles in adult and pediatric brain tumors of 31 genes related to
tumor
associated antigens (TAA) for possible use in immunotherapy.
METHODS: Thirty-seven brain
tumor
specimens from 11 adult and 26 pediatric patients were analyzed by quantitative real-time PCR for the relative expression of 31 TAPP mRNAs.
Histological diagnoses consisted of 16 glioblastomas, 4 low
grade
astrocytomas
, 10 juvenile pilocytic
astrocytomas
, and 7 ependymomas.
RESULTS: The adult
gliomas
expressed 94% (29 of 31) of the TAPP mRNAs evaluated compared with pediatric brain tumors that expressed 55-74% of the TAPP mRNAs, dependent on
tumor
histological
subtype
.
The pediatric brain tumors lacked expression of some genes associated with engendering
tumor
survival, such as hTert and Survivin.
Genetic Alliance.
consumer health - Brain Tumor, Adult
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2002 Aug 1;62(15):4364-8
[
12154041.001
]
[Cites]
Cancer Immunol Immunother. 2001 Sep;50(7):337-44
[
11676393.001
]
[Cites]
Nucleic Acids Res. 2001 May 1;29(9):e45
[
11328886.001
]
[Cites]
Cancer. 2003 Feb 15;97(4):1077-83
[
12569609.001
]
[Cites]
J Neurooncol. 2003 Aug-Sep;64(1-2):13-20
[
12952282.001
]
[Cites]
Cancer Res. 2004 Jul 15;64(14):4973-9
[
15256471.001
]
[Cites]
Br J Cancer. 2004 Nov 1;91(9):1656-62
[
15477864.001
]
[Cites]
J Cell Biol. 1989 Dec;109(6 Pt 1):2575-87
[
2687284.001
]
[Cites]
Hum Gene Ther. 1995 May;6(5):591-601
[
7578396.001
]
[Cites]
Cancer Immunol Immunother. 1997 Oct;45(2):77-87
[
9390198.001
]
[Cites]
Lancet. 1998 Mar 21;351(9106):882-3
[
9525374.001
]
[Cites]
J Neurosurg. 1998 Jul;89(1):42-51
[
9647171.001
]
[Cites]
J Biol Chem. 1999 Jan 15;274(3):1359-65
[
9880507.001
]
[Cites]
Br J Cancer. 2005 Jan 31;92(2):359-65
[
15655550.001
]
[Cites]
Neuro Oncol. 2005 Jul;7(3):225-35
[
16053697.001
]
[Cites]
Clin Cancer Res. 2005 Aug 1;11(15):5515-25
[
16061868.001
]
[Cites]
Brain Pathol. 2005 Oct;15(4):342-63
[
16389946.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):194-202
[
16492905.001
]
[Cites]
Oncogene. 2006 May 4;25(19):2818-26
[
16314830.001
]
[Cites]
Pediatr Blood Cancer. 2006 Jul;47(1):4-13
[
16534789.001
]
[Cites]
Int J Oncol. 2006 Jun;28(6):1555-60
[
16685456.001
]
[Cites]
Neurosurg Focus. 2000;9(6):e9
[
16817692.001
]
[Cites]
J Neuropathol Exp Neurol. 2006 Sep;65(9):905-13
[
16957584.001
]
[Cites]
Cancer Gene Ther. 2006 Dec;13(12):1052-60
[
16826191.001
]
[Cites]
Neurosurgery. 2006 Nov;59(5):988-99; discussioin 999-1000
[
17143233.001
]
[Cites]
J Neurooncol. 2007 Jan;81(2):139-48
[
17004103.001
]
[Cites]
Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):566-75
[
17255279.001
]
[Cites]
Clin Cancer Res. 2007 Sep 1;13(17):4960-3
[
17785545.001
]
[Cites]
Immunology. 2007 Dec;122(4):615-22
[
17645496.001
]
[Cites]
Oncogene. 2000 Feb 3;19(5):617-23
[
10698506.001
]
[Cites]
J Neurooncol. 1999;45(2):141-57
[
10778730.001
]
[Cites]
Clin Cancer Res. 2000 Jun;6(6):2209-18
[
10873070.001
]
[Cites]
Semin Radiat Oncol. 2001 Apr;11(2):152-62
[
11285553.001
]
[Cites]
Clin Cancer Res. 2002 Sep;8(9):2851-5
[
12231526.001
]
(PMID = 18259692.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA121258; United States / NINDS NIH HHS / NS / NS 046463; United States / NCI NIH HHS / CA / CA 121258; United States / NINDS NIH HHS / NS / R21 NS057829; United States / NINDS NIH HHS / NS / NS 054093; United States / NINDS NIH HHS / NS / NS 056300; United States / NINDS NIH HHS / NS / R21 NS056300; United States / NINDS NIH HHS / NS / R21 NS046463; United States / NINDS NIH HHS / NS / NS 057829
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Protein Precursors; 0 / RNA, Messenger
[Other-IDs]
NLM/ NIHMS572988; NLM/ PMC4005736
43.
Stark AM, Fritsch MJ, Claviez A, Dörner L, Mehdorn HM:
Management of tectal glioma in childhood.
Pediatr Neurol
; 2005 Jul;33(1):33-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Management of tectal
glioma
in childhood.
Tectal
glioma
is a topographical diagnosis including tumors of different histology, mainly low-
grade
astrocytomas
.
This report discusses the management of this rare
tumor
in children.
Clinical charts of 12 children with tectal
glioma
treated in our department between 1976 and 2001 were retrospectively reviewed.
The duration between first symptoms and the diagnosis of tectal
glioma
was in the range of 2 days to 9 years.
Ten patients presented with symptoms associated with increased intracranial pressure,
one
patient presented with ataxia, and in
one
case tectal
glioma
was an incidental
finding
.
First-line therapy was endoscopic third ventriculostomy in 5 cases (42%), ventriculoperitoneal shunting in 6 cases (50%), and combined partial
tumor
resection and shunting in
one
case.
Histology was obtained in 5 cases (low-
grade astrocytoma
, n = 4; ependymoma, n = 1).
Tectal
glioma
represents a distinct subgroup of brainstem tumors associated with a good (or favorable) prognosis.
Effective treatment for hydrocephalus is essential; the
tumor
should be monitored by regular clinical examination and magnetic resonance imaging.
Biopsy is warranted in cases with
tumor
progression.
[MeSH-major]
Brain Neoplasms / pathology. Brain Neoplasms / therapy.
Glioma
/ pathology.
Glioma
/ therapy. Superior Colliculi / pathology
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool.
Disease
Management. Female. Follow-Up Studies. Humans. Infant. Male. Retrospective Studies
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15876519.001).
[ISSN]
0887-8994
[Journal-full-title]
Pediatric neurology
[ISO-abbreviation]
Pediatr. Neurol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
44.
Mamelak AN, Rosenfeld S, Bucholz R, Raubitschek A, Nabors LB, Fiveash JB, Shen S, Khazaeli MB, Colcher D, Liu A, Osman M, Guthrie B, Schade-Bijur S, Hablitz DM, Alvarez VL, Gonda MA:
Phase I single-dose study of intracavitary-administered iodine-131-TM-601 in adults with recurrent high-grade glioma.
J Clin Oncol
; 2006 Aug 1;24(22):3644-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Phase I single-dose study of intracavitary-administered iodine-131-TM-601 in adults with recurrent high-
grade
glioma
.
PURPOSE: TM-601 binds to malignant brain
tumor
cells with high affinity and does not seem to bind to normal brain tissue.
Preclinical studies suggest that iodine-131 (131I) -TM-601 may be an effective targeted therapy for the treatment
of glioma
.
We evaluated the safety, biodistribution, and dosimetry of intracavitary-administered 131I-TM-601 in patients with recurrent
glioma
.
PATIENTS AND METHODS: Eighteen adult patients (17 with glioblastoma multiforme and
one
with anaplastic
astrocytoma
) with histologically documented recurrent
glioma
and a Karnofsky performance status of > or = 60%
who
were eligible for cytoreductive craniotomy were enrolled.
An intracavitary catheter with subcutaneous reservoir was placed in the
tumor
cavity during surgery.
Two weeks after surgery, patients received a single dose of 131I-TM-601 from
one of
three dosing panels (0.25, 0.50, or 1.0 mg of TM-601), each labeled with 10 mCi of 131I.
RESULTS: Intracavitary administration was
well
tolerated, with no dose-limiting toxicities observed.
131I-TM-601 bound to the
tumor
periphery and demonstrated long-term retention at the
tumor
with minimal uptake in any other organ
system
.
At day 180, four patients had radiographic stable
disease
, and
one
had a partial response.
Two of these patients further improved and were without evidence
of disease
for more than 30 months.
CONCLUSION: A single dose of 10 mCi 131I-TM-601 was
well
tolerated for 0.25 to 1.0 mg TM-601 and may have an antitumoral effect.
[MeSH-major]
Brachytherapy. Brain Neoplasms / radiotherapy.
Glioma
/ radiography. Iodine Radioisotopes / administration & dosage. Iodine Radioisotopes / adverse effects. Scorpion Venoms / administration & dosage. Scorpion Venoms / adverse effects
[MeSH-minor]
Adult. Aged. Female. Humans. Karnofsky Performance Status. Magnetic Resonance Imaging. Male. Middle Aged.
Neoplasm
Recurrence, Local / radiotherapy. Radiometry. Radiopharmaceuticals / administration & dosage. Radiopharmaceuticals / adverse effects. Radiotherapy Dosage. Survival Analysis. Time Factors. Tomography, Emission-Computed, Single-Photon. Treatment Outcome
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16877732.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Chlorotoxin; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Scorpion Venoms
45.
Yang Z, Wang Y, Fang J, Chen F, Liu J, Wu J, Wang Y:
Expression and aberrant promoter methylation of Wnt inhibitory factor-1 in human astrocytomas.
J Exp Clin Cancer Res
; 2010;29:26
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression and aberrant promoter methylation of Wnt inhibitory factor-1 in human
astrocytomas
.
BACKGROUND: Wnt inhibitory factor-1(WIF-1) acts as a Wnt-antagonists and
tumor
suppressor, but hypermethylation of WIF-1 gene promoter and low expression activate Wnt signaling aberrantly and induce the development of various human tumors.
With this work we intended to investigate the expression and promoter methylation status of WIF-1 gene in human
astrocytomas
.
METHODS: The tissue samples consisted of 53
astrocytomas
and 6 normal brain tissues.
RESULTS: The average expression levels of WIF-1 protein and mRNA in
astrocytomas
were decreased significantly compared with normal control tissues.
The protein and mRNA expression of WIF-1 gene in
astrocytomas
was decreased with the increase of pathological
grade
.
Furthermore, WIF-1 promoter methylation was observed by MS-PCR in
astrocytomas
which showed significant reduction of WIF-1 expression.
CONCLUSION: Our results demonstrate that the WIF-1 gene is frequently down-regulated or silenced in
astrocytomas
by aberrant promoter methylation.
This may be an important mechanism in
astrocytoma
carcinogenesis.
[MeSH-major]
Adaptor Proteins, Signal Transducing / biosynthesis.
Astrocytoma
/ metabolism. Brain Neoplasms / metabolism. DNA Methylation. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Cancer Res. 2003 Jun;9(6):2121-32
[
12796377.001
]
[Cites]
J Cell Sci. 2003 Jul 1;116(Pt 13):2627-34
[
12775774.001
]
[Cites]
N Engl J Med. 2003 Nov 20;349(21):2042-54
[
14627790.001
]
[Cites]
Cancer Res. 2004 Jul 15;64(14):4717-20
[
15256437.001
]
[Cites]
J Neurooncol. 2004 Jul;68(3):275-83
[
15332332.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Oct 8;323(1):229-34
[
15351726.001
]
[Cites]
Br J Cancer. 1997;75(1):2-8
[
9000591.001
]
[Cites]
Science. 1998 Sep 4;281(5382):1509-12
[
9727977.001
]
[Cites]
Nature. 1999 Apr 1;398(6726):422-6
[
10201372.001
]
[Cites]
Nature. 1999 Apr 1;398(6726):431-6
[
10201374.001
]
[Cites]
Oncogene. 2005 Nov 24;24(53):7946-52
[
16007117.001
]
[Cites]
Clin Cancer Res. 2006 Jan 15;12(2):383-91
[
16428476.001
]
[Cites]
Biochem Biophys Res Commun. 2006 Mar 10;341(2):635-40
[
16427602.001
]
[Cites]
Pathobiology. 2006;73(5):213-23
[
17314492.001
]
[Cites]
Curr Opin Cell Biol. 2007 Apr;19(2):150-8
[
17306971.001
]
[Cites]
Neuro Oncol. 2007 Jul;9(3):271-9
[
17504928.001
]
[Cites]
Acta Neuropathol. 2007 Aug;114(2):97-109
[
17618441.001
]
[Cites]
Cancer Lett. 2007 Nov 18;257(2):172-81
[
17709179.001
]
[Cites]
N Engl J Med. 2008 Jul 31;359(5):492-507
[
18669428.001
]
[Cites]
Gene Expr Patterns. 2008 Sep;8(7-8):515-22
[
18586116.001
]
[Cites]
Cancer Gene Ther. 2009 Apr;16(4):351-61
[
18949017.001
]
[Cites]
Int J Oncol. 2009 Jun;34(6):1743-8
[
19424593.001
]
[Cites]
Neurochem Res. 2009 Jul;34(7):1278-88
[
19148749.001
]
[Cites]
World J Gastroenterol. 2009 Jun 7;15(21):2595-601
[
19496188.001
]
[Cites]
Neoplasia. 2009 Jul;11(7):700-11
[
19568415.001
]
[Cites]
Neurochem Int. 2009 Sep;55(5):307-17
[
19576519.001
]
[Cites]
Cancer Res. 2000 Sep 1;60(17):4926-31
[
10987308.001
]
[Cites]
Nat Rev Genet. 2002 Jun;3(6):415-28
[
12042769.001
]
[Cites]
J Pathol. 2003 Oct;201(2):204-12
[
14517837.001
]
(PMID = 20334650.001).
[ISSN]
1756-9966
[Journal-full-title]
Journal of experimental & clinical cancer research : CR
[ISO-abbreviation]
J. Exp. Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Repressor Proteins; 0 / WIF1 protein, human
[Other-IDs]
NLM/ PMC2851677
46.
Watanabe T, Katayama Y, Yoshino A, Fukaya C, Yamamoto T:
Human interferon beta, nimustine hydrochloride, and radiation therapy in the treatment of newly diagnosed malignant astrocytomas.
J Neurooncol
; 2005 Mar;72(1):57-62
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Human interferon beta, nimustine hydrochloride, and radiation therapy in the treatment of newly diagnosed malignant
astrocytomas
.
Previous investigators have reported encouraging results for malignant
gliomas
treated using a combination of human interferon beta (IFN-beta) with nimustine hydrochloride (ACNU) and radiation therapy (termed IAR therapy).
This study was undertaken to examine further the efficacy of the IAR regimen followed by maintenance therapy with IFN-beta and ACNU in patients with newly diagnosed malignant
astrocytomas
.
Of 33 patients assessable
for a
response, 11 responded (33%), with 4 complete responses.
The estimated median overall survival (OS) was 16 months, with values of 58 and 13 months for anaplastic
astrocytoma
(AA) and glioblastoma (GB) patients, respectively.
The IAR therapy was safe and
well
tolerated.
Based on a statistical analysis of the factors that affected the PFS and OS, histologic
grade
, postoperative Karnofsky performance scale (KPS), and extent of surgery were identified as independent predictors.
In addition, they emphasize the importance
of a
preserved KPS after cytoreductive surgery, which could produce a potential benefit for adjuvant therapy and could ultimately lead to a prolonged survival.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Astrocytoma
/ drug therapy.
Astrocytoma
/ radiotherapy. Supratentorial Neoplasms / drug therapy. Supratentorial Neoplasms / radiotherapy
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Acta Neurochir (Wien). 1994;127(1-2):55-9
[
7942182.001
]
[Cites]
Cancer. 2001 Jul 15;92(2):420-33
[
11466698.001
]
[Cites]
J Clin Oncol. 2001 Jan 15;19(2):509-18
[
11208845.001
]
[Cites]
Acta Neurochir (Wien). 2000;142(6):633-8; discussion 639
[
10949437.001
]
[Cites]
Gan To Kagaku Ryoho. 1991 Feb;18(2):188-94
[
1992912.001
]
[Cites]
J Neurosurg. 1993 May;78(5):762-6
[
8385709.001
]
[Cites]
J Clin Neurosci. 2001 May;8(3):253-5
[
11386801.001
]
[Cites]
Clin Cancer Res. 1997 Mar;3(3):381-7
[
9815695.001
]
[Cites]
J Neurooncol. 2000 Aug;49(1):57-62
[
11131987.001
]
[Cites]
J Clin Oncol. 1991 Nov;9(11):1945-9
[
1658242.001
]
[Cites]
Neurosurgery. 1994 Jan;34(1):45-60; discussion 60-1
[
8121569.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1993 Jan 15;25(2):193-207
[
8380567.001
]
[Cites]
Neurosurg Rev. 1984;7(1):55-64
[
6379511.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1995 Apr 30;32(1):75-83
[
7721642.001
]
[Cites]
Cancer Lett. 1983 Sep;20(2):131-8
[
6199106.001
]
[Cites]
J Neurol Neurosurg Psychiatry. 1988 Jan;51(1):50-9
[
2832547.001
]
[Cites]
J Neurosurg. 2001 Aug;95(2):190-8
[
11780887.001
]
(PMID = 15803376.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0S726V972K / Nimustine; 77238-31-4 / Interferon-beta
47.
Zhi F, Chen X, Wang S, Xia X, Shi Y, Guan W, Shao N, Qu H, Yang C, Zhang Y, Wang Q, Wang R, Zen K, Zhang CY, Zhang J, Yang Y:
The use of hsa-miR-21, hsa-miR-181b and hsa-miR-106a as prognostic indicators of astrocytoma.
Eur J Cancer
; 2010 Jun;46(9):1640-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The use of hsa-miR-21, hsa-miR-181b and hsa-miR-106a as prognostic indicators of
astrocytoma
.
BACKGROUND: The aberrant expression of microRNAs (miRNAs) is associated with a variety
of diseases
including cancers.
In the present study, the miRNA expression profile was examined in
astrocytoma
, a malignant and prevalent intracranial tumour in adults.
METHODS: We screened the expression profile of 200 miRNAs in a training sample set consisting of 84
astrocytoma
samples and 20 normal adjacent tissue (NAT) samples using the method of stem-loop quantitative RT-PCR.
The significantly altered miRNAs were validated in another independent sample set consisting of 40
astrocytoma
samples and 40 NAT samples.
The correlation of the miRNA levels with survival in
astrocytoma
samples was estimated by performing Kaplan-Meier survival analysis and univariate/multivariate Cox proportional hazard regression analysis.
RESULTS: After a two-phase selection and validation process, seven miRNAs were found to have a significantly different expression profile in
astrocytoma
samples upon comparison to the NAT samples.
Unsupervised clustering analysis further revealed the great potential of the 7-miRNA profile to
differentiate
between tumours and normal brain tissues.
The down-regulation of hsa-miR-137 in
astrocytomas
was shown to be associated with advanced clinical stages of this
disease
.
CONCLUSIONS: Our results suggest a great potential for the use of miRNA profiling as a powerful diagnostic and prognostic marker in defining the signature
of astrocytomas
and in predicting the post-surgical outcome.
[MeSH-major]
Astrocytoma
/ metabolism. Biomarkers,
Tumor
/ metabolism. Brain Neoplasms / metabolism. MicroRNAs / metabolism
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
(PMID = 20219352.001).
[ISSN]
1879-0852
[Journal-full-title]
European journal of cancer (Oxford, England : 1990)
[ISO-abbreviation]
Eur. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / MIRN106 microRNA, human; 0 / MIRN21 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
48.
Jang FF, Wei W, De WM:
Vascular endothelial growth factor and basic fibroblast growth factor expression positively correlates with angiogenesis and peritumoural brain oedema in astrocytoma.
J Ayub Med Coll Abbottabad
; 2008 Apr-Jun;20(2):105-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Vascular endothelial growth factor and basic fibroblast growth factor expression positively correlates with angiogenesis and peritumoural brain oedema in
astrocytoma
.
BACKGROUND:
Astrocytoma
is the most malignant intracranial
neoplasm
and is characterized by high neovascularization and peritumoural brain oedema.
METHODS: The expression of two angiogenic growth factors, vascular endothelial growth factor and basic fibroblast growth factor were investigated using immunohistochemistry for
astrocytoma
from 82 patients and 11 normal human tissues.
RESULTS: The expression of vascular endothelial growth factor and basic fibroblast growth factor positively correlate with the pathological
grade
of
astrocytoma
, microvessel density numbers and brain oedema, which may be responsible for the increased tumour neovascularization and peritumoural brain oedema.
CONCLUSION: The results support the idea that inhibiting vascular endothelial growth factor and basic fibroblast growth factor are useful for the treatment of human
astrocytoma
and to improve patient's clinical outcomes and prognosis.
[MeSH-major]
Astrocytoma
/ blood supply. Brain Edema / etiology. Brain Neoplasms / blood supply. Fibroblast Growth Factor 2 / biosynthesis. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / biosynthesis
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19385471.001).
[ISSN]
1025-9589
[Journal-full-title]
Journal of Ayub Medical College, Abbottabad : JAMC
[ISO-abbreviation]
J Ayub Med Coll Abbottabad
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Pakistan
[Chemical-registry-number]
0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
49.
Mamedova L, Capra V, Accomazzo MR, Gao ZG, Ferrario S, Fumagalli M, Abbracchio MP, Rovati GE, Jacobson KA:
CysLT1 leukotriene receptor antagonists inhibit the effects of nucleotides acting at P2Y receptors.
Biochem Pharmacol
; 2005 Dec 19;71(1-2):115-25
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Montelukast and pranlukast were found to inhibit nucleotide-induced calcium mobilization in a human monocyte-macrophage like cell line, DMSO-
differentiated
U937 (dU937).
Therefore, these antagonists were studied functionally in a heterologous expression
system for
the human P2Y receptors.
In 1321N1
astrocytoma
cells stably expressing human P2Y(1,2,4,6) receptors, CysLT1 antagonists inhibited both the P2Y agonist-induced activation of phospholipase C and intracellular Ca2+ mobilization.
In control
astrocytoma
cells expressing an endogenous M3 muscarinic receptor, 10 microM montelukast had no effect on the carbachol-induced rise in intracellular Ca2+.
COS Scholar Universe.
author profiles
.
Guide to Pharmacology.
gene/protein/disease-specific - P2Y6 receptor - data and references
.
Hazardous Substances Data Bank.
MONTELUKAST
.
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16280122.001).
[ISSN]
0006-2952
[Journal-full-title]
Biochemical pharmacology
[ISO-abbreviation]
Biochem. Pharmacol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 DK031116-21
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Acetates; 0 / Chromones; 0 / DNA Primers; 0 / Membrane Proteins; 0 / Quinolines; 0 / Receptors, Leukotriene; 0 / Receptors, Purinergic P2; 0 / leukotriene D4 receptor; 0 / pranlukast; MHM278SD3E / montelukast; SY7Q814VUP / Calcium; UT0S826Z60 / Uridine Triphosphate
[Other-IDs]
NLM/ NIHMS31385; NLM/ PMC4967539
50.
Benesch M, Eder HG, Sovinz P, Raith J, Lackner H, Moser A, Urban C:
Residual or recurrent cerebellar low-grade glioma in children after tumor resection: is re-treatment needed? A single center experience from 1983 to 2003.
Pediatr Neurosurg
; 2006;42(3):159-64
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Residual or recurrent cerebellar low-
grade
glioma
in children after
tumor
resection: is re-treatment needed? A single center experience from 1983 to 2003.
PURPOSE: The aim of this study was to report on children with cerebellar low-
grade
glioma
(LGG),
who
were found to have progressive or nonprogresssive residual tumors or
tumor
recurrence after
tumor
resection.
RESULTS: Of 289 patients with CNS tumors referred between 1983 and 2003, 28 (9.7%) (15 male, 13 female; median age at diagnosis: 71 months) had cerebellar LGG (pilocytic
astrocytoma grade
I: n = 21; fibrillary
astrocytoma grade
II: n = 5; mixed hamartoma/pilocytic
astrocytoma
: n = 1; radiographic diagnosis: n = 1).
One
patient underwent biopsy.
Only 1 additional patient had to undergo second surgery due to
disease
progression.
CONCLUSIONS: A 'wait and see' strategy is justified in patients with nonprogressive recurrent or residual cerebellar LGG after primary
tumor
resection.
However, long-term follow-up with repeated MRI is mandatory in these patients to detect
disease
progression.
Second surgery is indicated only in patients with unequivocal
disease
progression, as documented by MRI.
[MeSH-major]
Astrocytoma
/ surgery. Cerebellar Neoplasms / surgery.
Neoplasm
Recurrence, Local / surgery.
Neoplasm
, Residual / surgery
[MeSH-minor]
Adolescent. Child. Child, Preschool.
Disease
Progression. Female. Follow-Up Studies. Humans. Infant. Magnetic Resonance Imaging. Male. Postoperative Complications / diagnosis. Postoperative Complications / mortality. Postoperative Complications / surgery. Reoperation. Retrospective Studies. Survival Rate
Genetic Alliance.
consumer health - Glioma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2006 S. Karger AG, Basel
(PMID = 16636617.001).
[ISSN]
1016-2291
[Journal-full-title]
Pediatric neurosurgery
[ISO-abbreviation]
Pediatr Neurosurg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Switzerland
51.
Prayson RA:
The utility of MIB-1/Ki-67 immunostaining in the evaluation of central nervous system neoplasms.
Adv Anat Pathol
; 2005 May;12(3):144-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The utility of MIB-1/Ki-67 immunostaining in the evaluation
of central nervous system
neoplasms.
The diagnosis and assignment of
grade
in neoplasms of the
central nervous system
(CNS), for the most part, are morphologically based and predicated on the interpretation of descriptions of what the phenotypic findings are
for a
particular
tumor
type.
Since assignment of
grade
and
tumor
type is the basis upon which therapeutic intervention is grounded, investigators have been searching for ancillary means by which morphologically based systems can be improved.
[MeSH-major]
Antibodies, Antinuclear / analysis. Antibodies, Monoclonal / analysis.
Central Nervous System
Neoplasms / pathology. Ki-67 Antigen / analysis
[MeSH-minor]
Astrocytoma
/ immunology.
Astrocytoma
/ pathology.
Glioma
/ immunology.
Glioma
/ pathology. Gliosis / immunology. Gliosis / pathology. Humans. Meningioma / pathology. Staining and Labeling
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15900115.001).
[ISSN]
1072-4109
[Journal-full-title]
Advances in anatomic pathology
[ISO-abbreviation]
Adv Anat Pathol
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Ki-67 Antigen; 0 / MIB-1 antibody
52.
Szeliga M, Sidoryk M, Matyja E, Kowalczyk P, Albrecht J:
Lack of expression of the liver-type glutaminase (LGA) mRNA in human malignant gliomas.
Neurosci Lett
; 2005 Feb 21;374(3):171-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Lack of expression of the liver-type glutaminase (LGA) mRNA in human malignant
gliomas
.
In the
central nervous system
(CNS), liver-type glutaminase (LGA) shows a unique nuclear localization suggesting its role in the regulation of transcription rather than in the cellular glutamine metabolism.
RT-PCR analysis of RNA derived from postoperative tissue samples revealed the absence or only traces of LGA mRNA in all (9) cases of malignant
gliomas
(
astrocytoma
anaplasticum, AA,
WHO
grade
III; glioblastoma multiforme,
WHO
grade
IV) examined.
The lack of LGA may be thus considered as a useful negative diagnostic marker of highly malignant
gliomas
in situ.
[MeSH-major]
Glioma
/ metabolism. Glutaminase / deficiency. Liver / metabolism
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15663956.001).
[ISSN]
0304-3940
[Journal-full-title]
Neuroscience letters
[ISO-abbreviation]
Neurosci. Lett.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / DNA, Complementary; 0 / RNA, Messenger; EC 3.5.1.2 / Glutaminase
53.
Korones DN, Smith A, Foreman N, Bouffet E:
Temozolomide and oral VP-16 for children and young adults with recurrent or treatment-induced malignant gliomas.
Pediatr Blood Cancer
; 2006 Jul;47(1):37-41
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Temozolomide and oral VP-16 for children and young adults with recurrent or treatment-induced malignant
gliomas
.
BACKGROUND: Children and young adults with recurrent or treatment-induced malignant
gliomas
have limited responses to temozolomide or oral VP-16 when either is administered as a single agent.
We postulated that a combination of these two drugs for patients with recurrent or treatment-induced malignant
gliomas
might result in better and more prolonged responses.
PROCEDURE: Eleven patients with recurrent or treatment-induced malignant
gliomas
were treated with varying combinations of temozolomide (150-210 mg/m2/d for 5 days) and oral VP-16 (50 mg/m2/d for 4-12 days).
Diagnoses included recurrent brain stem
glioma
(2), recurrent anaplastic
astrocytoma
(2), and glioblastoma (7) (3 treatment-induced, 2 malignant transformations of lower
grade
tumors, 1 recurrence, and 1 second
tumor
arising 10 months after diagnosis of medulloblastoma).
All 11 patients had received radiotherapy (including 4
who
received craniospinal radiation), and 7 had prior chemotherapy.
One
patient had a complete response (CR), six had partial responses (PR), and four had progressive
disease
(PD).
There was
one
grade
4 neutropenia, but no other
grade
3 or 4 toxicities.
CONCLUSIONS: These data suggest there is activity of temozolomide in combination with oral VP-16 for children and young adults with recurrent malignant
gliomas
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Glioma
/ drug therapy.
Neoplasm
Recurrence, Local / drug therapy. Neoplasms, Second Primary / drug therapy
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
DACARBAZINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2006 Wiley-Liss, Inc.
(PMID = 16047359.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
54.
Tews B, Felsberg J, Hartmann C, Kunitz A, Hahn M, Toedt G, Neben K, Hummerich L, von Deimling A, Reifenberger G, Lichter P:
Identification of novel oligodendroglioma-associated candidate tumor suppressor genes in 1p36 and 19q13 using microarray-based expression profiling.
Int J Cancer
; 2006 Aug 15;119(4):792-800
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Identification of novel oligodendroglioma-associated candidate
tumor
suppressor genes in 1p36 and 19q13 using microarray-based expression profiling.
Loss of heterozygosity (LOH) on chromosomal arms 1p and 19q is the most common genetic alteration in oligodendroglial tumors and associated with response to radio- and chemotherapy as
well
as favorable prognosis.
Using microsatellite analysis, we previously identified the chromosomal regions 1p36.22-p36.31 and 19q13.3, as candidate
tumor
suppressor gene regions being commonly deleted in these tumors.
To identify genes within these regions that are downregulated in oligodendroglial tumors with LOH 1p/19q, we performed cDNA microarray-based RNA expression profiling of 35
gliomas
with known allelic status on 1p and 19q, including 7 oligodendrogliomas and 8 diffuse
astrocytomas of World Health Organization
(
WHO
)
grade
II, as
well
as 14 anaplastic oligodendrogliomas and 6 anaplastic oligoastrocytomas
of WHO
grade
III.
Microarray analysis identified 8 genes from these regions (MGC4399, SRM, ICMT, RPL18, FTL, ZIN, FLJ10781 and DBP), which all showed significantly lower expression in 1p/19q-deleted
gliomas
when compared to
gliomas
without 1p/19q losses.
In addition, we found that the cytosolic phospholipase A2 (PLA2G4C) gene at 19q13.3 demonstrated significantly lower expression in anaplastic oligodendrogliomas (
WHO
grade
III) when compared to
well
-
differentiated
oligodendrogliomas (
WHO
grade
II).
[MeSH-major]
Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Oligodendroglioma / genetics. Oligonucleotide Array Sequence Analysis.
Tumor
Suppressor Proteins / genetics
Genetic Alliance.
consumer health - Oligodendroglioma
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2006 Wiley-Liss, Inc.
(PMID = 16550607.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Complementary; 0 / Tumor Suppressor Proteins
55.
Znidaric MT, Pucer A, Fatur T, Filipic M, Scancar J, Falnoga I:
Metal binding of metallothioneins in human astrocytomas (U87 MG, IPDDC-2A).
Biometals
; 2007 Oct;20(5):781-92
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Metal binding of metallothioneins in human
astrocytomas
(U87 MG, IPDDC-2A).
Astroglia cells structurally and nutritionally support neurons in the
central nervous system
.
They play an important role in guiding the construction of the
nervous system
and controlling the chemical and ionic environment of neurons.
Our aim was to establish the inducibility and metal binding of MTs in two human
astrocytoma
cell lines, U87 MG (
astrocytoma
-glioblastoma,
grade
IV) and IPDDC-2A (
astrocytoma
,
grade
II), on exposure to cadmium chloride (1 microM).
We showed that MTs are constitutively expressed in both human
astrocytoma
cell lines.
In accordance with the higher malignancy
grade
of U87 MG, the amount of MTs was higher in U87 MG than in IPDDC-2A cells.
[MeSH-major]
Astrocytoma
/ metabolism. Metallothionein / metabolism. Metals / metabolism
[MeSH-minor]
Cadmium Chloride / metabolism. Cadmium Chloride / pharmacology. Cadmium Chloride / toxicity. Cell Line,
Tumor
. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. Protein Binding / physiology
Hazardous Substances Data Bank.
CADMIUM CHLORIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17115260.001).
[ISSN]
0966-0844
[Journal-full-title]
Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine
[ISO-abbreviation]
Biometals
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Metals; 9038-94-2 / Metallothionein; J6K4F9V3BA / Cadmium Chloride
56.
Raco A, Piccirilli M, Landi A, Lenzi J, Delfini R, Cantore G:
High-grade intramedullary astrocytomas: 30 years' experience at the Neurosurgery Department of the University of Rome "Sapienza".
J Neurosurg Spine
; 2010 Feb;12(2):144-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
High-
grade
intramedullary
astrocytomas
: 30 years' experience at the Neurosurgery Department of the University of Rome "Sapienza".
OBJECT: The goal in this study was to review a series of patients
who
underwent surgical removal of intramedullary high-
grade
gliomas
, focusing on the functional outcome, recurrence rates, and technical problems continually debated in neurosurgical practice.
METHODS: Between December 1976 and December 2006, 22 patients underwent removal of intramedullary high-
grade
gliomas
.
RESULTS: Histological examinations showed 10
Grade
III
astrocytomas
and 12 glioblastomas.
Only 2 of the 22 high-
grade
astrocytomas
could be completely removed.
In this series, multimodality treatment of intramedullary high-
grade
astrocytomas
has been shown to increase length of survival without improving the neurological status.
[MeSH-major]
Astrocytoma
/ surgery. Spinal Cord Neoplasms / surgery
[MeSH-minor]
Adolescent. Adult. Cervical Vertebrae. Child. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged.
Neoplasm
Recurrence, Local. Neurosurgical Procedures / methods. Neurosurgical Procedures / mortality. Rome. Spinal Cord / pathology. Spinal Cord / surgery. Thoracic Vertebrae. Time Factors. Treatment Outcome. Young Adult
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
J Neurosurg Spine. 2010 Feb;12(2):141-2; discussion 142-3
[
20121347.001
]
(PMID = 20121348.001).
[ISSN]
1547-5646
[Journal-full-title]
Journal of neurosurgery. Spine
[ISO-abbreviation]
J Neurosurg Spine
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
57.
Fellows GA, Wright AJ, Sibtain NA, Rich P, Opstad KS, McIntyre DJ, Bell BA, Griffiths JR, Howe FA:
Combined use of neuroradiology and 1H-MR spectroscopy may provide an intervention limiting diagnosis of glioblastoma multiforme.
J Magn Reson Imaging
; 2010 Nov;32(5):1038-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
GBM is the most common and aggressive primary brain
tumor
, with mean survival under a year.
MATERIALS AND METHODS: Eighty-nine patients had clinical computed tomography (CT) and MR imaging and 1.5T SV SE (1)H-MRS with PRESS localization for neuroradiological diagnosis and
tumor classification
with spectroscopic and automated pattern recognition analysis (TE 30 ms, TR 2000 ms, spectral width 2500 Hz and 2048 data points, 128-256 signal averages were acquired, depending on voxel size (8 cm(3) to 4 cm(3)).
RESULTS: The 18 stereotactic biopsies revealed 14 GBM, 2
grade
II
astrocytomas
, 1 lymphoma, and 1 anaplastic
astrocytoma
.
We do not advocate the replacement of biopsy in all patients; instead our data suggest a specific intervention limiting role for the use of (1)H-MRS in brain
tumor
diagnosis.
Genetic Alliance.
consumer health - Glioblastoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - CT Scans
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
© 2010 Wiley-Liss, Inc.
(PMID = 21031506.001).
[ISSN]
1522-2586
[Journal-full-title]
Journal of magnetic resonance imaging : JMRI
[ISO-abbreviation]
J Magn Reson Imaging
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / C12A/A1209; United Kingdom / Cancer Research UK / / C8807/A3870
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
58.
Yang Z, Wang Y, Fang J, Chen F, Liu J, Wu J, Wang Y, Song T, Zeng F, Rao Y:
Downregulation of WIF-1 by hypermethylation in astrocytomas.
Acta Biochim Biophys Sin (Shanghai)
; 2010 Jun 15;42(6):418-25
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Downregulation of WIF-1 by hypermethylation in
astrocytomas
.
Wnt inhibitory factor-1 (WIF-1) acts as a Wnt antagonist and
tumor
suppressor, but hypermethylation of WIF-1 gene promoter and low expression of WIF-1 activate Wnt signaling aberrantly and induce the development of several human tumors.
By using RT-PCR, immunohistochemistry and methylation-specific PCR, we analyzed the expression and methylation of WIF-1 in 4 normal brain tissues, 35 freshly resected
astrocytoma
tissues and 4 glioblastoma-derived cell lines.
Significant downregulation of WIF-1 mRNA and protein expression levels was observed in
astrocytoma
tissues compared with normal brain tissues.
Significant association between WIF-1 downregulation and pathological
grade
of astrocytomas
was found.
WIF-1 gene aberrant methylation was observed in 19 of 35 (54.29%)
tumor
samples.
Our results suggested that the WIF-1 gene is frequently silenced in
astrocytoma
by aberrant promoter methylation.
This may be an important mechanism in
astrocytoma
carcinogenesis.
[MeSH-major]
Adaptor Proteins, Signal Transducing / genetics.
Astrocytoma
/ genetics. DNA Methylation. Repressor Proteins / genetics
[MeSH-minor]
Azacitidine / analogs & derivatives. Azacitidine / metabolism. Cell Line,
Tumor
. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Promoter Regions, Genetic. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Wnt Proteins / genetics. beta Catenin / genetics
Hazardous Substances Data Bank.
AZACITIDINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20539942.001).
[ISSN]
1745-7270
[Journal-full-title]
Acta biochimica et biophysica Sinica
[ISO-abbreviation]
Acta Biochim. Biophys. Sin. (Shanghai)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / WIF1 protein, human; 0 / Wnt Proteins; 0 / beta Catenin; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
59.
Ellert-Miklaszewska A, Grajkowska W, Gabrusiewicz K, Kaminska B, Konarska L:
Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors.
Brain Res
; 2007 Mar 16;1137(1):161-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The efficacy of cannabinoids against high-
grade
glioma
in animal models, mediated by two specific receptors, CB1 and CB2, raised promises for targeted treatment of the most frequent and malignant primary brain tumors.
Most glioblastomas expressed very high levels of CB2 receptors and the expression correlated with
tumor
grade
.
Interestingly, some benign pediatric
astrocytic
tumors, such as subependymal giant cell
astrocytoma
(SEGA), which may occasionally cause mortality owing to progressive growth, also displayed high CB2 immunoreactivity.
Our results suggest that the CB2 receptor expression depends primarily on the histopathological origin of the brain
tumor
cells and differentiation state, reflecting the
tumor
grade
.
[MeSH-minor]
Adolescent. Adult. Age Factors.
Astrocytoma
/ metabolism. Child. Glioblastoma / metabolism. Histocompatibility Antigens / metabolism. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction / methods
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17239827.001).
[ISSN]
0006-8993
[Journal-full-title]
Brain research
[ISO-abbreviation]
Brain Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Histocompatibility Antigens; 0 / Receptor, Cannabinoid, CB2
60.
Somasundaram K, Reddy SP, Vinnakota K, Britto R, Subbarayan M, Nambiar S, Hebbar A, Samuel C, Shetty M, Sreepathi HK, Santosh V, Hegde AS, Hegde S, Kondaiah P, Rao MR:
Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive astrocytoma.
Oncogene
; 2005 Oct 27;24(47):7073-83
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive
astrocytoma
.
Astrocytoma
is the most common type of brain cancer constituting more than half of all brain tumors.
With an aim to identify markers describing
astrocytoma
progression, we have carried out microarray analysis of
astrocytoma
samples of different grades using cDNA microarray containing 1152 cancer-specific genes.
Data analysis identified several differentially regulated genes between normal brain tissue and
astrocytoma
as
well
as between grades II/III
astrocytoma
and glioblastoma multiforme (GBM;
grade
IV).
As ASCL has been implicated in neuroendocrine, medullary thyroid and small-cell lung cancers, we chose to examine the role of ASCL1 in the
astrocytoma
development.
Our data revealed that ASCL1 is overexpressed in progressive
astrocytoma
as evidenced by increased levels of ASCL1 transcripts in 85.71% (6/7) of
grade
II diffuse
astrocytoma
(DA), 90% (9/10) of
grade
III anaplastic
astrocytoma
(AA) and 87.5% (7/8) of secondary GBMs, while the majority of primary
de
novo GBMs expressed similar to or less than normal brain levels (66.67%; 8/12).
ASCL1 upregulation in progressive
astrocytoma
is accompanied by inhibition of Notch signaling as seen by uninduced levels of HES1, a transcriptional target of Notch1, increased levels of HES6, a dominant-negative inhibitor of HES1-mediated repression of ASCL1, and increased levels of Notch ligand Delta1, which is capable of inhibiting Notch signaling by forming intracellular Notch ligand autonomous complexes.
Our results imply that inhibition of Notch signaling may be an important early event in the development of
grade
II DA and subsequent progression to
grade
III AA and secondary GBM.
[MeSH-major]
Astrocytoma
/ genetics. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Membrane Proteins / metabolism. Signal Transduction. Transcription Factors / metabolism
[MeSH-minor]
Basic Helix-Loop-Helix Transcription Factors. Brain / metabolism. Brain / pathology. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Brain Neoplasms / pathology.
Disease
Progression. Gene Expression Profiling. Helix-Loop-Helix Motifs. Humans. Oligonucleotide Array Sequence Analysis. RNA,
Neoplasm
/ genetics. RNA,
Neoplasm
/ metabolism. Receptors, Notch. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16103883.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / ASCL1 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / RNA, Neoplasm; 0 / Receptors, Notch; 0 / Transcription Factors
61.
Pöpperl G, Kreth FW, Herms J, Koch W, Mehrkens JH, Gildehaus FJ, Kretzschmar HA, Tonn JC, Tatsch K:
Analysis of 18F-FET PET for grading of recurrent gliomas: is evaluation of uptake kinetics superior to standard methods?
J Nucl Med
; 2006 Mar;47(3):393-403
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Analysis of 18F-FET PET for grading of recurrent
gliomas
: is evaluation of uptake kinetics superior to standard methods?
The aim of the present study was to evaluate whether extended analyses
of O
-(2-18F-fluoroethyl)-L-tyrosine (FET) uptake kinetics provide results superior to those of standard
tumor
-to-background ratios in predicting
tumor
grade
in patients with pretreated
gliomas
.
METHODS: Dynamic 18F-FET PET studies (0-40 min after injection of 180 MBq of 18F-FET) were performed on 45
glioma
patients with suspected
tumor
recurrence after multimodal treatment.
For the standard method, tumoral maximal standardized uptake
value
(SUVmax) and the ratio to the background were derived from a summed image 20-40 min after injection.
Results were correlated with the histopathologic findings of MRI/PET-guided stereotactic biopsies and were evaluated with respect to their discriminatory power to separate low- from high-
grade
tumors using receiver-operating characteristic (ROC) analyses.
RESULTS: The parameters taking into account the individual time course of 18F-FET uptake were able to
differentiate
low-
grade
from high-
grade
recurrent
astrocytomas
with high diagnostic accuracy, reaching the best differentiation with a sensitivity and specificity of 92% and an area under the ROC curve (AUC) of 0.94.
Time-activity curves (5-40 min after injection) slightly and steadily increased in
tumor
-free patients and in low-
grade
tumors, whereas high-
grade
tumors showed an early peak around 10-15 min after injection followed by a decrease.
CONCLUSION: This study has shown differences in the dynamics of 18F-FET uptake between recurrent low- and high-
grade
gliomas
.
[MeSH-major]
Brain Neoplasms / metabolism. Brain Neoplasms / radionuclide imaging.
Glioma
/ metabolism.
Glioma
/ radionuclide imaging.
Neoplasm
Recurrence, Local / metabolism.
Neoplasm
Recurrence, Local / radionuclide imaging. Tyrosine / analogs & derivatives
MedlinePlus Health Information.
consumer health - Brain Tumors
.
Hazardous Substances Data Bank.
L-TYROSINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
J Nucl Med. 2006 May;47(5):806
(PMID = 16513607.001).
[ISSN]
0161-5505
[Journal-full-title]
Journal of nuclear medicine : official publication, Society of Nuclear Medicine
[ISO-abbreviation]
J. Nucl. Med.
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / O-(2-fluoroethyl)tyrosine; 0 / Radiopharmaceuticals; 42HK56048U / Tyrosine
62.
Tatevossian RG, Lawson AR, Forshew T, Hindley GF, Ellison DW, Sheer D:
MAPK pathway activation and the origins of pediatric low-grade astrocytomas.
J Cell Physiol
; 2010 Mar;222(3):509-14
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
MAPK pathway activation and the origins of pediatric low-
grade
astrocytomas
.
Low-
grade
astrocytomas
(LGAs) are the most common type of brain
tumor
in children.
[MeSH-major]
Astrocytoma
/ enzymology. Brain Neoplasms / enzymology. MAP Kinase Signaling
System
. Mitogen-Activated Protein Kinases / metabolism
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19937730.001).
[ISSN]
1097-4652
[Journal-full-title]
Journal of cellular physiology
[ISO-abbreviation]
J. Cell. Physiol.
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
[Number-of-references]
66
63.
Ferletta M, Uhrbom L, Olofsson T, Pontén F, Westermark B:
Sox10 has a broad expression pattern in gliomas and enhances platelet-derived growth factor-B--induced gliomagenesis.
Mol Cancer Res
; 2007 Sep;5(9):891-7
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Sox10 has a broad expression pattern in
gliomas
and enhances platelet-derived growth factor-B--induced gliomagenesis.
In a previously published insertional mutagenesis screen for candidate brain
tumor
genes in the mouse using a Moloney mouse leukemia virus encoding platelet-derived growth factor (PDGF)-B, the Sox10 gene was tagged in five independent tumors.
All Moloney murine leukemia virus/PDGFB tumors had a high protein expression of Sox10 independently of malignant
grade
or
tumor
type.
Infection with RCAS-SOX10 alone did not induce any
gliomas
.
Combined infection of RCAS-SOX10 and RCAS-PDGFB in wild-type Ntv-a mice yielded
a tumor
frequency of 12%, and in Ntv-a Arf-/- mice the
tumor
frequency was 30%.
This indicates that Sox10 alone is not sufficient to induce gliomagenesis but acts synergistically with PDGFB in
glioma
development.
We investigated the expression of Sox10 in other human tumors and in a number
of gliomas
.
The Sox10 expression was restricted to
gliomas
and melanomas.
All
glioma
types expressed Sox10, and tumors of low-
grade
glioma
had a much broader distribution of Sox10 compared with high-
grade
gliomas
.
[MeSH-major]
Brain Neoplasms / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic.
Glioma
/ genetics.
Glioma
/ pathology. High Mobility Group Proteins / genetics. Platelet-Derived Growth Factor / physiology. Transcription Factors / genetics
[MeSH-minor]
Animals.
Astrocytoma
/ genetics. Chickens. Glioblastoma / genetics. Humans. Intermediate Filament Proteins / genetics. Melanoma / genetics. Mice. Nerve Tissue Proteins / genetics. Nestin. Promoter Regions, Genetic. SOXE Transcription Factors
MedlinePlus Health Information.
consumer health - Brain Tumors
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17855658.001).
[ISSN]
1541-7786
[Journal-full-title]
Molecular cancer research : MCR
[ISO-abbreviation]
Mol. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Platelet-Derived Growth Factor; 0 / SOX10 protein, human; 0 / SOXE Transcription Factors; 0 / Sox10 protein, mouse; 0 / Transcription Factors
64.
Jacques TS, Eldridge C, Patel A, Saleem NM, Powell M, Kitchen ND, Thom M, Revesz T:
Mixed glioneuronal tumour of the fourth ventricle with prominent rosette formation.
Neuropathol Appl Neurobiol
; 2006 Apr;32(2):217-20
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Our cases demonstrate the morphological features of the 'rosette-forming glioneuronal tumour of the fourth ventricle', a recently identified tumour characterised by its unique location, neurocytic pseudo-rosette formation and the presence
of a
low
grade astrocytoma
component.
However, the clinical data available including the cases presented here, along with the histological features, suggest that these are low
grade
tumours with a good prognosis after surgical resection.
[MeSH-minor]
Adult.
Astrocytoma
/ metabolism.
Astrocytoma
/ pathology.
Astrocytoma
/ physiopathology. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Neurocytoma / metabolism. Neurocytoma / pathology. Neurocytoma / physiopathology
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16599951.001).
[ISSN]
0305-1846
[Journal-full-title]
Neuropathology and applied neurobiology
[ISO-abbreviation]
Neuropathol. Appl. Neurobiol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
65.
Combs SE, Schulz-Ertner D, Thilmann C, Edler L, Debus J:
Fractionated stereotactic radiation therapy in the management of primary oligodendroglioma and oligoastrocytoma.
Int J Radiat Oncol Biol Phys
; 2005 Jul 1;62(3):797-802
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
RESULTS: Fractionated stereotactic RT was
well
tolerated in all patients, without side effects.
With regard to histology, overall survival rates in the
World Health Organization
(
WHO
)
Grade
II group were 89% and 74% at 5 and 10 years, respectively.
In patients with
WHO
Grade
III tumors, overall survival rates at 5 and 10 years were 69% and 46%, respectively.
In FSRT, the
tumor
volume can be irradiated with high doses, sparing volume of normal brain tissue.
[MeSH-major]
Astrocytoma
/ surgery. Oligodendroglioma / surgery. Stereotaxic Techniques. Supratentorial Neoplasms / surgery
Genetic Alliance.
consumer health - Oligoastrocytoma
.
Genetic Alliance.
consumer health - Oligodendroglioma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15936562.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
66.
Quon H, Abdulkarim B:
Adjuvant treatment of anaplastic oligodendrogliomas and oligoastrocytomas.
Cochrane Database Syst Rev
; 2008;(2):CD007104
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Also, the
value of
chromosome 1p and 19q deletions as prognostic and predictive markers is only beginning to be defined.
To investigate the prognostic and predictive
value of
loss of heterozygosity of chromosomes 1p and 19q.
Outcomes analyzed include overall survival (OS), progression-free survival (PFS), and treatment toxicity greater than or equal to
grade
3.
SEARCH STRATEGY: Cochrane
Central
Register for Controlled Trials (
CENTRAL
, Issue 4,2006), MEDLINE (1966 to 2006) and EMBASE (1988 to 2006) were searched.
The predictive
value of
1p and 19q co-deletions is less clear with
one
study observing a longer PFS with chemotherapy, while the other study did not.
Tumors with 1p and 19q co-deletions are associated with better OS and may indicate a more chemo-responsive
tumor
.
[MeSH-major]
Astrocytoma
/ drug therapy. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[UpdateIn]
Cochrane Database Syst Rev. 2014;5:CD007104
[
24833028.001
]
(PMID = 18425979.001).
[ISSN]
1469-493X
[Journal-full-title]
The Cochrane database of systematic reviews
[ISO-abbreviation]
Cochrane Database Syst Rev
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
11
67.
Saunders DE, Phipps KP, Wade AM, Hayward RD:
Surveillance imaging strategies following surgery and/or radiotherapy for childhood cerebellar low-grade astrocytoma.
J Neurosurg
; 2005 Mar;102(2 Suppl):172-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Surveillance imaging strategies following surgery and/or radiotherapy for childhood cerebellar low-
grade astrocytoma
.
OBJECT: The authors sought to evaluate surveillance strategies for the detection and monitoring of residual and recurrent
disease
in children with cerebellar low-
grade
astrocytomas
(CLGAs) treated surgically or with radiotherapy.
(2) those with residual
disease
with no immediate adjuvant therapy; and (3) those
who
received radiotherapy for residual/recurrent
disease
.
METHODS: Magnetic resonance (MR) imaging studies and clinical data obtained in children with CLGA
who
presented between January 1988 and September 1998 were reviewed.
Eighty-four children were followed
for a
mean period of 73 months (range 2-159 months).
One
child died.
Following an incomplete resection, radiologically detected
tumor
progression leading to further treatment was detected at 7, 9, 12, 13, and 20 months, respectively, and an additional six tumors regressed or stablized.
For follow up of residual
tumor
, 6-month interval imaging for at least 3 years, yearly images for another 2 years, and subsequent 2-year imaging is recommended.
[MeSH-major]
Astrocytoma
/ diagnosis. Cerebellar Neoplasms / diagnosis. Magnetic Resonance Imaging.
Neoplasm
, Residual / diagnosis. Tomography, X-Ray Computed
[MeSH-minor]
Adolescent. Cerebellum / pathology. Cerebellum / radiography. Cerebellum / surgery. Child. Child, Preschool.
Disease
Progression. Female. Follow-Up Studies. Humans. Infant. Male.
Neoplasm
Recurrence, Local / epidemiology.
Neoplasm
Staging. Postoperative Care. Remission, Spontaneous. Time Factors
Genetic Alliance.
consumer health - Cerebellar Astrocytoma, Childhood
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16156227.001).
[ISSN]
0022-3085
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
68.
Donato G, Iofrida G, Lavano A, Volpentesta G, Signorelli F, Pallante PL, Berlingieri MT, Pierantoni MG, Palmieri D, Conforti F, Maltese L, Tucci L, Amorosi A, Fusco A:
Analysis of UbcH10 expression represents a useful tool for the diagnosis and therapy of astrocytic tumors.
Clin Neuropathol
; 2008 Jul-Aug;27(4):219-23
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Analysis of UbcH10 expression represents a useful tool for the diagnosis and therapy
of astrocytic
tumors.
Previous studies suggest the expression of UbcH10 gene, that codes
for a
protein belonging to the ubiquitin-conjugating enzyme family, as a valid indicator of the proliferative and aggressive status of tumors of different origin.
Therefore, to look for possible tools to be used as diagnostic markers in
astrocytic
neoplasias, we investigated UbcH10 expression in normal brain, gliosis and low-
grade
and high-
grade
astrocytic
tumors by immunohistochemistry.
UbcH10 expression was observed in low-
grade astrocytoma
and in glioblastoma.
Our data indicate a clear correlation between UbcH10 expression and the histological
grade
of the
astrocytic
tumors.
[MeSH-major]
Astrocytoma
/ diagnosis.
Astrocytoma
/ metabolism. Biomarkers,
Tumor
/ analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Ubiquitin-Conjugating Enzymes / biosynthesis
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18666437.001).
[ISSN]
0722-5091
[Journal-full-title]
Clinical neuropathology
[ISO-abbreviation]
Clin. Neuropathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
69.
Chamberlain MC, Johnston S:
Bevacizumab for recurrent alkylator-refractory anaplastic oligodendroglioma.
Cancer
; 2009 Apr 15;115(8):1734-43
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Bevacizumab-related toxicity included fatigue (14 patients; 4
grade
3), leukopenia (9; 1
grade
3), anemia (5; 0
grade
3), hypertension (5; 1
grade
3), deep vein thrombosis (4; 1
grade
3), and wound dehiscence (2; 1
grade
3).
Fifteen (68%) patients demonstrated a partial radiographic response, 1 (5.0%) demonstrated stable
disease
, and 6 (27%) demonstrated progressive
disease
after 2 cycles of bevacizumab.
Time to
tumor
progression ranged from 1 to 18 months (median, 6.75 months).
[MeSH-minor]
Adult. Antibodies, Monoclonal, Humanized. Antineoplastic Agents, Alkylating / therapeutic use.
Astrocytoma
/ drug therapy. Bevacizumab. Chromosomes, Human, Pair 1.
Disease
-Free Survival. Drug Resistance,
Neoplasm
. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis
Genetic Alliance.
consumer health - Anaplastic Oligodendroglioma
.
Genetic Alliance.
consumer health - Oligodendroglioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19197992.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents, Alkylating; 2S9ZZM9Q9V / Bevacizumab
70.
Sankar T, Kuznetsov YE, Ryan RW, Caramanos Z, Antel SB, Arnold DL, Preul MC:
The metabolic epicenter of supratentorial gliomas: a 1H-MRSI study.
Can J Neurol Sci
; 2009 Nov;36(6):696-706
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The metabolic epicenter of supratentorial
gliomas
: a 1H-MRSI study.
BACKGROUND: Assessing the impact
of glioma
location on prognosis remains elusive.
We approached the problem using multivoxel proton magnetic resonance spectroscopic imaging (1H-MRSI) to define
a tumor
"metabolic epicenter", and examined the relationship of metabolic epicenter location to survival and histopathological
grade
.
METHODS: We studied 54 consecutive patients with a supratentorial
glioma
(
astrocytoma
or oligodendroglioma,
WHO
grades II-IV).
The metabolic epicenter in each
tumor
was defined as the 1H-MRSI voxel containing maximum intra-tumoral choline on preoperative imaging.
Tumor
location was considered the X-Y-Z coordinate position, in a standardized stereotactic space, of the metabolic epicenter.
Correlation between epicenter location and survival or
grade
was assessed.
RESULTS: Metabolic epicenter location correlated significantly with patient survival for all tumors (r2 = 0.30, p = 0.0002) and
astrocytomas
alone (r2 = 0.32, p = 0.005).
A predictive model based on both metabolic epicenter location and histopathological
grade
accounted for 70% of the variability in survival, substantially improving on histology alone to predict survival.
Location also correlated significantly with
grade
(r2 = 0.25, p = 0.001): higher
grade
tumors had a metabolic epicenter closer to the midpoint of the brain.
CONCLUSIONS: The concept of the metabolic epicenter eliminates several problems related to existing methods of classifying
glioma
location.
The location of the metabolic epicenter is strongly correlated with overall survival and histopathological
grade
, suggesting that it reflects biological factors underlying
glioma
growth and malignant dedifferentiation.
These findings may be clinically relevant to predicting patterns of local
glioma
recurrence, and in planning resective surgery or radiotherapy.
[MeSH-major]
Glioma
/ diagnosis. Magnetic Resonance Spectroscopy. Supratentorial Neoplasms / diagnosis. Supratentorial Neoplasms / metabolism
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
(L)-ASPARTIC ACID
.
Hazardous Substances Data Bank.
CHOLINE CHLORIDE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19960747.001).
[ISSN]
0317-1671
[Journal-full-title]
The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
[ISO-abbreviation]
Can J Neurol Sci
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Canada
[Chemical-registry-number]
0 / Protons; 30KYC7MIAI / Aspartic Acid; N91BDP6H0X / Choline
71.
Combs SE, Thilmann C, Edler L, Debus J, Schulz-Ertner D:
Efficacy of fractionated stereotactic reirradiation in recurrent gliomas: long-term results in 172 patients treated in a single institution.
J Clin Oncol
; 2005 Dec 1;23(34):8863-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Efficacy of fractionated stereotactic reirradiation in recurrent
gliomas
: long-term results in 172 patients treated in a single institution.
PURPOSE: To evaluate the efficacy of fractionated stereotactic radiotherapy (FSRT) performed as reirradiation in 172 patients with recurrent low- and high-
grade
gliomas
.
PATIENTS AND METHODS: Between 1990 and 2004, 172 patients with recurrent
gliomas
were treated with FSRT as reirradiation in a single institution.
Seventy-
one
patients suffered from
WHO
grade
2
gliomas
.
WHO
grade
3
gliomas
were diagnosed in 42 patients, and 59 patients were diagnosed with glioblastoma multiforme (GBM).
The median time between primary radiotherapy and reirradiation was 10 months for GBM, 32 months
for WHO
grade
3 tumors, and 48 months for
grade
2
astrocytomas
.
RESULTS: Median overall survival after primary diagnosis was 21 months for patients with GBM, 50 months for patients with
WHO
grade
3
gliomas
, and 111 months for patients with
WHO
grade
2
gliomas
.
Median survival after reirradiation was 8 months for patients with GBM, 16 months for patients with
grade
3 tumors, and 22 months for patients with low-
grade
gliomas
.
Progression-free survival after FSRT was 5 months for GBM, 8 months
for WHO
grade
3 tumors, and 12 months for low-
grade
gliomas
.
CONCLUSION: FSRT is
well
tolerated and may be effective in patients with recurrent
gliomas
.
[MeSH-major]
Central Nervous System
Neoplasms / surgery.
Glioma
/ surgery.
Neoplasm
Recurrence, Local / surgery. Radiosurgery / methods
[MeSH-minor]
Adolescent. Adult. Aged.
Astrocytoma
/
classification
.
Astrocytoma
/ pathology.
Astrocytoma
/ surgery. Child. Child, Preschool.
Disease
-Free Survival. Female. Follow-Up Studies. Glioblastoma /
classification
. Glioblastoma / pathology. Glioblastoma / surgery. Humans. Male. Middle Aged. Multivariate Analysis.
Neoplasm
Staging. Time Factors. Treatment Outcome
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16314646.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article
[Publication-country]
United States
72.
Gabilondo AM, Hostalot C, Garibi JM, Meana JJ, Callado LF:
Monoamine oxidase B activity is increased in human gliomas.
Neurochem Int
; 2008 Jan;52(1-2):230-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Monoamine oxidase B activity is increased in human
gliomas
.
Glial tumours are the most common type of brain
neoplasm
in humans.
Tumour
classification
and grading represent key factors for patient management.
There were no significant differences in MAO-B activity between glioblastoma multiformes (n=11) and low-
grade
astrocytomas
(n=3) or anaplastic
astrocytomas
(n=6).
In conclusion, the present results demonstrate a significant and selective increase in MAO-B activity in human
gliomas
when compared with meningiomas or non-tumoural tissue.
These results suggest that the quantification of MAO-B activity may be a useful diagnostic tool
for differentiating
glial tumours from other types of brain tumours or surrounding normal brain tissue.
[MeSH-major]
Brain Neoplasms / enzymology.
Glioma
/ enzymology. Monoamine Oxidase / metabolism
MedlinePlus Health Information.
consumer health - Brain Tumors
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17624626.001).
[ISSN]
0197-0186
[Journal-full-title]
Neurochemistry international
[ISO-abbreviation]
Neurochem. Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 1.4.3.4 / Monoamine Oxidase
73.
Khwaja FW, Reed MS, Olson JJ, Schmotzer BJ, Gillespie GY, Guha A, Groves MD, Kesari S, Pohl J, Van Meir EG:
Proteomic identification of biomarkers in the cerebrospinal fluid (CSF) of astrocytoma patients.
J Proteome Res
; 2007 Feb;6(2):559-70
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Proteomic identification of biomarkers in the cerebrospinal fluid (CSF) of
astrocytoma
patients.
The monitoring of changes in the protein composition of the cerebrospinal fluid (CSF) can be used as a sensitive indicator
of central nervous system
(CNS) pathology, yet its systematic application to analysis of CNS neoplasia has been limited.
There is a pressing need for both a better understanding of gliomagenesis and the development of reliable biomarkers of the
disease
.
In this report, we used two proteomic techniques, two-dimensional gel electrophoresis (2-
DE
), and cleavable Isotope-Coded Affinity Tag (cICAT) to compare CSF proteomes to identify
tumor
- and
grade
-specific biomarkers in patients bearing brain tumors of differing histologies and grades.
Retrospective analyses were performed on 60 samples derived from
astrocytomas WHO
grade
II, III, and IV, schwannomas, metastastic brain tumors, inflammatory samples, and non-neoplastic controls.
We identified 103 potential
tumor
-specific markers of which 20 were high-
grade astrocytoma
-specific.
These investigations allowed us to identify a spectrum of signature proteins that could be used to distinguish CSF derived from control patients versus those with low- (AII) or high-
grade
(AIV)
astrocytoma
.
These proteins may represent new diagnostic, prognostic, and
disease
follow-up markers when used alone or in combination.
These candidate biomarkers may also have functional properties that play a critical role in the development and malignant progression of human
astrocytomas
, thus possibly representing novel therapeutic targets for this highly lethal
disease
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2005 May 15;65(10):4088-96
[
15899798.001
]
[Cites]
J Clin Oncol. 2005 May 20;23(15):3614-21
[
15908672.001
]
[Cites]
Cancer Res. 2005 May 15;65(10):4051-8
[
15899794.001
]
[Cites]
Cancer Res. 2005 Mar 15;65(6):2303-13
[
15781644.001
]
[Cites]
Acta Neurol Belg. 2004 Dec;104(4):148-53
[
15742604.001
]
[Cites]
Lab Invest. 2005 Mar;85(3):328-41
[
15716863.001
]
[Cites]
FASEB J. 2005 Jan;19(1):153-4
[
15522907.001
]
[Cites]
Eur J Hum Genet. 2005 Jan;13(1):118-20
[
15470364.001
]
[Cites]
Nat Biotechnol. 1999 Oct;17(10):994-9
[
10504701.001
]
[Cites]
J Exp Med. 1997 Oct 20;186(8):1201-12
[
9334359.001
]
[Cites]
Oncogene. 1997 Jan 16;14(2):171-83
[
9010219.001
]
[Cites]
J Immunol. 1996 Mar 1;156(5):1714-21
[
8596018.001
]
[Cites]
Glia. 1995 Nov;15(3):264-88
[
8586463.001
]
[Cites]
Immunol Today. 1992 Dec;13(12):507-12
[
1463583.001
]
[Cites]
Nature. 1992 Oct 29;359(6398):845-8
[
1279432.001
]
[Cites]
J Invest Dermatol. 1991 Mar;96(3):318-22
[
2002252.001
]
[Cites]
Am J Pathol. 1991 Feb;138(2):349-58
[
1992762.001
]
[Cites]
Eur J Pediatr. 1988 Oct;148(1):3-8
[
3058481.001
]
[Cites]
Cancer. 1983 Jul 1;52(1):101-4
[
6189578.001
]
[Cites]
Dis Markers. 2005;21(2):81-92
[
15920295.001
]
[Cites]
Proteomics. 2005 Aug;5(13):3223, 3225
[
16104055.001
]
[Cites]
BMC Genomics. 2005;6:145
[
16242023.001
]
[Cites]
J Dermatol Sci. 2005 Dec;40(3):157-68
[
16150577.001
]
[Cites]
Clin Cancer Res. 2006 Nov 1;12(21):6331-6
[
17085642.001
]
[Cites]
Int J Cancer. 2003 Sep 10;106(4):521-7
[
12845647.001
]
[Cites]
Clin Cancer Res. 2000 Jan;6(1):102-11
[
10656438.001
]
[Cites]
Adv Exp Med Biol. 2000;477:173-85
[
10849745.001
]
[Cites]
Histol Histopathol. 2000 Jul;15(3):971-81
[
10963139.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):559-64
[
11209055.001
]
[Cites]
Clin J Oncol Nurs. 2000 Jul-Aug;4(4):153-8
[
11261094.001
]
[Cites]
Int J Neuropsychopharmacol. 2001 Mar;4(1):93-102
[
11343634.001
]
[Cites]
J Neurooncol. 2001 Jun;53(2):149-60
[
11716067.001
]
[Cites]
Adv Anat Pathol. 2002 Jan;9(1):24-36
[
11756757.001
]
[Cites]
Neuron. 2002 Jul 3;35(1):25-38
[
12123606.001
]
[Cites]
J Neuropathol Exp Neurol. 2002 Sep;61(9):767-77
[
12230323.001
]
[Cites]
Cancer Res. 2002 Nov 1;62(21):6270-7
[
12414657.001
]
[Cites]
J Proteome Res. 2002 Jan-Feb;1(1):47-54
[
12643526.001
]
[Cites]
Nat Rev Cancer. 2003 Apr;3(4):267-75
[
12671665.001
]
[Cites]
Cancer J. 2003 May-Jun;9(3):214-21
[
12952306.001
]
[Cites]
J Neuropathol Exp Neurol. 2003 Aug;62(8):855-62
[
14503641.001
]
[Cites]
Nature. 2003 Oct 30;425(6961):905
[
14586448.001
]
[Cites]
Lab Invest. 2004 Apr;84(4):397-405
[
14990981.001
]
[Cites]
Clin Biochem. 2004 Nov;37(11):943-52
[
15498520.001
]
[Cites]
J Natl Cancer Inst. 1979 Mar;62(3):485-91
[
216840.001
]
[Cites]
Clin Chem. 1980 Aug;26(9):1317-22
[
7398046.001
]
(PMID = 17269713.001).
[ISSN]
1535-3893
[Journal-full-title]
Journal of proteome research
[ISO-abbreviation]
J. Proteome Res.
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / RR 02878; United States / NCI NIH HHS / CA / R01 CA086335; United States / NCI NIH HHS / CA / R01 CA086335-05; United States / NCRR NIH HHS / RR / M01 RR000039; United States / NCRR NIH HHS / RR / RR 12878; United States / NCRR NIH HHS / RR / M01 RR 00039; United States / NCRR NIH HHS / RR / RR 13948; United States / NCI NIH HHS / CA / CA 86335
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Affinity Labels; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proteome
[Other-IDs]
NLM/ NIHMS61862; NLM/ PMC2566942
74.
Schwer AL, Damek DM, Kavanagh BD, Gaspar LE, Lillehei K, Stuhr K, Chen C:
A phase I dose-escalation study of fractionated stereotactic radiosurgery in combination with gefitinib in patients with recurrent malignant gliomas.
Int J Radiat Oncol Biol Phys
; 2008 Mar 15;70(4):993-1001
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A phase I dose-escalation study of fractionated stereotactic radiosurgery in combination with gefitinib in patients with recurrent malignant
gliomas
.
PURPOSE: To determine the maximum tolerated dose (MTD) of fractionated stereotactic radiosurgery (SRS) with gefitinib in patients with recurrent malignant
gliomas
.
Eligible patients had pathologically proved recurrent anaplastic
astrocytoma
or glioblastoma.
Patients started gefitinib (250 mg/day) 7 days before SRS and continued
for 1
year or until
disease
progression.
Dose-limiting toxicity (DLT) was any
Grade
3 toxicity.
Grade
1-2 gefitinib-related dermatitis and diarrhea were common (10 and 7 patients, respectively).
CONCLUSION: Fractionated SRS to a dose of 36 Gy in three fractions is
well
tolerated with gefitinib at daily dose of 250 mg.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Brain Neoplasms / therapy.
Glioma
/ therapy.
Neoplasm
Recurrence, Local / therapy. Quinazolines / therapeutic use. Radiosurgery / methods
[MeSH-minor]
Adult. Aged.
Astrocytoma
/ drug therapy.
Astrocytoma
/ surgery.
Astrocytoma
/ therapy. Dose Fractionation. Female. Humans. Male. Maximum Tolerated Dose. Mental Status Schedule. Middle Aged. Prospective Studies. Treatment Outcome
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17967517.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
75.
Arjona D, Rey JA, Taylor SM:
Early genetic changes involved in low-grade astrocytic tumor development.
Curr Mol Med
; 2006 Sep;6(6):645-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Early genetic changes involved in low-
grade
astrocytic tumor
development.
Astrocytomas
represent the most common form of glial tumors.
The most malignant
grade
of these tumors, glioblastoma multiforme, may arise as a malignant progression from low-
grade astrocytoma
through anaplastic
astrocytoma
to secondary GBM, or else it may arise "
de
novo" as primary GBM.
Since malignant transformation is a multistep process, we summarize in this review the earliest genetic changes that seem to be involved in the appearance and development of low-
grade
astrocytic
tumors, where early detection and treatment could be possible.
[MeSH-major]
Astrocytoma
/ genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. Models, Genetic.
Tumor
Suppressor Proteins / genetics
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17022734.001).
[ISSN]
1566-5240
[Journal-full-title]
Current molecular medicine
[ISO-abbreviation]
Curr. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Tumor Suppressor Proteins
[Number-of-references]
80
76.
Kaderali Z, Lamberti-Pasculli M, Rutka JT:
The changing epidemiology of paediatric brain tumours: a review from the Hospital for Sick Children.
Childs Nerv Syst
; 2009 Jul;25(7):787-93
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
METHODS: We classified 1,866 surgical pathology cases of brain tumours in children under the age of 19 according to the
World Health Organization
2007 consensus and analysed them by gender, histological tumour type, age distribution and decade.
The main histological tumour types were low-
grade
(I/II)
astrocytomas
(26.4%), medulloblastoma (10.6%), anaplastic
astrocytoma
/glioblastoma multiforme (7.1%) and ependymoma (7.0%).
Over three decades, an increasing proportion of certain tumour types, including pilocytic
astrocytoma
, atypical teratoma/rhabdoid tumours and neuronal/mixed neuronal-glial tumours was seen.
Any changes in the epidemiology of childhood
central nervous system
tumours over the past three decades may be attributed in part to changing
classification
systems, improved imaging technologies and developments in epilepsy surgery; however, continued surveillance remains important.
[MeSH-minor]
Age Factors.
Astrocytoma
/ epidemiology.
Astrocytoma
/ pathology. Canada / epidemiology. Child. Ependymoma / epidemiology. Ependymoma / pathology. Glioblastoma / epidemiology. Glioblastoma / pathology. Humans. Medulloblastoma / epidemiology. Medulloblastoma / pathology.
Neoplasm
Staging. Neoplasms, Complex and Mixed / epidemiology. Neoplasms, Complex and Mixed / pathology. Neoplasms, Nerve Tissue / epidemiology. Neoplasms, Nerve Tissue / pathology. Rhabdoid
Tumor
/ epidemiology. Rhabdoid
Tumor
/ pathology. Risk Factors. Sex Factors. Teratoma / epidemiology. Teratoma / pathology. Time Factors
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Paediatr Perinat Epidemiol. 1996 Jul;10(3):319-38
[
8822774.001
]
[Cites]
J Neuropathol Exp Neurol. 2001 Mar;60(3):248-62
[
11245209.001
]
[Cites]
J Natl Cancer Inst. 1998 Sep 2;90(17):1269-77
[
9731733.001
]
[Cites]
Cancer. 2000 May 15;88(10):2342-9
[
10820357.001
]
[Cites]
Toxicol Appl Pharmacol. 2004 Sep 1;199(2):118-31
[
15313584.001
]
[Cites]
Cancer. 1999 May 1;85(9):2077-90
[
10223251.001
]
[Cites]
J Natl Cancer Inst. 1993 Nov 17;85(22):1871-2
[
8230273.001
]
[Cites]
Int J Cancer. 2006 Jun 1;118(11):2809-15
[
16380987.001
]
[Cites]
Int J Cancer. 2003 May 20;105(1):88-91
[
12672035.001
]
[Cites]
Childs Nerv Syst. 2005 Nov;21(11):940-4
[
16044344.001
]
[Cites]
Childs Nerv Syst. 2001 Sep;17(9):503-11
[
11585322.001
]
[Cites]
Cancer. 1997 Apr 1;79(7):1381-93
[
9083161.001
]
[Cites]
Cancer. 2000 Mar 15;88(6):1492-3
[
10717635.001
]
[Cites]
Childs Nerv Syst. 1991 Jun;7(3):150-3
[
1878869.001
]
[Cites]
Neuro Oncol. 2006 Jan;8(1):27-37
[
16443945.001
]
[Cites]
Cancer. 1996 Aug 1;78(3):532-41
[
8697401.001
]
[Cites]
Pediatr Neurosurg. 2000 Jun;32(6):321-6
[
10971194.001
]
[Cites]
J Natl Cancer Inst. 1993 Jul 7;85(13):1024-5
[
8515483.001
]
[Cites]
Acta Neurochir (Wien). 1993;123(1-2):14-24
[
8213273.001
]
[Cites]
J Natl Cancer Inst. 1990 Oct 17;82(20):1594-6
[
2213900.001
]
[Cites]
J Pediatr Hematol Oncol. 2003 Nov;25(11):842-4
[
14608192.001
]
[Cites]
Environ Health Perspect. 1995 Sep;103 Suppl 6:177-84
[
8549470.001
]
(PMID = 19082611.001).
[ISSN]
1433-0350
[Journal-full-title]
Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
[ISO-abbreviation]
Childs Nerv Syst
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Germany
[Number-of-references]
30
77.
Hulleman E, Helin K:
Molecular mechanisms in gliomagenesis.
Adv Cancer Res
; 2005;94:1-27
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Glioma
, and in particular high-
grade astrocytoma
termed glioblastoma multiforme (GBM), is the most common primary
tumor of
the brain.
Modeling
of astrocytomas
by genetic manipulation of mice suggests that deregulation of the pathways that control gliogenesis during normal brain development, such as the differentiation of neural stem cells (NSCs) into astrocytes, might contribute to GBM formation.
Use of novel techniques including large-scale genomics and proteomics in combination with relevant mouse models will most likely provide novel insights into the molecular mechanisms underlying
glioma
formation and will hopefully lead to development of treatment modalities for GBM.
[MeSH-major]
Brain Neoplasms /
classification
. Brain Neoplasms / physiopathology.
Glioma
/
classification
. Signal Transduction / physiology
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16095998.001).
[ISSN]
0065-230X
[Journal-full-title]
Advances in cancer research
[ISO-abbreviation]
Adv. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
155
78.
Gil-Benso R, Lopez-Gines C, Benito R, López-Guerrero JA, Callaghan RC, Pellín A, Roldán P, Cerdá-Nicolas M:
Concurrent EGFR amplification and TP-53 mutation in glioblastomas.
Clin Neuropathol
; 2007 Sep-Oct;26(5):224-31
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
A genetic alteration that is significantly more frequent in primary than in secondary glioblastomas, the latter arising from preceding low-
grade
gliomas
, is epidermal growth factor receptor gene (EGFR) amplification, whereas TP-53 mutations are significantly more frequent in low-
grade
gliomas
and secondary glioblastomas derived there- from.
We report the histological and genetic study of two glioblastomas,
one
case arising
de
novo and the other case arising 3 years after a previously diagnosed anaplastic
astrocytoma
, with concurrent EGFR amplification and TP-53 mutation.
[MeSH-minor]
Astrocytoma
/ genetics.
Astrocytoma
/ metabolism.
Astrocytoma
/ pathology. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17907599.001).
[ISSN]
0722-5091
[Journal-full-title]
Clinical neuropathology
[ISO-abbreviation]
Clin. Neuropathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
EC 2.7.10.1 / Receptor, Epidermal Growth Factor
79.
Eoli M, Bissola L, Bruzzone MG, Pollo B, Maccagnano C, De Simone T, Valletta L, Silvani A, Bianchessi D, Broggi G, Boiardi A, Finocchiaro G:
Reclassification of oligoastrocytomas by loss of heterozygosity studies.
Int J Cancer
; 2006 Jul 1;119(1):84-90
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Oligoastrocytomas (OAs) are
WHO
grade
II or III tumors composed
of a
mixture of 2 neoplastic cell types morphologically resembling the cells in oligodendrogliomas and diffuse
astrocytomas
.
Investigations on the genetic profile of OAs may yield important information for their
classification
and help for their clinical management.
We have studied, in 94 OAs (46
WHO
grade
II and 48
WHO
grade
III), the patterns of loss of heterozygosity (LOH) of 4 genomic regions: 1p, 19q, 17p and 10q.
OAs without LOH on 1p behave like
WHO
grade
II or III diffuse
astrocytomas
: they have shorter survival, MRI characteristics implying malignancy and genetic alterations associated with
tumor
progression.
OAs with LOH on 1p, on the other hand, behave like
WHO
grade
II or III oligodendrogliomas with 1p loss: they are associated with longer survival and do not have MRI or genetic alterations associated with malignancy.
These findings suggest that the definition of OAs or mixed
gliomas
could be reshaped in agreement with the genetic information.
[MeSH-major]
Astrocytoma
/
classification
.
Astrocytoma
/ genetics. Brain Neoplasms /
classification
. Brain Neoplasms / genetics. Loss of Heterozygosity
[MeSH-minor]
Adult. Analysis of Variance. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 19.
Disease
Progression.
Disease
-Free Survival. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Survival Analysis
MedlinePlus Health Information.
consumer health - Brain Tumors
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16432842.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
80.
Combs SE, Gutwein S, Thilmann C, Debus J, Schulz-Ertner D:
Reirradiation of recurrent WHO grade III astrocytomas using fractionated stereotactic radiotherapy (FSRT).
Strahlenther Onkol
; 2005 Dec;181(12):768-73
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Reirradiation of recurrent
WHO
grade
III
astrocytomas
using fractionated stereotactic radiotherapy (FSRT).
PURPOSE: To assess the effect of reirradiation in recurrent
WHO
grade
III
astrocytomas
.
PATIENTS AND METHODS: From January 1995 to July 2003, 40 patients with
grade
III
gliomas
were treated with fractionated stereotactic reirradiation at the time point of recurrence.
RESULTS: Radiotherapy was
well
tolerated by all patients.
No toxicities > CTC
grade
2 developed.
CONCLUSION: Fractionated stereotactic radiotherapy is
well
tolerated and effective in patients with recurrent
grade
III
astrocytomas
.
[MeSH-major]
Astrocytoma
/ mortality.
Astrocytoma
/ surgery. Brain Neoplasms / mortality. Brain Neoplasms / surgery.
Neoplasm
Recurrence, Local / mortality.
Neoplasm
Recurrence, Local / surgery. Radiosurgery / statistics & numerical data
[MeSH-minor]
Adult. Aged. Dose Fractionation. Female. Germany / epidemiology. Humans. Incidence. Male. Middle Aged. Prognosis. Risk Assessment / methods. Risk Factors. Severity of Illness Index. Survival Analysis. Survival Rate. Treatment Outcome.
World Health Organization
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16362786.001).
[ISSN]
0179-7158
[Journal-full-title]
Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
[ISO-abbreviation]
Strahlenther Onkol
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Germany
81.
Nishikawa R, Shibui S, Maruno M, Sugiyama K, Sato S, Fujimaki T, Takahashi H, Wakabayashi T, Takahashi J, Kochi M, Nakamura H, Sawamura Y, Ikeda J, Hori T, Aoki T, Matsutani M:
[Efficacy and safety of monotherapy with temozolomide in patients with anaplastic astrocytoma at first relapse--a phase II clinical study].
Gan To Kagaku Ryoho
; 2006 Sep;33(9):1279-85
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Efficacy and safety of monotherapy with temozolomide in patients with anaplastic
astrocytoma
at first relapse--a phase II clinical study].
The efficacy and safety of temozolomide were evaluated in 32 patients with anaplastic
astrocytoma
at first relapse.
Temozolomide was administered orally once daily for the first five days
of a
28-day cycle, at a dose of 150 or 200 mg/m(2)/day.
The response rate determined by independent
central
review of MRI was 34% (95% confidence interval: 18.6%-53.2%), with 3 complete response and 8 partial response.
The incidence of constipation (50%) and nausea (25%) was high,but these events were all mild or moderate in severity except in
one
subject with constipation,and could be managed with standard laxatives and antiemetics.
The main laboratory test abnormalities (total incidence and incidence of
grade
3/4 change) were lymphocytopenia (50%, 25%), neutropenia (47%, 6%), leukopenia (38%, 3%), thrombocytopenia (31%, 9%), and increased GPT (25%, 3%).
Temozolomide was shown to have good efficacy and tolerability in patients with anaplastic
astrocytoma
at first relapse.
[MeSH-major]
Antineoplastic Agents, Alkylating / therapeutic use.
Astrocytoma
/ drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives
[MeSH-minor]
Adult. Aged. Anorexia / chemically induced.
Disease
-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Leukopenia / chemically induced. Male. Middle Aged
Genetic Alliance.
consumer health - Anaplastic Astrocytoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
Hazardous Substances Data Bank.
DACARBAZINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16969025.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Clinical Trial, Phase II; English Abstract; Journal Article; Multicenter Study
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
82.
Beetz C, Brodoehl S, Patt S, Kalff R, Deufel T:
Low expression but infrequent genomic loss of the putative tumour suppressor DBCCR1 in astrocytoma.
Oncol Rep
; 2005 Feb;13(2):335-40
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Low expression but infrequent genomic loss of the putative tumour suppressor DBCCR1 in
astrocytoma
.
The present study addressed expression of DBCCR1 in
gliomas
, specifically in
astrocytomas
, using semi-quantitative RT-PCR on 25 tumours of different malignancy
grade
and on 5 control brain tissue samples.
Genomic deletion of the DBCCR1 locus at 9q32-33 was also investigated, together with the CDKN2A locus at 9p21, by loss of heterozygosity analysis in a second series of 26
astrocytic
tumours.
We found that DBCCR1 mRNA expression is markedly reduced in the majority of tumour samples compared to controls, and that this reduction significantly correlates with tumour
grade
.
Genomic loss of the DBCCR1 region was found in only 5 of 24 (21%) informative samples, with no obvious correlation to tumour
grade
, while loss of the CDKN2A locus was observed in 13 of 21 (62%) informative samples with high-
grade
tumours being affected more often.
In contrast to the situation in bladder cancer, the prevalent inactivation of DBCCR1 seen at the expression level in
astrocytomas
is not primarily caused by genomic loss of the gene.
[MeSH-major]
Astrocytoma
/ genetics. Brain Neoplasms / genetics. Genes,
Tumor
Suppressor.
Tumor
Suppressor Proteins / genetics
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15643521.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / DBC1 protein, human; 0 / Tumor Suppressor Proteins
83.
Marcorelles P, Fallet-Bianco C, Oury JF, van Wallenghem E, Parent P, Labadie G, Lagarde N, Laquerrière A:
Fetal aqueductal glioneuronal hamartoma: a clinicopathological and physiopathological study of three cases.
Clin Neuropathol
; 2005 Jul-Aug;24(4):155-62
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Histological examination evidenced a nodular,
well
-demarcated mass producing into the aqueductal lumen, and containing numerous immature proliferating glioneuronal cells.
Immunohistochemical analyses did not suggest a developmental
abnormality of
the subcommissural organ but rather a hamartomatous malformative process.
Post-natal cases have been described in the cerebello-pontine angle or in the quadrigeminal plate, and have always been diagnosed as pilocytic or low-
grade
astrocytomas
.
In our cases, the lesions could be related to so-called pencil
glioma
, sometimes associated with type 1 neurofibromatosis and, to our knowledge, have never been described prior to birth.
The occurrence during fetal life and the progressive maturation of the nodules are more likely in favor
of a
hamartomatous process.
CONCLUSION: Even though they could sporadically occur, an accurate genetic counseling should be required in order to ensure that there is no familial history of Recklinghausen
disease
, and to provide a more precise evaluation of recurrence risk.
[MeSH-major]
Brain Neoplasms / pathology. Cerebral Aqueduct / pathology. Fetal
Diseases
/ pathology.
Glioma
/ pathology. Hamartoma / pathology
[MeSH-minor]
Abortion, Induced. Adult. Brain
Diseases
/ pathology. Brain
Diseases
/ ultrasonography. Female. Humans. Hydrocephalus / pathology. Hydrocephalus / ultrasonography. Neuroglia / pathology. Neurons / pathology. Pregnancy. Ultrasonography, Prenatal
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Fetal Health and Development
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16033131.001).
[ISSN]
0722-5091
[Journal-full-title]
Clinical neuropathology
[ISO-abbreviation]
Clin. Neuropathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
84.
Edwards LA, Thiessen B, Dragowska WH, Daynard T, Bally MB, Dedhar S:
Inhibition of ILK in PTEN-mutant human glioblastomas inhibits PKB/Akt activation, induces apoptosis, and delays tumor growth.
Oncogene
; 2005 May 19;24(22):3596-605
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Inhibition of ILK in PTEN-mutant human glioblastomas inhibits PKB/Akt activation, induces apoptosis, and delays
tumor
growth.
The
tumor
suppressor gene phosphatase and tensin homologue (PTEN) regulates the phosphatidylinositol-3'-kinase (PI3K) signaling pathway and has been shown to correlate with poor prognosis in high-
grade
astrocytomas
when mutational inactivation or loss of the PTEN gene occurs.
5 mg/kg), exhibited stable
disease
with < or =7% increase in
tumor
volume over the 3-week course of treatment.
In contrast, animals treated with an oligonucleotide control or saline exhibited a >100% increase in
tumor
volume over the same time period.
[MeSH-minor]
3-Phosphoinositide-Dependent Protein Kinases. Animals. Apoptosis / physiology. Blotting, Western. Cell Line,
Tumor
. Enzyme Activation / physiology. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mutation. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Proto-Oncogene Proteins c-akt.
Tumor
Suppressor Proteins / genetics
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
PhosphoSitePlus.
gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15782140.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.1.- / integrin-linked kinase; EC 2.7.11.1 / 3-Phosphoinositide-Dependent Protein Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
85.
Hu CH, Fang XM, Hu XY, Cui L:
Analysis of the mismatched manifestation between rCBF and rCBV maps in cerebral astrocytomas.
Clin Imaging
; 2009 Nov-Dec;33(6):417-23
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Analysis of the mismatched manifestation between rCBF and rCBV maps in cerebral
astrocytomas
.
OBJECTIVE: To explore the mismatched manifestation between regional cerebral blood flow (rCBF) and regional cerebral blood volume (rCBV)
of astrocytomas
.
METHODS: Both conventional and perfusion CT were performed on 29 patients with pathologically confirmed
astrocytomas
(15 cases in Grades I-II, 14 cases in Grades III-IV).
RESULTS: Twelve low-
grade
astrocytomas
showed low or medium values of both rCBF (46.95+/-22.92 ml 100 g(-1) mm(-1)) and rCBV (5.74+/-3.61 ml 100 g(-1)); 12 high-
grade
astrocytomas
showed high values of both rCBF (95.44+/-42.58 ml 100 g(-1) min(-1)) and rCBV (9.24+/-5.32 ml 100g(-1)).
However, the remaining five
astrocytomas
were mismatched, showing reduced rCBF
value
and increased rCBV
value
in the same ROI.
The discrepancy may mislead to an inaccuracy of perfusion CT in grading
gliomas
.
CONCLUSIONS: The mismatched manifestation between rCBF and rCBV occasionally exists in some areas
of astrocytomas
.
Hence, attention should be paid to assessments in preoperative grading
of astrocytomas
and in monitoring therapeutic effects.
[MeSH-major]
Astrocytoma
/ physiopathology.
Astrocytoma
/ radiography. Brain Neoplasms / physiopathology. Brain Neoplasms / radiography. Cerebrovascular Circulation. Perfusion Imaging / methods. Tomography, X-Ray Computed / methods
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - CT Scans
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19857800.001).
[ISSN]
1873-4499
[Journal-full-title]
Clinical imaging
[ISO-abbreviation]
Clin Imaging
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
86.
Cao Y, Tsien CI, Nagesh V, Junck L, Ten Haken R, Ross BD, Chenevert TL, Lawrence TS:
Survival prediction in high-grade gliomas by MRI perfusion before and during early stage of RT [corrected].
Int J Radiat Oncol Biol Phys
; 2006 Mar 01;64(3):876-85
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Survival prediction in high-
grade
gliomas
by MRI perfusion before and during early stage of RT [corrected].
PURPOSE: To determine whether cerebral blood volume (CBV) and cerebral blood flow can predict the response of high-
grade
gliomas
to radiotherapy (RT) by taking into account spatial heterogeneity and temporal changes in perfusion.
METHODS AND MATERIALS: Twenty-three patients with high-
grade
gliomas
underwent conformal RT, with magnetic resonance imaging perfusion before and at Weeks 1-2 and 3-4 during RT.
Tumor
perfusion was classified as high, medium, or low.
The prognostic values of pre-RT perfusion and the changes during RT for early prediction
of tumor
response to RT were evaluated.
RESULTS: The fractional high-CBV
tumor
volume before RT and the fluid-attenuated inversion recovery imaging
tumor
volume were identified as predictors for survival (p = 0.01).
Changes in
tumor
CBV during the early treatment course also predicted for survival.
Better survival was predicted by a decrease in the fractional low-CBV
tumor
volume at Week
1 of
RT vs. before RT, a decrease in the fractional high-CBV
tumor
volume at Week 3 vs. Week
1 of
RT, and a smaller pre-RT fluid-attenuated inversion recovery imaging
tumor
volume (p = 0.01).
CONCLUSION: Early temporal changes during RT in heterogeneous regions of high and low perfusion in
gliomas
might predict for different physiologic responses to RT.
This might also open the opportunity to identify
tumor
subvolumes that are radioresistant and might benefit from intensified RT.
[MeSH-major]
Astrocytoma
/ blood supply.
Astrocytoma
/ radiotherapy. Brain Neoplasms / blood supply. Brain Neoplasms / radiotherapy. Cerebrovascular Circulation. Magnetic Resonance Imaging / methods
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):960
(PMID = 16298499.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R21 CA113699; United States / NCI NIH HHS / CA / R21 CA11369901; United States / NCI NIH HHS / CA / P01 CA85878; United States / NCI NIH HHS / CA / 2 PO1 CA59827
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 7S5I7G3JQL / Dexamethasone
87.
Petridis AK, Wedderkopp H, Hugo HH, Maximilian Mehdorn H:
Polysialic acid overexpression in malignant astrocytomas.
Acta Neurochir (Wien)
; 2009 Jun;151(6):601-3; discussion 603-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Polysialic acid overexpression in malignant
astrocytomas
.
METHODS: Intra-operatively collected biopsies from 30 patients with different
astrocytoma
grades were immuno-histochemically examined to identify expression of PSA.
RESULTS:
Astrocytoma grade
I and II had 4% PSA expressing cells whereas in
grade
III and IV the number of PSA expressing cells was 45%.
CONCLUSION: In this short communication we show that highly malignant
astrocytomas
express significantly more PSA compared to less malignant
astrocytomas
.
[MeSH-major]
Astrocytoma
/ metabolism.
Astrocytoma
/ pathology. Biomarkers,
Tumor
/ metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Sialic Acids / metabolism
[MeSH-minor]
Animals. Biopsy. Cell Adhesion / physiology. Cell Differentiation / physiology. Cell Movement / physiology. Cell Proliferation.
Disease
Models, Animal. Humans. Immunohistochemistry. Mice.
Neoplasm
Invasiveness / diagnosis.
Neoplasm
Invasiveness / physiopathology.
Neoplasm
Proteins / physiology. Nerve Tissue Proteins / physiology. Neural Cell Adhesion Molecules / metabolism. Stem Cells / cytology. Stem Cells / metabolism
MedlinePlus Health Information.
consumer health - Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19387537.001).
[ISSN]
0942-0940
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Austria
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Neural Cell Adhesion Molecules; 0 / Sialic Acids; 0 / UCC1 protein, human; 0 / polysialic acid
88.
Wolff JE, Berrak S, Koontz Webb SE, Zhang M:
Nitrosourea efficacy in high-grade glioma: a survival gain analysis summarizing 504 cohorts with 24193 patients.
J Neurooncol
; 2008 May;88(1):57-63
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Nitrosourea efficacy in high-
grade
glioma
: a survival gain analysis summarizing 504 cohorts with 24193 patients.
Even though past studies have suggested efficacy of nitrosourea drugs in patients with high-
grade
glioma
and temozolomide has recently been shown significantly to be beneficial, no conclusive comparisons between these agents have been published.
We performed a survival gain analysis of 364 studies describing 24,193 patients with high-
grade
glioma
treated in 504 cohorts, and compared the effects of drugs.
The most frequent diagnoses were glioblastoma multiforme (GBM) (72%) and anaplastic
astrocytoma
(22%).
The outcome was influenced by several of the known prognostic factors including the histological
grade
, if the tumors were newly diagnosed or recurrent, the completeness of resection, patients' age, and gender.
This information allowed the calculation
of a
predicted mOS for each cohort based on their prognostic factors independent of treatment.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy.
Glioma
/ drug therapy. Nitrosourea Compounds / therapeutic use
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Astrocytoma
/ drug therapy.
Astrocytoma
/ pathology. Carmustine / adverse effects. Carmustine / therapeutic use. Clinical Trials as Topic. Cohort Studies. Data Interpretation, Statistical. Databases, Factual. Female. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Lomustine / adverse effects. Lomustine / therapeutic use. Male. Nimustine / adverse effects. Nimustine / therapeutic use. Reproducibility of Results. Selection Bias. Survival Analysis. Treatment Outcome
Genetic Alliance.
consumer health - Glioma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Hazardous Substances Data Bank.
LOMUSTINE
.
Hazardous Substances Data Bank.
Carmustine
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Int J Cancer. 1996 Feb 8;65(4):506-12
[
8621235.001
]
[Cites]
J Neurooncol. 2006 Sep;79(3):281-7
[
16598416.001
]
[Cites]
Neuro Oncol. 2006 Jan;8(1):12-26
[
16443944.001
]
[Cites]
Eur J Cancer. 1991;27(5):630-8
[
1828975.001
]
[Cites]
Stat Med. 2002 Jun 15;21(11):1559-73
[
12111920.001
]
[Cites]
J Clin Epidemiol. 2006 Oct;59(10):1102-9
[
16980151.001
]
[Cites]
Surg Neurol. 2005 Feb;63(2):162-9; discussion 169
[
15680662.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1990 Feb;18(2):321-4
[
2154418.001
]
[Cites]
Cancer Res. 1965 Dec;25(11):1876-81
[
5858571.001
]
[Cites]
Acta Neurochir (Wien). 2006 Mar;148(3):269-75; discussion 275
[
16482400.001
]
[Cites]
Neurol Med Chir (Tokyo). 2001 Mar;41(3):115-9; discussion 119-20
[
11372553.001
]
[Cites]
Cancer. 2005 Aug 15;104(4):825-32
[
15981281.001
]
[Cites]
J Cancer Res Clin Oncol. 1999 Aug-Sep;125(8-9):481-6
[
10480340.001
]
[Cites]
Anticancer Res. 2005 Sep-Oct;25(5):3585-90
[
16101184.001
]
[Cites]
AJNR Am J Neuroradiol. 2005 Nov-Dec;26(10):2466-74
[
16286386.001
]
[Cites]
J Clin Oncol. 2003 Apr 15;21(8):1485-91
[
12697871.001
]
[Cites]
N Engl J Med. 2005 Mar 10;352(10 ):987-96
[
15758009.001
]
(PMID = 18253699.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 16672
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Nitrosourea Compounds; 0S726V972K / Nimustine; 7BRF0Z81KG / Lomustine; U68WG3173Y / Carmustine
89.
Pirotte B, Goldman S, Van Bogaert P, David P, Wikler D, Rorive S, Brotchi J, Levivier M:
Integration of [11C]methionine-positron emission tomographic and magnetic resonance imaging for image-guided surgical resection of infiltrative low-grade brain tumors in children.
Neurosurgery
; 2005 Jul;57(1 Suppl):128-39; discussion 128-39
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Integration of [11C]methionine-positron emission tomographic and magnetic resonance imaging for image-guided surgical resection of infiltrative low-
grade
brain tumors in children.
OBJECTIVE: To evaluate the interest of integrating positron emission tomography (PET) images with the radiolabeled tracer [(11)C]methionine (Met) into the image-guided navigation planning of infiltrative low-
grade
brain tumors (LGBTs) in children.
METHODS: Twenty-two children underwent combined Met-PET with magnetic resonance imaging (MRI) scans in the planning
of a
navigation procedure.
These children presented an LGBT (
astrocytomas
, 10; oligodendrogliomas, 4; ependymomas, 4; gangliogliomas, 4) located close to functional areas.
Tumor
boundaries were ill-defined on MRI (including T2-weighted and fluid-attenuated inversion-recovery scans) and could not be clearly identified for allowing a complete, or at least a large, image-guided resection.
The PET tracer Met was chosen because of its higher sensitivity and specificity than MRI to detect
tumor
tissue.
The quality
of tumor
resection was assessed by an early postoperative MRI and Met-PET workup.
RESULTS: In 20 of the 22 children with ill-defined LGBTs, PET improved
tumor
delineation and contributed to define a final target contour different from that obtained with MRI alone.
Met-PET guidance allowed a total resection of Met uptake in 17 cases that were considered total
tumor
resections because the operative margin left in place contained nontumor tissue.
CONCLUSION: These data suggested that Met-PET guidance could help to improve the number of total resections and the amount
of tumor
removed in infiltrative LGBTs in children.
[MeSH-minor]
Adolescent. Child. Child, Preschool. Female. Humans. Image Enhancement / methods. Infant. Male.
Neoplasm
Invasiveness. Radiopharmaceuticals. Subtraction Technique. Systems Integration
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
Hazardous Substances Data Bank.
(L)-Methionine
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15987579.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Radiopharmaceuticals; 58576-49-1 / carbon-11 methionine; AE28F7PNPL / Methionine
90.
Dixit VD, Weeraratna AT, Yang H, Bertak D, Cooper-Jenkins A, Riggins GJ, Eberhart CG, Taub DD:
Ghrelin and the growth hormone secretagogue receptor constitute a novel autocrine pathway in astrocytoma motility.
J Biol Chem
; 2006 Jun 16;281(24):16681-90
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Ghrelin and the growth hormone secretagogue receptor constitute a novel autocrine pathway in
astrocytoma
motility.
Originally thought of as a stomach-derived endocrine peptide acting via its receptors in the
central nervous system
to stimulate food intake and growth hormone expression, ghrelin and its receptor (growth hormone secretagogue receptor (GHS-R)) are widely expressed in a number of organ systems, including cancer cells.
However, the direct functional role of ghrelin and its receptor in tumors
of central nervous system
origin remains to be defined.
Here, we demonstrate that the human
astrocytoma
cell lines U-118, U-87, CCF-STTG1, and SW1088 express 6-, 11-, 15-, and 29-fold higher levels of GHS-R compared with primary normal human astrocytes.
The ligation of GHS-R by ghrelin on these cells resulted in an increase in intracellular calcium mobilization, protein kinase C activation, actin polymerization, matrix metalloproteinase-2 activity, and
astrocytoma
motility.
In addition, ghrelin led to actin polymerization and membrane ruffling on cells, with the specific co-localization of the small GTPase Rac1 with GHS-R on the leading edge of the
astrocytoma
cells and imparting the
tumor
cells with a motile phenotype.
Disruption of the endogenous ghrelin/GHS-R pathway by RNA interference resulted in diminished motility, matrix metalloproteinase activity, and Rac expression, whereas
tumor
cells stably overexpressing GHS-R exhibited increased cell motility.
The relevance of ghrelin and GHS-R expression was verified in clinically relevant tissues from 20 patients with oligodendrogliomas and
grade
II-IV
astrocytomas
.
Analysis
of a central nervous system tumor
tissue microarray revealed that strong GHS-R and ghrelin expression was significantly more common in high
grade
tumors compared with low
grade
ones.
Together, these findings suggest a novel role for the ghrelin/GHS-R axis in
astrocytoma
cell migration and invasiveness of cancers
of central nervous system
origin.
[MeSH-major]
Astrocytoma
/ metabolism. Peptide Hormones / physiology. Receptors, G-Protein-Coupled / physiology
[MeSH-minor]
Calcium / metabolism. Cell Line,
Tumor
. Cell Movement.
Central Nervous System
/ metabolism. Ghrelin. Humans. Models, Biological. Peptides. RNA Interference. Receptors, Cell Surface / metabolism. Receptors, Ghrelin
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Endocrinol Metab. 2001 Apr;86(4):1738-45
[
11297611.001
]
[Cites]
Genes Dev. 2001 Jun 1;15(11):1311-33
[
11390353.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Jun;54(6):759-68
[
11422110.001
]
[Cites]
Nat Rev Neurosci. 2001 Aug;2(8):551-60
[
11483998.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Aug;86(8):3996-9
[
11502844.001
]
[Cites]
Neuro Oncol. 1999 Apr;1(2):109-19
[
11550306.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Oct;86(10):4984-90
[
11600575.001
]
[Cites]
Biochem Biophys Res Commun. 2002 Jan 11;290(1):552-7
[
11779207.001
]
[Cites]
Endocrinology. 2002 Feb;143(2):484-91
[
11796502.001
]
[Cites]
J Biol Chem. 2002 Feb 15;277(7):5667-74
[
11724768.001
]
[Cites]
Oncologist. 2002;7(1):17-33
[
11854544.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jun;87(6):2988
[
12050285.001
]
[Cites]
Curr Treat Options Oncol. 2000 Dec;1(5):459-68
[
12057153.001
]
[Cites]
Cancer Cell. 2002 Apr;1(3):279-88
[
12086864.001
]
[Cites]
J Pharmacol Exp Ther. 2002 Aug;302(2):822-7
[
12130749.001
]
[Cites]
Biochem Biophys Res Commun. 2002 Dec 20;299(5):739-43
[
12470640.001
]
[Cites]
J Biol Chem. 2002 Dec 20;277(51):49481-7
[
12388552.001
]
[Cites]
J Cell Biol. 2002 Dec 23;159(6):1029-37
[
12486113.001
]
[Cites]
J Biol Chem. 2003 Jan 3;278(1):64-70
[
12414809.001
]
[Cites]
Histol Histopathol. 2003 Jan;18(1):207-16
[
12507300.001
]
[Cites]
Am J Pathol. 2003 Feb;162(2):645-54
[
12547722.001
]
[Cites]
Cell. 2003 Feb 21;112(4):453-65
[
12600310.001
]
[Cites]
Nat Cell Biol. 2003 Mar;5(3):185-7
[
12646870.001
]
[Cites]
Cytokine Growth Factor Rev. 2003 Apr;14(2):113-22
[
12651223.001
]
[Cites]
J Cell Biol. 2003 Apr 28;161(2):417-27
[
12707305.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jul;88(7):3117-20
[
12843152.001
]
[Cites]
Biochem Biophys Res Commun. 2003 Sep 19;309(2):464-8
[
12951072.001
]
[Cites]
J Biol Chem. 2003 Oct 17;278(42):40601-6
[
12902325.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13513-8
[
14595012.001
]
[Cites]
Science. 2003 Dec 5;302(5651):1690-1
[
14657480.001
]
[Cites]
Horm Metab Res. 2003 Nov-Dec;35(11-12):740-50
[
14710353.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Jan;89(1):400-9
[
14715878.001
]
[Cites]
Eur J Endocrinol. 2004 Feb;150(2):173-84
[
14763915.001
]
[Cites]
Cancer Cell. 2004 Mar;5(3):201-2
[
15050909.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4679-84
[
15070777.001
]
[Cites]
Circulation. 2004 May 11;109(18):2221-6
[
15117840.001
]
[Cites]
J Biol Chem. 2004 May 21;279(21):22118-23
[
15037605.001
]
[Cites]
J Clin Invest. 2004 Jul;114(1):57-66
[
15232612.001
]
[Cites]
BMC Cancer. 2004 Jul 21;4:39
[
15265232.001
]
[Cites]
Nat Rev Cancer. 2004 Aug;4(8):579-91
[
15286738.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Aug;89(8):3739-44
[
15292299.001
]
[Cites]
Clin Cancer Res. 2004 Aug 15;10(16):5622-9
[
15328205.001
]
[Cites]
J Physiol. 2004 Sep 15;559(Pt 3):729-37
[
15272046.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 May 27;94(11):5854-9
[
9159164.001
]
[Cites]
Pathol Oncol Res. 1998;4(3):230-41
[
9761943.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Dec;83(12):4314-20
[
9851770.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):226-31
[
9874800.001
]
[Cites]
EMBO J. 1999 Feb 1;18(3):501-11
[
9927410.001
]
[Cites]
FASEB J. 1999 May;13(8):781-92
[
10224222.001
]
[Cites]
J Neuroendocrinol. 1999 Jul;11(7):491-502
[
10444306.001
]
[Cites]
Circulation. 2004 Dec 14;110(24):3674-9
[
15569841.001
]
[Cites]
Endocrinology. 2005 Jan;146(1):355-64
[
15471959.001
]
[Cites]
Diabetes. 2005 Jan;54(1):259-67
[
15616037.001
]
[Cites]
Am J Physiol Endocrinol Metab. 2005 Mar;288(3):E486-92
[
15507538.001
]
[Cites]
Endocrinology. 2005 Mar;146(3):1514-22
[
15564328.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Mar;90(3):1798-804
[
15585554.001
]
[Cites]
Endocr Rev. 2005 Apr;26(2):203-50
[
15561803.001
]
[Cites]
J Clin Endocrinol Metab. 2005 May;90(5):2920-6
[
15713718.001
]
[Cites]
Gastroenterology. 2005 Jul;129(1):8-25
[
16012930.001
]
[Cites]
Nature. 1999 Dec 9;402(6762):656-60
[
10604470.001
]
[Cites]
J Nutr Health Aging. 1999;3(2):92-101
[
10885804.001
]
[Cites]
J Natl Cancer Inst. 2000 Sep 20;92(18):1472-89
[
10995803.001
]
[Cites]
Science. 2000 Oct 13;290(5490):333-7
[
11030651.001
]
[Cites]
Nature. 2000 Oct 19;407(6806):908-13
[
11057670.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14478-83
[
11121050.001
]
[Cites]
Annu Rev Immunol. 2001;19:397-421
[
11244042.001
]
[Cites]
Clin J Oncol Nurs. 2000 Jul-Aug;4(4):153-8
[
11261094.001
]
(PMID = 16527811.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 AG000758-10
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Ghrelin; 0 / Peptide Hormones; 0 / Peptides; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; SY7Q814VUP / Calcium
[Other-IDs]
NLM/ NIHMS41150; NLM/ PMC2271047
91.
Kessler R, Bleichert F, Warnke JP, Eschrich K:
6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is up-regulated in high-grade astrocytomas.
J Neurooncol
; 2008 Feb;86(3):257-64
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is up-regulated in high-
grade
astrocytomas
.
We investigated the PFKFB3 expression in 40 human
astrocytic gliomas
and 20 non-neoplastic brain tissue specimens.
The PFKFB3 protein levels were markedly elevated in high-
grade
astrocytomas
relative to low-
grade
astrocytomas
and corresponding non-neoplastic brain tissue, whereas no significant increase of PFKFB3 mRNA was observed in high-
grade
astrocytomas
when compared with control tissue.
The findings demonstrate that PFKFB3 up-regulation is a hallmark of high-
grade
astrocytomas
offering an explanation for high glycolytic flux and lactate production in these tumors.
[MeSH-major]
Astrocytoma
/ metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Phosphofructokinase-2 / metabolism. Up-Regulation / physiology
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Acta Neuropathol. 2007 Mar;113(3):295-302
[
17235514.001
]
[Cites]
Science. 1956 Feb 24;123(3191):309-14
[
13298683.001
]
[Cites]
Am J Pathol. 2007 May;170(5):1445-53
[
17456751.001
]
[Cites]
Anticancer Res. 1997 May-Jun;17(3C):1903-11
[
9216643.001
]
[Cites]
EMBO J. 2005 May 18;24(10):1852-62
[
15861128.001
]
[Cites]
Mol Endocrinol. 1997 Apr;11(4):490-502
[
9092801.001
]
[Cites]
Magn Reson Med. 2003 Feb;49(2):223-32
[
12541241.001
]
[Cites]
FEBS Lett. 2006 May 29;580(13):3308-14
[
16698023.001
]
[Cites]
Genes Dev. 2001 Jun 1;15(11):1311-33
[
11390353.001
]
[Cites]
J Biochem. 1997 Jul;122(1):122-8
[
9276680.001
]
[Cites]
Trends Biochem Sci. 2001 Jan;26(1):30-5
[
11165514.001
]
[Cites]
Lab Invest. 2000 Jan;80(1):65-72
[
10653004.001
]
[Cites]
Neurology. 1982 Dec;32(12 ):1323-9
[
6983044.001
]
[Cites]
Oncogene. 2006 Nov 23;25(55):7225-34
[
16715124.001
]
[Cites]
J Biol Chem. 2002 Feb 22;277(8):6183-7
[
11744734.001
]
[Cites]
Cancer Res. 1999 Nov 15;59(22):5830-5
[
10582706.001
]
[Cites]
Neuropathology. 2005 Mar;25(1):1-7
[
15822813.001
]
[Cites]
Brain Res Mol Brain Res. 1994 Nov;27(1):51-7
[
7877454.001
]
[Cites]
Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903
[
3477813.001
]
[Cites]
Curr Opin Clin Nutr Metab Care. 2001 Sep;4(5):411-8
[
11568503.001
]
[Cites]
Proc Natl Acad Sci U S A. 1981 Jun;78(6):3483-6
[
6455662.001
]
[Cites]
Cytogenet Cell Genet. 1998;83(3-4):214-7
[
10072580.001
]
[Cites]
Biochimie. 2005 Nov;87(11):1005-10
[
15925437.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5881-7
[
12384552.001
]
[Cites]
Int J Cancer. 1994 Jan 2;56(1):72-7
[
8262681.001
]
[Cites]
Acta Neurochir (Wien). 1998;140(1):14-9
[
9522902.001
]
[Cites]
Biochem Biophys Res Commun. 1998 Jan 26;242(3):680-4
[
9464277.001
]
[Cites]
Trends Biochem Sci. 1995 Nov;20(11):465-70
[
8578590.001
]
[Cites]
J Exp Med. 2003 Aug 4;198(3):475-81
[
12885872.001
]
[Cites]
Curr Opin Clin Nutr Metab Care. 2006 Sep;9(5):535-9
[
16912547.001
]
[Cites]
Brain Res Mol Brain Res. 2001 Mar 5;87(2):190-5
[
11245921.001
]
[Cites]
Br J Cancer. 1996 Sep;74(6):839-45
[
8826847.001
]
[Cites]
Cancer. 2000 Jun 1;88(11):2606-18
[
10861440.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):3047-52
[
10077634.001
]
[Cites]
Biochem J. 2004 Aug 1;381(Pt 3):561-79
[
15170386.001
]
[Cites]
Cancer Res. 2001 Mar 1;61(5):2154-61
[
11280780.001
]
[Cites]
J Neurooncol. 1995;24(2):153-61
[
7562002.001
]
(PMID = 17805487.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; EC 2.7.1.105 / PFKFB3 protein, human; EC 2.7.1.105 / Phosphofructokinase-2
92.
Paolillo M, Barbieri A, Zanassi P, Schinelli S:
Expression of endothelins and their receptors in glioblastoma cell lines.
J Neurooncol
; 2006 Aug;79(1):1-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
In this study we have investigated the expression and the amounts of preproET-1, preproET-2, ETA and ETB receptors mRNA by classical RT-PCR and quantitative real-time PCR in
one
human low
grade astrocytoma
cell line and eight human glioblastoma cell lines.
Although the majority of glioblastoma cell lines in culture express ET isoforms and ET receptors, we conclude that ET-1 and the ETB receptors are likely to mediate the effects of the ET
system
in glioblastoma cell lines.
[MeSH-minor]
Blotting, Western. Cell Line,
Tumor
. Enzyme-Linked Immunosorbent Assay. Extracellular Signal-Regulated MAP Kinases / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression. Gene Expression Profiling. Humans. Phosphorylation. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Glioblastoma
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Neurosci. 2001 Nov 15;21(22):8842-53
[
11698596.001
]
[Cites]
Biochim Biophys Acta. 1996 May 28;1311(3):155-63
[
8664342.001
]
[Cites]
Cancer. 2005 Sep 1;104(5):1049-57
[
16007684.001
]
[Cites]
J Cardiovasc Pharmacol. 2004 Nov;44 Suppl 1:S136-9
[
15838263.001
]
[Cites]
J Neuropathol Exp Neurol. 1997 Apr;56(4):435-9
[
9100674.001
]
[Cites]
J Transl Med. 2004 May 27;2(1):16
[
15165288.001
]
[Cites]
Cancer Res. 2004 Feb 15;64(4):1436-43
[
14973117.001
]
[Cites]
Cancer Res. 2004 Dec 15;64(24):8945-53
[
15604257.001
]
[Cites]
Br J Cancer. 2001 Nov 30;85(11):1759-63
[
11742499.001
]
[Cites]
J Chem Neuroanat. 2004 May;27(2):87-98
[
15121213.001
]
[Cites]
J Cardiovasc Pharmacol. 2000;35(4 Suppl 2):S3-5
[
10976772.001
]
[Cites]
Nat Rev Cancer. 2003 Feb;3(2):110-6
[
12563310.001
]
[Cites]
Glia. 2003 Aug;43(2):185-9
[
12838510.001
]
[Cites]
J Cardiovasc Pharmacol. 2000 Nov;36(5 Suppl 1):S390-2
[
11078429.001
]
[Cites]
J Cardiovasc Pharmacol. 1995;26 Suppl 3:S104-6
[
8587332.001
]
[Cites]
Lab Invest. 2000 Nov;80(11):1681-9
[
11092528.001
]
[Cites]
J Neurol Sci. 1995 Dec;134(1-2):26-32
[
8747839.001
]
[Cites]
J Cardiovasc Pharmacol. 2004 Nov;44 Suppl 1:S132-5
[
15838262.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6381-4
[
12438219.001
]
[Cites]
Brain Res Mol Brain Res. 2005 Jun 13;137(1-2):77-88
[
15950764.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10954-9
[
12941866.001
]
[Cites]
Curr Drug Targets CNS Neurol Disord. 2002 Dec;1(6):543-53
[
12769596.001
]
(PMID = 16557350.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Endothelins; 0 / RNA, Messenger; 0 / Receptors, Endothelin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
93.
MacDonald TJ, Pollack IF, Okada H, Bhattacharya S, Lyons-Weiler J:
Progression-associated genes in astrocytoma identified by novel microarray gene expression data reanalysis.
Methods Mol Biol
; 2007;377:203-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Progression-associated genes in
astrocytoma
identified by novel microarray gene expression data reanalysis.
Astrocytoma
is graded as pilocytic (
WHO
grade I
), diffuse (
WHO
grade
II), anaplastic (
WHO
grade
III), and glioblastoma multiforme (
WHO
grade
IV).
The progression from low- to high-
grade astrocytoma
is associated with distinct molecular changes that vary with patient age, yet the prognosis of high-
grade
tumors in children and adults is equally dismal.
Whether specific gene expression changes are consistently associated with all high-
grade
astrocytomas
, independent of patient age, is not known.
To address this question, we reanalyzed the microarray datasets comprising
astrocytomas
from children and adults, respectively.
We identified nine genes consistently dysregulated in high-
grade
tumors, using four novel tests for identifying differentially expressed genes.
Four genes encoding ribosomal proteins (RPS2, RPS8, RPS18, RPL37A) were upregulated, and five genes (APOD, SORL1, SPOCK2, PRSS11, ID3) were downregulated in high-
grade
by all tests.
Expression results were validated using a third
astrocytoma
dataset.
APOD, the most differentially expressed gene, has been shown to inhibit
tumor
cell and vascular smooth muscle cell proliferation.
This suggests that dysregulation of APOD may be critical for malignant
astrocytoma
formation, and thus a possible novel universal target for therapeutic intervention.
Further investigation is needed to evaluate the role of APOD, as
well
as the other genes identified, in malignant
astrocytoma
development.
[MeSH-major]
Astrocytoma
/ genetics. Biomarkers,
Tumor
/ genetics. Brain Neoplasms / genetics. Gene Expression. Oligonucleotide Array Sequence Analysis / methods
[MeSH-minor]
Adult. Child. Chromosomes, Human. Cluster Analysis. Data Interpretation, Statistical.
Disease
Progression. Gene Expression Regulation, Neoplastic. Humans. Models, Genetic.
Neoplasm
Recurrence, Local. Reproducibility of Results
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17634619.001).
[ISSN]
1064-3745
[Journal-full-title]
Methods in molecular biology (Clifton, N.J.)
[ISO-abbreviation]
Methods Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
49
94.
Zhang W, Zhao J, Guo D, Zhong W, Shu J, Luo Y:
[Application of susceptibility weighted imaging in revealing intratumoral blood products and grading gliomas].
J Radiol
; 2010 Apr;91(4):485-90
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Application of susceptibility weighted imaging in revealing intratumoral blood products and grading
gliomas
].
[Transliterated title]
Rôle
de
l'IRM
de
susceptibilité magnétique dans
la
mise
en
évidence
de
produits
de
dégradation
de
l'hémoglobine intratumoraux et dans
la classification
des gliomes.
The purpose of our study was to evaluate the application of SWI for revealing inratumoral blood products and diagnosing high-
grade
gliomas
.
MATERIALS AND METHODS: Conventional MR sequences and SWI were performed in 32 patients, 10 low-
grade
gliomas
(1
grade I
and 9
grade
II) and 22 high-
grade
gliomas
(8
grade
III and 14
grade
IV).
Logistic regression and Receiver operating characteristic (ROC) curve analysis were used to evaluate the diagnostic
value of
SWI for high-
grade
gliomas
.
No statistical difference was found in detection rate of blood products between low-
grade
and high-
grade
group.
According to the result of logistic regression, the frequency of blood products and the diameter of maximum blood products were significant determinants of high-
grade
gliomas
.
The result of ROC analysis indicated that with an optimal cut-off point (0.67), the sensitivity, specificity, positive predictive
value
and negative predictive
value for
diagnosing high-
grade
gliomas
with blood products detected by SWI were 81.8%, 80.0%, 90.0%, and 66.6%, respectively.
With a high-
grade
gliomas
risk estimation model based on two variables, satisfied sensitivity, specificity, PPV and NPV were obtained.
Thus, SWI could be a useful adjunct sequence in
glioma
grading.
[MeSH-major]
Blood Proteins / analysis. Brain Neoplasms / diagnosis.
Glioma
/ diagnosis. Image Processing, Computer-Assisted / methods. Magnetic Resonance Imaging / methods
[MeSH-minor]
Adult. Aged.
Astrocytoma
/ diagnosis.
Astrocytoma
/ pathology. Female. Glioblastoma / diagnosis. Glioblastoma / pathology. Hemorrhage / diagnosis. Hemorrhage / pathology. Humans. Male. Middle Aged. Predictive
Value of
Tests. Sensitivity and Specificity. Young Adult
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20514004.001).
[ISSN]
0221-0363
[Journal-full-title]
Journal de radiologie
[ISO-abbreviation]
J Radiol
[Language]
fre
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Blood Proteins
95.
Bodey B, Kaiser HE, Siegel SE:
Epidermal growth factor receptor (EGFR) expression in childhood brain tumors.
In Vivo
; 2005 Sep-Oct;19(5):931-41
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The results demonstrated the presence of c-erbB-2 (HER-2) and c-erbB-4 (HER-4) in 10 to 50% of the neoplastic cells of high-
grade
glial tumors with high immunoreactivity, while c-erbB-3 (HER-3) was only detected in less than 10% of the neoplastically-transformed cells.
Medulloblastoma is the most common malignant brain
tumor
that occurs during childhood.
Multimodality treatment regimens have substantially improved survival in this
disease
; however, the
tumor
is incurable in about
one
-third of patients with medulloblastoma, and the current treatment has a detrimental effect on long-term survivors.
[MeSH-minor]
Alkaline Phosphatase / metabolism. Antibodies, Monoclonal / chemistry. Antigens / biosynthesis.
Astrocytoma
/ metabolism. Child, Preschool. Humans. Immunohistochemistry. Infant. Infant, Newborn. Medulloblastoma / metabolism. Medulloblastoma / therapy. Receptor, ErbB-2 / biosynthesis. Receptor, ErbB-3 / biosynthesis. Receptor, ErbB-4
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16097449.001).
[ISSN]
0258-851X
[Journal-full-title]
In vivo (Athens, Greece)
[ISO-abbreviation]
In Vivo
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 3.1.3.1 / Alkaline Phosphatase
96.
Nabika S, Kiya K, Satoh H, Mizoue T, Kondo H, Katagiri M, Nishisaka T, Sugiyama K, Kurisu K:
Prognostic significance of expression patterns of EGFR family, p21 and p27 in high-grade astrocytoma.
Hiroshima J Med Sci
; 2010 Dec;59(4):65-70
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Prognostic significance of expression patterns of EGFR family, p21 and p27 in high-
grade astrocytoma
.
The goal of this study was to investigate the relationship among immunohistochemical expression of epithelial growth factor receptor (EGFR) family proteins, p21, p27 and prognosis in patients with high-
grade astrocytoma
.
Expression of EGFR family proteins (c-erbB-1, c-erbB-2, c-erbB-3, c-erbB-4), p21 and p27 and Ki-67 labeling index (LI) were studied in 59 samples of high-
grade astrocytoma
.
[MeSH-major]
Astrocytoma
/ mortality. Breast Neoplasms / mortality. Cyclin-Dependent Kinase Inhibitor p21 / analysis. Intracellular Signaling Peptides and Proteins / analysis. Receptor, Epidermal Growth Factor / analysis
MedlinePlus Health Information.
consumer health - Breast Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21361082.001).
[ISSN]
0018-2052
[Journal-full-title]
Hiroshima journal of medical sciences
[ISO-abbreviation]
Hiroshima J. Med. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Intracellular Signaling Peptides and Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4
97.
Schittenhelm J, Psaras T:
Glioblastoma with granular cell astrocytoma features: a case report and literature review.
Clin Neuropathol
; 2010 Sep-Oct;29(5):323-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Glioblastoma with granular cell
astrocytoma
features: a case report and literature review.
We present the case
of a
69-year old patient with a contrast enhancing, partially cystic lesion of the right temporal lobe, involving the ventricle and extending into the occipital lobe.
The resected
tumor
showed histological features
of a
glioblastoma with granular cell
astrocytoma
features, lacking amplification of the EGFR gene region and IDH1R132H mutation.
Literature review of 59 cases showed a 12-month overall survival of 11.7% for high-
grade
and 40% for low-
grade
granular cell
astrocytomas
.
In 35% more than
one
cerebral lobe was affected.
[MeSH-major]
Astrocytoma
/ pathology. Brain Neoplasms / pathology. Glioblastoma / pathology
Genetic Alliance.
consumer health - Glioblastoma
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20860896.001).
[ISSN]
0722-5091
[Journal-full-title]
Clinical neuropathology
[ISO-abbreviation]
Clin. Neuropathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Germany
98.
Nowak S, Zukiel R, Barciszewska AM, Barciszewski J:
The diagnosis and therapy of brain tumours.
Folia Neuropathol
; 2005;43(3):193-6
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The clinical outcome, especially the survival rates of the patients with brain tumours depend on tumour
grade
expressing its malignancy.
A prognosis for glioblastomas (
WHO
IV) is very poor, but
for astrocytomas
(
WHO
I and II) it is relatively favourable.
There is evidence that oxidative stress and reactive oxygen species (ROS) are crucial in the etiology and progression
of a
number of human
diseases
, including neoplasms.
In addition to all four basic nucleotides: adenosine (A), guanosine (G), tymidine (T) and cytosine (C), 5-methylcytosine (m5C) is a rare but normal component of cellular DNA and occurs mainly within a sequence
of a
structural gene or in regulatory regions.
Because thymine is a normal DNA base, therefore the product of spontaneous deamination of m5C is not so easily detected by cell's DNA repair
system
.
Thus, 5-methylcytosine residue constitutes a mutational hotspot and DNA methylation pattern in patients might be useful as a primary diagnostic tool or as a marker for early detection of relapse of the
disease
.
The high sequence-specificity of RNAi makes it a new, promising tool in a gene-function analysis as
well
as in potential therapeutics development.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16245217.001).
[ISSN]
1641-4640
[Journal-full-title]
Folia neuropathologica
[ISO-abbreviation]
Folia Neuropathol
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
Poland
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / RNA, Small Interfering
[Number-of-references]
29
99.
Mawrin C, Kirches E, Schneider-Stock R, Boltze C, Vorwerk CK, von Mawrin A, Kirches E, Schneider-Stock R, Boltze C, Vorwerk CK, von Mawrin A, Kirches E, Schneider-Stock R, Boltze C, Vorwerk CK, von Mawrin A, Kirches E, Schneider-Stock R, Boltze C, Vorwerk CK, von Deimling A, Stoltenburg-Didinge G, Bornemann A, Romeike B, Sellhaus B, Dietzmann K:
Alterations of cell cycle regulators in gliomatosis cerebri.
J Neurooncol
; 2005 Apr;72(2):115-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Gliomatosis cerebri (GC) is regarded as a rare glial
neoplasm of
unknown origin, and a detailed analysis of molecular alterations underlying this
disease
has started only recently.
However, because GC characteristically affects large parts of the brain and spinal cord, the distribution of genetic alterations may be highly variable between different
tumor
areas.
Additionally,
tumor
areas with varying degrees of differentiation may be present, raising the possibility to model the genetic events associated with
astrocytoma
progression.
Here we analyzed various
tumor
regions with features of low-
grade
and high-
grade
astrocytomas
from 9 autopsy-proven GC cases for the immunoexpression of the cell cycle-controlling proteins mdm2, p21, p27/kip1, p16, and Rb.
Furthermore, allelic losses of the CDKN2A gene and
of a
PTEN flanking region of chromosome 10 were determined.
We detected
tumor
regions with immunoexpression of p21 only rarely in our series, without association to the
tumor
grade
.
The expression of p27(kip1) showed a clear reduction with increasing
astrocytoma
malignancy in 7 cases.
Allelic loss of the CDKN2A gene occurred in 5 patients but was not related to the
tumor
grading, nor to the intensity of p16 immunoexpression.
EGFR amplification was also absent in our series, but
one
case demonstrated EGFR expression only in the high-
grade
tumor
area.
Allelic losses on chromosome 10 were found in
one
out of six informative cases.
However, marked differences in the immunoexpression, as
well
as in the distribution of genetic aberrations were seen between different
tumor
samples within a given case.
The distribution of the alterations suggests that these molecular genetic changes represent secondary events, which may develop within
tumor
clones derived from a common founder
tumor
clone characterized by extraordinary spreading through the brain.
Moreover, the detected aberrations in gliomatosis cerebri can reflect the
tumor
progression associated with secondary malignant
astrocytoma
formation even within a single case.
[MeSH-major]
Astrocytoma
/ genetics. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 10 / genetics. Neoplasms, Neuroepithelial / genetics. Neoplasms, Neuroepithelial / pathology
Genetic Alliance.
consumer health - Gliomatosis Cerebri
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cell Mol Life Sci. 1999 Jan;55(1):96-107
[
10065155.001
]
[Cites]
Brain Pathol. 1993 Jul;3(3):255-68
[
8293185.001
]
[Cites]
J Neuropathol Exp Neurol. 2002 Sep;61(9):806-14
[
12230327.001
]
[Cites]
Neurosci Lett. 1997 Oct 3;234(2-3):127-30
[
9364514.001
]
[Cites]
Nature. 1985 Jan 10-18;313(5998):144-7
[
2981413.001
]
[Cites]
Neuroradiology. 2000 Aug;42(8):612-5
[
10997568.001
]
[Cites]
Hum Pathol. 1997 Oct;28(10):1166-79
[
9343324.001
]
[Cites]
Acta Neurochir (Wien). 2000;142(4):469-72
[
10883346.001
]
[Cites]
Cancer Res. 2000 Jan 15;60(2):417-24
[
10667596.001
]
[Cites]
Prog Cell Cycle Res. 1997;3:125-34
[
9552411.001
]
[Cites]
J Neuropathol Exp Neurol. 1997 Feb;56(2):180-5
[
9034372.001
]
[Cites]
Br J Cancer. 1995 Nov;72(5):1230-3
[
7577473.001
]
[Cites]
Clin Neuropathol. 1999 Jul-Aug;18(4):190-7
[
10442461.001
]
[Cites]
Lab Invest. 2000 Jan;80(1):65-72
[
10653004.001
]
[Cites]
J Child Neurol. 1995 Jan;10(1):37-45
[
7539465.001
]
[Cites]
J Neurooncol. 2001 Oct;55(1):11-7
[
11804278.001
]
[Cites]
Nat Genet. 1994 Sep;8(1):23-6
[
7987388.001
]
[Cites]
Genes Chromosomes Cancer. 1995 Oct;14(2):149-53
[
8527397.001
]
[Cites]
Oncogene. 1995 Nov 16;11(10):2021-8
[
7478521.001
]
[Cites]
Neurology. 1974 Jun;24(6):504-11
[
4499966.001
]
[Cites]
Eur Radiol. 2001;11(2):303-8
[
11218032.001
]
[Cites]
Ann Neurol. 2002 Oct;52(4):390-9
[
12325066.001
]
[Cites]
Clin Neuropathol. 1985 Jul-Aug;4(4):135-48
[
4053456.001
]
[Cites]
Acta Neuropathol. 2003 Jun;105(6):529-36
[
12734658.001
]
[Cites]
Int J Oncol. 1998 Aug;13(2):325-9
[
9664128.001
]
[Cites]
Brain Tumor Pathol. 1998;15(2):111-6
[
10328549.001
]
[Cites]
Hum Pathol. 2003 Jan;34(1):102-6
[
12605375.001
]
[Cites]
Neuro Oncol. 1999 Jan;1(1):44-51
[
11550301.001
]
[Cites]
Cancer Res. 1995 May 1;55(9):1941-5
[
7728764.001
]
[Cites]
Cell. 1993 Nov 19;75(4):805-16
[
8242751.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2965-9
[
1557402.001
]
[Cites]
Biochem Biophys Res Commun. 1999 Aug 11;261(3):890-6
[
10441521.001
]
[Cites]
J Neuropathol Exp Neurol. 1998 Jul;57(7):684-9
[
9690672.001
]
[Cites]
Cancer Res. 1988 Oct 1;48(19):5546-51
[
2901288.001
]
(PMID = 15925990.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 9007-49-2 / DNA; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
100.
Essig M, Giesel F, Stieltjes B, Weber MA:
[Functional imaging for brain tumors (perfusion, DTI and MR spectroscopy)].
Radiologe
; 2007 Jun;47(6):513-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
In cases of brain
tumor
, PWI aids in grading and better differentiation in diagnostics as
well
as for pre-therapeutic planning.
In addition, the course of treatment, both after chemo- as
well
as radiotherapy in combination with surgical treatment, can be optimized.
PWI allows better estimates of biological activity and aggressiveness in low
grade
brain tumors, and in the case
of WHO
grade
II
astrocytoma
showing anaplasically transformed
tumor
areas, allows more rapid visu-alization and a better prediction of the course of the
disease
than conventional MRI diagnostics.
Diffusion MRI, due to the directional dependence of the diffusion, can illustrate the course and direction of the nerve fibers, as
well
as reconstructing the nerve tracts in the cerebrum, pons and cerebellum 3-dimensionally.
Diffusion imaging can be used for describing brain tumors, for evaluating contralateral involvement and the course of the nerve fibers near the
tumor
.
DWI can also not
differentiate
accurately between cystic and necrotic brain tumors, or between metastases and brain abscesses.
Diagnostic problems such as the differentiation between neoplastic and non-neoplastic lesions, grading cerebral
glioma
and distinguishing between primary brain tumors and metastases can be resolved.
[MeSH-major]
Biomarkers,
Tumor
/ analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Diffusion Magnetic Resonance Imaging / methods. Magnetic Resonance Spectroscopy / methods
MedlinePlus Health Information.
consumer health - Brain Tumors
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Radiologe. 2005 Apr;45(4):327-39
[
15800783.001
]
[Cites]
AJNR Am J Neuroradiol. 2000 Oct;21(9):1603-10
[
11039338.001
]
[Cites]
Neuroradiology. 2006 Apr;48 Suppl 1:3-8
[
16699847.001
]
[Cites]
Radiologe. 2004 Jul;44(7):723-32; quiz 733-4
[