[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
Items 1 to 100 of about 132
1. Shaw EJ, Haylock B, Husband D, du Plessis D, Sibson DR, Warnke PC, Walker C: Gene expression in oligodendroglial tumors. Anal Cell Pathol (Amst); 2010;33(2):81-94
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression in oligodendroglial tumors.
  • BACKGROUND: Oligodendroglial tumors with 1p/19q loss are more likely to be chemosensitive and have longer survival than those with intact 1p/19q, but not all respond to chemotherapy, warranting investigation of the biological basis of chemosensitivity.
  • METHODS: Gene expression profiling was performed using amplified antisense RNA from 28 oligodendroglial tumors treated with chemotherapy (26 serial stereotactic biopsy, 2 resection).
  • RESULTS: Unsupervised hierarchical clustering showed clustering of multiple samples from the same case in 14/17 cases and identified subgroups associated with tumor grade and 1p/19q status.
  • IQGAP1, INA, TGIF1, NR2F2 and MYCBP were differentially expressed in oligodendroglial tumors with 1p/19q loss.
  • CONCLUSION: Gene expression profiling using serial stereotactic biopsies indicated greater homogeneity within tumors than between tumors.
  • Genes associated with 1p/19q status or response were identified warranting further elucidation of their role in oligodendroglial tumors.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Cluster Analysis. Drug Resistance, Neoplasm / genetics. Female. Gene Expression. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Principal Component Analysis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Cell Oncol (Dordr). 2011 Aug;34(4):407-8
  • (PMID = 20966545.001).
  • [ISSN] 2210-7185
  • [Journal-full-title] Analytical cellular pathology (Amsterdam)
  • [ISO-abbreviation] Anal Cell Pathol (Amst)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4605574
  •  go-up   go-down


2. Xiong NX, Zhao HY, Zhang FC, He ZQ: Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor. Neurosci Bull; 2007 Jan;23(1):41-5
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor.
  • The present study is to explore the relationship between the expression of Nogo-A and the malignancy of oligodendroglial tumors in patients.
  • METHODS: Tumor tissue samples with different malignancy grade were obtained from the hospitals.
  • The samples used for detection had been diagnosed as oligodendroglial tumors (oligodendroglioma or anaplastic oligodendroglioma).
  • The correlation test between the Nogo-A expression and the morphological changes (the percentages of atypical cells and mitotic cells in the tumors) related to the malignancy of tumor tissues was performed.
  • RESULTS: There was significant negative correlation between the Nogo-A expression and the morphological change of tumor tissues according to immunohistochemistry.
  • CONCLUSION: Nogo-A expression was negatively correlated with the malignancy grade of oligodendroglial tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Myelin Proteins / metabolism. Oligodendroglioma / diagnosis. Oligodendroglioma / metabolism
  • [MeSH-minor] Adult. Down-Regulation / physiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mitotic Index. Neoplasm Invasiveness / diagnosis. Nogo Proteins. Predictive Value of Tests

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2002 May 1;22(9):3553-67 [11978832.001]
  • [Cites] J Neurosci. 2003 Jul 2;23 (13):5393-406 [12843238.001]
  • [Cites] Oncogene. 2001 Jul 5;20(30):3929-36 [11494121.001]
  • [Cites] J Mol Neurosci. 2005;25(1):1-6 [15781961.001]
  • [Cites] J Cell Physiol. 2003 Aug;196 (2):312-8 [12811824.001]
  • [Cites] Nature. 2000 Jan 27;403(6768):434-9 [10667796.001]
  • [Cites] J Biol Chem. 2003 May 23;278(21):19280-5 [12639960.001]
  • [Cites] Nature. 2000 Jan 27;403(6768):439-44 [10667797.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):149-58 [9426071.001]
  • [Cites] J Neurochem. 2004 Sep;90(5):1156-62 [15312170.001]
  • [Cites] Oncogene. 2003 Mar 6;22(9):1390-9 [12618765.001]
  • [Cites] Oncogene. 2000 Nov 23;19(50):5736-46 [11126360.001]
  • [Cites] Biochem J. 2005 Oct 15;391(Pt 2):433-40 [16095439.001]
  • [Cites] Oncogene. 2004 Apr 15;23(17):2977-87 [15021917.001]
  • [Cites] Apoptosis. 2003 Jan;8(1):5-9 [12510146.001]
  • (PMID = 17592524.001).
  • [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 / Biomarkers, Tumor; 0 / Myelin Proteins; 0 / Nogo Proteins; 0 / RTN4 protein, human
  •  go-up   go-down


3. Weller M, Berger H, Hartmann C, Schramm J, Westphal M, Simon M, Goldbrunner R, Krex D, Steinbach JP, Ostertag CB, Loeffler M, Pietsch T, von Deimling A, German Glioma Network: Combined 1p/19q loss in oligodendroglial tumors: predictive or prognostic biomarker? Clin Cancer Res; 2007 Dec 1;13(23):6933-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined 1p/19q loss in oligodendroglial tumors: predictive or prognostic biomarker?
  • PURPOSE: The combined loss of genetic material on chromosomes 1p and 19q is strongly associated with favorable outcome in patients with WHO grade 3 anaplastic oligodendroglial tumors.
  • The prognostic value of 1p/19q loss in WHO grade 2 oligodendroglial tumors is less well defined.
  • CONCLUSIONS: Combined 1p/19q loss is not a sensitive prognostic biomarker in patients with oligodendroglial tumors who do not receive radiotherapy or chemotherapy.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Astrocytoma / pathology. Biomarkers, Tumor / genetics. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18056167.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


Advertisement
4. Järvelä S, Parkkila S, Bragge H, Kähkönen M, Parkkila AK, Soini Y, Pastorekova S, Pastorek J, Haapasalo H: Carbonic anhydrase IX in oligodendroglial brain tumors. BMC Cancer; 2008;8:1
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carbonic anhydrase IX in oligodendroglial brain tumors.
  • METHODS: This study was set out to investigate the role of CA IX in a series of 86 oligodendroglial brain tumors (71 primary and 15 recurrent; 48 pure oligodendrogliomas and 40 mixed oligoastrocytomas).
  • RESULTS: 80% of the tumors showed CA IX expression by immunohistochemistry.
  • Tumors with moderate or strong CA IX expression had decreased level of cell proliferation compared to weak or no CA IX expression (median 2.9 vs. 5.8, p = 0.015).
  • CA IX correlated with two antioxidative enzymes, manganese superoxide dismutase (MnSOD) and regulatory gammaglutamylcysteine synthetase (GLCL-R): CA IX expression was significantly higher in MnSOD-positive tumors (p = 0.008) and decreased in GLCL-R-positive tumors (p = 0.044).
  • CONCLUSION: CA IX was proved to be an independent prognostic indicator in oligodendroglial brain tumors, and it also correlates reversely with cell proliferation.
  • It may have a role in the biology of oligodendrogliomas, and most interestingly, as it is mainly expressed in tumor tissue, CA IX could serve as a target molecule for anticancer treatments.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Brain Neoplasms / enzymology. Carbonic Anhydrases / metabolism. Oligodendroglioma / enzymology
  • [MeSH-minor] Adult. Cell Proliferation. Follow-Up Studies. Humans. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6567-71 [15475445.001]
  • [Cites] Gastroenterology. 1997 Feb;112(2):398-408 [9024293.001]
  • [Cites] Cancer Res. 1982 May;42(5):1955-61 [7066906.001]
  • [Cites] Am J Med. 1991 Sep 30;91(3C):14S-22S [1928205.001]
  • [Cites] Virology. 1992 Apr;187(2):620-6 [1312272.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):3113-7 [8464931.001]
  • [Cites] Int J Cancer. 1993 May 8;54(2):268-74 [8486430.001]
  • [Cites] Anal Quant Cytol Histol. 1994 Aug;16(4):261-8 [7524516.001]
  • [Cites] J Pathol. 1994 Dec;174(4):275-82 [7884589.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):279-85 [9665489.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Mar 15;61(4):1197-207 [15752902.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7259-66 [16103077.001]
  • [Cites] Histol Histopathol. 2005 Oct;20(4):1173-7 [16136500.001]
  • [Cites] Bioorg Med Chem Lett. 2005 Nov 1;15(21):4872-6 [16165351.001]
  • [Cites] Neuro Oncol. 2005 Oct;7(4):465-75 [16212811.001]
  • [Cites] Biochem J. 2005 Nov 15;392(Pt 1):83-92 [16083424.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):473-7 [16428489.001]
  • [Cites] J Neurooncol. 2006 Apr;77(2):131-40 [16292483.001]
  • [Cites] Neurosurgery. 1999 Dec;45(6):1279-91; discussion 191 [10598694.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7075-83 [11156414.001]
  • [Cites] Am J Pathol. 2001 Mar;158(3):905-19 [11238039.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1750-7 [11410516.001]
  • [Cites] Mol Hum Reprod. 2001 Jul;7(7):611-6 [11420383.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):5262-7 [11431368.001]
  • [Cites] Annu Rev Biophys Biomol Struct. 2001;30:421-55 [11441809.001]
  • [Cites] Cancer. 2001 Jul 1;92(1):165-71 [11443623.001]
  • [Cites] J Clin Oncol. 2001 Aug 15;19(16):3660-8 [11504747.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6394-9 [11522632.001]
  • [Cites] Neurology. 2001 Oct 9;57(7):1278-81 [11591848.001]
  • [Cites] Cancer Res. 2001 Nov 1;61(21):7992-8 [11691824.001]
  • [Cites] J Hepatol. 2001 Nov;35(5):643-9 [11690711.001]
  • [Cites] J Neurooncol. 2001 Oct;55(1):29-37 [11804280.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1205-12 [11861405.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]
  • [Cites] Neuropathol Appl Neurobiol. 2002 Apr;28(2):89-94 [11972795.001]
  • [Cites] Med Res Rev. 2003 Mar;23(2):146-89 [12500287.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Feb;62(2):111-26 [12578221.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):155-64 [12744469.001]
  • [Cites] Int J Cancer. 2003 Jul 20;105(6):873-81 [12767076.001]
  • [Cites] Am J Respir Crit Care Med. 2003 Jun 15;167(12):1600-19 [12796054.001]
  • [Cites] Exp Cell Res. 2003 Nov 1;290(2):332-45 [14567991.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Jan 5;14(1):217-23 [14684331.001]
  • [Cites] Int J Oncol. 2004 Apr;24(4):995-1004 [15010840.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Feb 23;14(4):869-73 [15012984.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6160-5 [15342400.001]
  • [Cites] Annu Rev Biochem. 1995;64:375-401 [7574487.001]
  • [Cites] J Enzyme Inhib Med Chem. 2004 Jun;19(3):199-229 [15499993.001]
  • (PMID = 18173856.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2245965
  •  go-up   go-down


5. Ramirez C, Bowman C, Maurage CA, Dubois F, Blond S, Porchet N, Escande F: Loss of 1p, 19q, and 10q heterozygosity prospectively predicts prognosis of oligodendroglial tumors--towards individualized tumor treatment? Neuro Oncol; 2010 May;12(5):490-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of 1p, 19q, and 10q heterozygosity prospectively predicts prognosis of oligodendroglial tumors--towards individualized tumor treatment?
  • The purpose of this study was to determine whether chromosome 10q loss is a predictor of tumor aggressiveness and poor clinical outcome in patients with oligodendroglial tumors alone or together with loss of heterozygosity (LOH) on chromosomes 1p and 19q.
  • A microsatellite analysis was performed on sections from 130 patients with grade II and grade III oligodendroglial tumors to assess the allelic status of chromosomes 1p, 19q, and 10q, plus detailed clinical and radiological information was taken prospectively.
  • There was a significant association between LOH status and the tumors' response to chemotherapy: 92.3% with 1p19q LOH, 83.3% without allelic losses, 50% with 1p19q10q LOH, and 14.5% with 10q LOH.
  • 10q LOH predicted a survival disadvantage in patients with oligodendroglial tumors irrespective of 1p/19q LOH status.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 19 / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Drug Resistance, Neoplasm / genetics. Female. Humans. Kaplan-Meier Estimate. Loss of Heterozygosity. Male. Microsatellite Repeats. Middle Aged. Precision Medicine / methods. Prognosis. Young Adult


6. Klink B, Schlingelhof B, Klink M, Stout-Weider K, Patt S, Schrock E: Glioblastomas with oligodendroglial component - common origin of the different histological parts and genetic subclassification. Anal Cell Pathol (Amst); 2010;33(1):37-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastomas with oligodendroglial component - common origin of the different histological parts and genetic subclassification.
  • BACKGROUND: Glioblastomas are the most common and most malignant brain tumors in adults.
  • A small subgroup of glioblastomas contains areas with histological features of oligodendroglial differentiation (GBMO).
  • Our objective was to genetically characterize the oligodendroglial and the astrocytic parts of GBMOs and correlate morphologic and genetic features with clinical data.
  • METHODS: The oligodendroglial and the "classic" glioblastoma parts of 13 GBMO were analyzed separately by interphase fluorescence in situ hybridization (FISH) on paraffin sections using a custom probe set (regions 1p, 1q, 7q, 10q, 17p, 19q, cen18, 21q) and by comparative genomic hybridization (CGH) of microdissected paraffin embedded tumor tissue.
  • RESULTS: We identified four distinct genetic subtypes in 13 GBMOs: an "astrocytic" subtype (9/13) characterized by +7/-10; an "oligodendroglial" subtype with -1p/-19q (1/13); an "intermediate" subtype showing +7/-1p (1/13), and an "other" subtype having none of the former aberrations typical for gliomas (2/13).
  • The different histological tumor parts of GBMO revealed common genetic changes in all tumors and showed additional aberrations specific for each part.
  • CONCLUSION: Our findings demonstrate the monoclonal origin of GBMO followed by the development of the astrocytic and oligodendroglial components.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Glioblastoma / genetics. Glioblastoma / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted. Imaging, Three-Dimensional. In Situ Hybridization, Fluorescence. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20966543.001).
  • [ISSN] 2210-7185
  • [Journal-full-title] Analytical cellular pathology (Amsterdam)
  • [ISO-abbreviation] Anal Cell Pathol (Amst)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4605661
  •  go-up   go-down


7. Möllemann M, Wolter M, Felsberg J, Collins VP, Reifenberger G: Frequent promoter hypermethylation and low expression of the MGMT gene in oligodendroglial tumors. Int J Cancer; 2005 Jan 20;113(3):379-85
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent promoter hypermethylation and low expression of the MGMT gene in oligodendroglial tumors.
  • We report on the analysis of 52 oligodendroglial tumors for MGMT promoter methylation, as well as mRNA and protein expression.
  • In 46 of 52 tumors (88%), we detected MGMT promoter hypermethylation as defined by methylation of more than 50% of the sequenced CpG sites.
  • Real-time reverse transcription-PCR showed reduced MGMT mRNA levels relative to non-neoplastic brain tissue in the majority of tumors with hypermethylation.
  • Similarly, immunohistochemical analysis showed either no or only small fractions of MGMT positive tumor cells.
  • MGMT promoter hypermethylation was significantly more frequent and the percentage of methylated CpG sites in the investigated MGMT promoter fragment was significantly higher in tumors with loss of heterozygosity on chromosome arms 1p and 19q as compared to tumors without allelic losses on these chromosomes arms.
  • Taken together, our data suggest that MGMT hypermethylation and low or absent expression are frequent in oligodendroglial tumors and likely contribute to the chemosensitivity of these tumors.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. DNA Methylation. O(6)-Methylguanine-DNA Methyltransferase / genetics. Oligodendroglioma / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. CpG Islands. Female. Humans. Immunoenzyme Techniques. Loss of Heterozygosity. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15455350.001).
  • [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 / RNA, Messenger; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  •  go-up   go-down


8. Qu M, Olofsson T, Sigurdardottir S, You C, Kalimo H, Nistér M, Smits A, Ren ZP: Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas. Acta Neuropathol; 2007 Feb;113(2):129-36
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas.
  • Oligoastrocytomas are glial tumours consisting of a mixture of neoplastic astrocytic and oligodendroglial cells.
  • In the majority of cases (9/11), the oligodendroglial and astrocytic components of an individual oligoastrocytoma displayed the same genotype.
  • In one case, the oligodendroglial part of the tumour showed LOH19q, whereas the astrocytic part showed TP53 mutation (codon 273).
  • In another case, we found LOH 1p/19q in the oligodendroglial component, but two retained areas on chromosome 1p in the astrocytic component of the tumour.
  • The two cases of biphasic oligoastrocytomas in our sample that display a different genotype in the astrocytic and oligodendroglial part of the tumour show that different components of an oligoastrocytoma may be derived from different cell clones during neoplastic transformation.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / genetics. Brain Neoplasms / classification. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / genetics

  • 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 = 17031656.001).
  • [ISSN] 0001-6322
  • [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] 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


9. Preusser M, Birner P, Ambros IM, Ambros PF, Budka H, Harris AL, Hainfellner JA: DEC1 expression in 1p-aberrant oligodendroglial neoplasms. Histol Histopathol; 2005 10;20(4):1173-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DEC1 expression in 1p-aberrant oligodendroglial neoplasms.
  • BACKGROUND: Expression of hypoxia-related tissue factors in 1p-aberrant oligodendroglial neoplasms diminishes patient outcome.
  • In our study, we assessed the expression of DEC1 in 1p aberrant oligodendroglial neoplasms and its association with necrosis and expression of hypoxia-inducible factor 1alpha (HIF-1alpha), carbonic anhydrase-9 (CA9), and vascular endothelial growth factor-mRNA (VEGF).
  • MATERIALS AND METHODS: 44 primary and 16 recurrent oligodendroglial neoplasms with 1p-aberrations were investigated immunohistochemically for the expression of DEC1, HIF-1alpha, and CA9.
  • RESULTS: DEC1 was expressed in tumor cell nuclei, and occasionally in nuclei of endothelial cells, and glial and neuronal cells of surrounding brain tissue.
  • High expression (>10% of tumor cells immunolabeled) of DEC1 was found in 56 cases, low expression (<10% of tumor cells immunolabeled) was found in 3 cases.
  • CONCLUSION: DEC1 expression is found in the majority of 1p-aberrant oligodendroglial neoplasms and does not correlate with necrosis or expression of HIF-1alpha, CA9, VEGF.
  • Thus, immunohistochemical analysis of DEC1 expression is in our hands not suitable for detection of tissue hypoxia in this type of primary brain tumor.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adult. Biomarkers. Female. Humans. Hypoxia / diagnosis. Hypoxia / genetics. Hypoxia / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. Male. Necrosis. RNA, Messenger / metabolism. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16136500.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DEC1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


10. Jenkinson MD, Smith TS, Brodbelt AR, Joyce KA, Warnke PC, Walker C: Apparent diffusion coefficients in oligodendroglial tumors characterized by genotype. J Magn Reson Imaging; 2007 Dec;26(6):1405-12
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apparent diffusion coefficients in oligodendroglial tumors characterized by genotype.
  • PURPOSE: To investigate whether oligodendroglial tumors with or without 1p/19q loss differ in their diffusion-weighted imaging characteristics.
  • Oligodendroglial tumors with or without 1p/19q loss differ in their therapeutic responsiveness and prognosis, and recent reports also suggest that these tumors may differ in their magnetic resonance characteristics and blood volume.
  • 1) around tumor margins to generate pixel histograms;.
  • 2) over minimum and maximum tumor ADC;.
  • 3) on areas comparable to the highest choline (Cho)/creatine (Cr) ratio determined from chemical shift imaging (CSI); and 4) across tumor margins to measure the ADC transition coefficient (ATC).
  • RESULTS: Tumor ADC was significantly different from normal brain (P < 0.001).
  • ADC and ATC were not significantly different between oligodendroglial subtypes or grades.
  • Tumors with intact 1p/19q had higher maximum (P = 0.021) and histogram ADC (P = 0.015), and greater ATC (P = 0.001) compared to those with 1p/19q loss, which may reflect differences in edema and cellularity.
  • CONCLUSION: This preliminary study identified differences in ADC and ATC between oligodendroglial tumor genotypes that may reflect underlying biology.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Allelic Imbalance. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Genotype. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17968881.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


11. Huang L, Jiang T, Yuan F, Li GL, Liu EZ, Wang ZC: Correlations between molecular profile and tumor location in Chinese patients with oligodendroglial tumors. Clin Neurol Neurosurg; 2008 Dec;110(10):1020-4
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlations between molecular profile and tumor location in Chinese patients with oligodendroglial tumors.
  • OBJECTIVE: To investigate possible correlations between molecular alterations and tumor location in Chinese patients with oligodendroglial tumors.
  • Correlations between molecular profile and tumor location were made by chi-square and Fisher's exact tests.
  • RESULTS: Oligodendroglial tumors located in the nontemporal lobes were significantly more likely to have combination of LOH 1p and LOH 19q than tumors arising in the insula, temporal lobe, and temporal with another lobe (p=0.001).
  • In contrast to the oligodendroglial tumors, we detected no association between molecular alterations and location for diffuse astrocytomas.
  • CONCLUSION: We conclude that molecular subsets of oligodendroglial tumors may arise preferentially in certain lobes of the brain, with tumors having LOH 1p and LOH 19q occurring most frequently in the nontemporal lobes.
  • These findings suggest that molecular subsets of oligodendroglial tumors may arise from site-specific precursor cells, which has provided some information for the current management of these neoplasms in China.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebral Cortex / metabolism. Cerebral Cortex / pathology. Chi-Square Distribution. Child. China. Chromatography, High Pressure Liquid / methods. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Humans. Loss of Heterozygosity. Male. Microsatellite Repeats / genetics. Middle Aged. Retrospective Studies. Temporal Lobe / metabolism. Temporal Lobe / pathology. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18845382.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


12. Mikami S, Hirose Y, Yoshida K, Kawase T, Ohnishi A, Nagashima K, Mukai M, Okada Y, Ikeda E: Predominant expression of OLIG2 over ID2 in oligodendroglial tumors. Virchows Arch; 2007 May;450(5):575-84
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predominant expression of OLIG2 over ID2 in oligodendroglial tumors.
  • This study aims to examine if the analysis of OLIG2 and ID2 expression in glioma tissues helps the differential diagnosis of chemosensitive oligodendroglial tumors from astrocytic tumors.
  • Expression levels of OLIG2 and ID2 in 11 oligodendroglial and 27 astrocytic tumors were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR, and immunohistochemistry.
  • The mean expression level of OLIG2 was higher in oligodendroglial tumors than astrocytic tumors, but some astrocytic tumors showed high OLIG2 expression, indicating that OLIG2 cannot be an independent marker of oligodendroglial tumors.
  • No significant difference was observed between ID2 expression in oligodendroglial tumors and astrocytic tumors.
  • It was notable that OLIG2 expression was predominant over ID2 expression in oligodendroglial tumors, while ID2 expression was predominant over OLIG2 expression in astrocytic tumors.
  • These results indicate that the immunohistochemical study on the relative expression level of OLIG2 to ID2 can be a useful screening for oligodendroglial tumors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Brain Neoplasms / metabolism. Inhibitor of Differentiation Protein 2 / metabolism. Nerve Tissue Proteins / metabolism. Oligodendroglia / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / metabolism. Astrocytoma / secondary. Astrocytoma / surgery. Biomarkers, Tumor / metabolism. Child. Chromosome Deletion. Chromosomes, Human, Pair 1. Female. Fluorescent Antibody Technique, Direct. Gene Expression. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization. Oligodendroglioma / metabolism. Oligodendroglioma / secondary. Oligodendroglioma / surgery. RNA, Messenger / metabolism

  • 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 = 17431671.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / RNA, Messenger
  •  go-up   go-down


13. Bannykh SI, Stolt CC, Kim J, Perry A, Wegner M: Oligodendroglial-specific transcriptional factor SOX10 is ubiquitously expressed in human gliomas. J Neurooncol; 2006 Jan;76(2):115-27
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oligodendroglial-specific transcriptional factor SOX10 is ubiquitously expressed in human gliomas.
  • Whereas prototypical examples of the tumors have distinct pathogenetic and prognostic differences, the majority of the gliomas falls in the intermediate category and their distinction is problematic.
  • The transcriptional factor SOX10 is one of the key determinants of oligodendroglial differentiation.
  • High levels of expression were also found in pilocytic astrocytoma, consistent with recent studies suggesting that pilocytic astrocytomas have greater overlap with oligodendroglial than astrocytic tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. Glioma / metabolism. High Mobility Group Proteins / biosynthesis. Oligodendroglia / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytes / metabolism. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / metabolism. Biomarkers, Tumor / metabolism. Blotting, Western. Child. Child, Preschool. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nerve Tissue Proteins / metabolism. SOXE Transcription Factors

  • 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 = 16205963.001).
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / Nerve Tissue Proteins; 0 / OLIG1 protein, human; 0 / OLIG2 protein, human; 0 / SOX10 protein, human; 0 / SOXE Transcription Factors; 0 / Transcription Factors
  •  go-up   go-down


14. Walker C, du Plessis DG, Joyce KA, Fildes D, Gee A, Haylock B, Husband D, Smith T, Broome J, Warnke PC: Molecular pathology and clinical characteristics of oligodendroglial neoplasms. Ann Neurol; 2005 Jun;57(6):855-65
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular pathology and clinical characteristics of oligodendroglial neoplasms.
  • To evaluate the role of molecular genetics in the routine clinic, we investigated allelic imbalance at 1p36, 19q13, 17p13, 10p12-15, and 10q22-26 and p53 mutation in 100 oligodendroglial neoplasms diagnosed at a single treatment center between 2000 and 2003.
  • Genotype was unrelated to tumor location and could not distinguish high-grade tumors that presented de novo from those that progressed from a previous lower grade malignancy.
  • In this recently diagnosed unselected series, clinical differences in tumors with and without the -1p/-19q genotype support a genetic approach to aid diagnosis and prognostication for oligodendroglial neoplasms.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 19. Female. Genetic Testing. Genotype. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / pathology. Phenotype. Prognosis. Tumor Suppressor Protein p53 / genetics

  • 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 = 15929038.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


15. McCarthy BJ, Propp JM, Davis FG, Burger PC: Time trends in oligodendroglial and astrocytic tumor incidence. Neuroepidemiology; 2008;30(1):34-44
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Time trends in oligodendroglial and astrocytic tumor incidence.
  • BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.
  • METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.
  • CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.
  • Minimizing misclassification of glial tumors will be essential for accurately assessing incidence, survival, and mortality rates, as well as for identifying homogeneous subgroups for epidemiologic and treatment studies.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Child. Child, Preschool. Humans. Incidence. Infant. Infant, Newborn. Middle Aged. Registries / statistics & numerical data. Time. United States / epidemiology

  • 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
  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18259099.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  •  go-up   go-down


16. Absaliamova OV, Korshunov AG, Loshakov VA, Kobiakov GL, Golanov AV, Urakov SV, Amanov RD, Lichinitser MR: [Influence of molecular-genetic factors on prognosis in patients with oligodendroglial tumors]. Zh Vopr Neirokhir Im N N Burdenko; 2009 Jan-Mar;(1):17-23; discussion 23-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Influence of molecular-genetic factors on prognosis in patients with oligodendroglial tumors].
  • Previous studies demonstrated that patients with oligodendroglial tumors (OT) have longer overall and recurrence free survival than patients with other glial tumors of the same grade.
  • In the series of 241 cases (107 male, 134 female patients, median age -- 38 years, (16-73)) we analyzed the impact of histology, tumor grade and genetic alterations on time to tumor progression (TTP).
  • All patients underwent surgical resection of tumor or biopsy from 2000 to 2005.
  • The type of tumor (pure or mixed) didn't influence survival.
  • TTP of patients with grade II and grade III tumors was 37.7 and 48.2 months, respectively (p = 0.035).
  • In pure O codeletion 1p19q was detected more frequently (in O -- 75%, in AO -- 56%) than in mixed tumors (in OA -- 31%, in AOA -- 35%).
  • None of the tumors with 1pl9q deletion had other genetic alterations.
  • Pure O more frequently had 1p19q deletion than mixed tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosome Deletion. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Young Adult

  • 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 = 19507310.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


17. Whitmore RG, Krejza J, Kapoor GS, Huse J, Woo JH, Bloom S, Lopinto J, Wolf RL, Judy K, Rosenfeld MR, Biegel JA, Melhem ER, O'Rourke DM: Prediction of oligodendroglial tumor subtype and grade using perfusion weighted magnetic resonance imaging. J Neurosurg; 2007 Sep;107(3):600-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediction of oligodendroglial tumor subtype and grade using perfusion weighted magnetic resonance imaging.
  • Perfusion weighted magnetic resonance (MR) imaging allows for noninvasive determination of relative tumor blood volume (rTBV) and has been used to predict the grade of astrocytic neoplasms.
  • The aim of this study was to use perfusion weighted MR imaging to predict tumor grade and cytogenetic profile in oligodendroglial neoplasms.
  • METHODS: Thirty patients with oligodendroglial neoplasms who underwent preoperative perfusion MR imaging were retrospectively identified.
  • Tumors were classified by histopathological grade and stratified into two cytogenetic groups: 1p or 1p and 19q loss of heterozygosity (LOH) (Group 1), and 19q LOH only on intact alleles (Group 2).
  • Tumor blood volume was calculated in relation to contralateral white matter.
  • Multivariate logistic regression analysis was used to develop predictive models of cytogenetic profile and tumor grade.
  • CONCLUSIONS: Oligodendroglial classification models derived from advanced imaging will improve the accuracy of tumor grading, provide prognostic information, and have potential to influence treatment decisions.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Loss of Heterozygosity / genetics. Magnetic Resonance Angiography. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Blood Volume. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Tumor Burden

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17886561.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA-90586
  • [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
  •  go-up   go-down


18. Kim SH, Kim H, Kim TS: Clinical, histological, and immunohistochemical features predicting 1p/19q loss of heterozygosity in oligodendroglial tumors. Acta Neuropathol; 2005 Jul;110(1):27-38
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, histological, and immunohistochemical features predicting 1p/19q loss of heterozygosity in oligodendroglial tumors.
  • To identify a better diagnostic criteria for oligodendroglial tumors, we investigated the clinical, histological, and immunohistochemical features that would be able to predict a 1p/19q loss of heterozygosity (LOH) in these tumors.
  • We performed a PCR-based LOH test with the 1p and 19q microsatellite markers by microdissecting tumor in 56 samples (44 oligodendrogliomas and 12 mixed oligoastrocytomas) of paraffin-embedded tissue.
  • Patients with oligodendroglial tumors with 1p/19q LOH had a statistically significant better prognosis for overall survival.
  • Comparative analysis of several features indicated that the 1p/19q LOH tumors were associated with two histological features, "tumor cellularity" and "perinuclear halo," and low O(6)-methylguanine-DNA-methyltransferase (MGMT) expression and high cytoplasmic glutathione S-transferase pi (GST-pi) expression.
  • Using the new features, we could predict the 1p/19q status of oligodendroglial tumors with greater than 90% accuracy.
  • Therefore, applying these features in clinical practice, would be helpful in clarifying oligodendroglial tumor diagnosis.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Glioma / diagnosis. Glioma / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Child. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction. Sensitivity and Specificity. Survival Analysis


19. Idbaih A, Boisselier B, Marie Y, El Hallani S, Sanson M, Crinière E, Rodero M, Carpentier C, Paris S, Laigle-Donadey F, Ducray F, Hoang-Xuan K, Delattre JY: TP53 codon 72 polymorphism, p53 expression, and 1p/19q status in oligodendroglial tumors. Cancer Genet Cytogenet; 2007 Sep;177(2):103-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TP53 codon 72 polymorphism, p53 expression, and 1p/19q status in oligodendroglial tumors.
  • Such results were also reported in brain tumors, notably in astrocytomas.
  • This SNP has never been precisely investigated in oligodendroglial tumors.
  • We retrospectively analyzed blood samples of 275 oligodendroglial tumor patients for the TP53 codon 72 polymorphism and compared them with a series of 144 healthy controls.
  • This suggests no association between oligodendroglial tumors and the SNP in codon 72 of TP53.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Codon. Oligodendroglioma / genetics. Polymorphism, Genetic / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Aged. Astrocytoma / genetics. Astrocytoma / metabolism. Case-Control Studies. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Female. Genotype. Glioma / genetics. Glioma / metabolism. Humans. Immunoenzyme Techniques. Male. Microsatellite Repeats. Middle Aged. Prognosis. Survival Rate

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17854663.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


20. Jenkinson MD, Smith TS, Joyce K, Fildes D, du Plessis DG, Warnke PC, Walker C: MRS of oligodendroglial tumors: correlation with histopathology and genetic subtypes. Neurology; 2005 Jun 28;64(12):2085-9
Hazardous Substances Data Bank. CHOLINE CHLORIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MRS of oligodendroglial tumors: correlation with histopathology and genetic subtypes.
  • BACKGROUND: Oligodendroglial neoplasms with combined loss of chromosomes 1p and 19q may have a good prognosis and respond to procarbazine-lomustine (CCNU)-vincristine (PCV) chemotherapy.
  • OBJECTIVE: To determine whether single voxel magnetic resonance spectroscopy (SV-MRS) obtained through routine clinical practice distinguishes between histopathologic and genetic subtypes of oligodendroglial tumors.
  • METHODS: Forty-eight patients with oligodendroglial tumors (19 oligodendrogliomas and 29 oligoastrocytomas) underwent molecular genetic analysis to determine allelic imbalance in chromosomes 1p36 and 19q13.
  • SV-MRS was obtained pretherapy to determine tumor metabolite ratios.
  • RESULTS: Grade III oligodendroglial tumors had higher choline (Mann-Whitney; p = 0.002), methyl lipid (Mann-Whitney; p = 0.002), and combined methylene lipid and lactate ratios (Mann-Whitney; p < 0.001) than grade II tumors.
  • Lactate did not distinguish between tumor types (Fisher exact test; p = 0.342) or grade (Fisher exact test; p = 0.452).
  • There were no significant associations when tumors were analyzed according to histopathology or genetic subtypes.
  • CONCLUSION: As a noninvasive diagnostic tool used in routine clinical practice, SV-MRS has the potential benefit of determining oligodendroglial tumor grade but not subtypes classified by histopathology or molecular genetics.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Magnetic Resonance Spectroscopy / standards. Oligodendroglioma / diagnosis
  • [MeSH-minor] Adult. Aged. Allelic Imbalance / genetics. Choline / metabolism. DNA Mutational Analysis. Diagnosis, Differential. Female. Gene Expression Regulation, Neoplastic / genetics. Genetic Testing. Genotype. Humans. Lactic Acid / metabolism. Lipids / analysis. Male. Middle Aged. Predictive Value of Tests

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LACTIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15985578.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipids; 33X04XA5AT / Lactic Acid; N91BDP6H0X / Choline
  •  go-up   go-down


21. Xu M, See SJ, Ng WH, Arul E, Back MF, Yeo TT, Lim CC: Comparison of magnetic resonance spectroscopy and perfusion-weighted imaging in presurgical grading of oligodendroglial tumors. Neurosurgery; 2005 May;56(5):919-26; discussion 919-26
MedlinePlus Health Information. consumer health - MRI Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of magnetic resonance spectroscopy and perfusion-weighted imaging in presurgical grading of oligodendroglial tumors.
  • OBJECTIVE: Oligodendroglial tumors form an uncommon, but distinct, subgroup of gliomas with longer survival, better treatment response, and characteristic genetic alterations.
  • Noninvasive grading of oligodendroglial tumors using functional and metabolic magnetic resonance imaging may be helpful in guiding the treatment approach and predicting malignant transformation of these tumors.
  • We assessed the ability of tumor contrast enhancement, normalized cerebral blood volume, normalized choline, and the presence of either lactate or lipid metabolites to correctly predict the World Health Organization tumor grade.
  • The accuracy of tumor grading using each method was also compared.
  • RESULTS: Tumor contrast enhancement (P = 0.069) and normalized cerebral blood volume (P = 0.181) were not significantly different between low and high-grade oligodendrogliomas.
  • The MRSI measurement of normalized choline was significantly higher in high-grade (2.82 +/- 0.64) than in low-grade (1.62 +/- 0.46) oligodendrogliomas (P < 0.001), and the presence of lactate or lipid metabolites also correctly predicted high-grade tumors (P = 0.014).
  • CONCLUSION: MRSI measurements are more accurate than perfusion-weighted magnetic resonance imaging or conventional contrast enhancement in differentiating oligodendroglial tumor grade.
  • In these inherently vascular tumors, metabolic measurements of mitosis and necrosis may be better than measures of neovascularity in presurgical grading.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Magnetic Resonance Imaging / methods. Magnetic Resonance Spectroscopy / methods. Oligodendroglioma / diagnosis. Oligodendroglioma / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Observer Variation. Preoperative Care. Reproducibility of Results. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15854239.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


22. Hergersberg M, Mariani L, Vassella E, Murtin C, Weis J, Moschopulos M, Laeng H, Landolt H, Huber A, Roelcke U: Age at diagnosis and loss of heterozygosity on chromosome 1p and 19q in oligodendroglial tumors. J Neurooncol; 2006 Nov;80(2):215-7
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age at diagnosis and loss of heterozygosity on chromosome 1p and 19q in oligodendroglial tumors.
  • The age distribution and incidence of loss of heterozygosity (LOH) of 1p and 19q was analyzed in 85 oligodendroglial tumors WHO II and III.
  • The peak of tumor manifestation was in the age group of 35 to 55 years.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Loss of Heterozygosity / genetics. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Age of Onset. Aging / physiology. Female. Humans. Male. Middle Aged. O(6)-Methylguanine-DNA Methyltransferase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16685464.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  •  go-up   go-down


23. Kanamori M, Kumabe T, Sonoda Y, Nishino Y, Watanabe M, Tominaga T: Predictive factors for overall and progression-free survival, and dissemination in oligodendroglial tumors. J Neurooncol; 2009 Jun;93(2):219-28
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictive factors for overall and progression-free survival, and dissemination in oligodendroglial tumors.
  • The pattern of recurrence and predictive factors for tumor progression, dissemination and survival in oligodendroglial tumors were investigated.
  • 56 consecutive patients with oligodendroglial tumors were retrospectively analyzed to determine the predictive significance of various factors, including World Health Organization grade, loss of chromosomes 1p and 19q, and immunohistochemical features of TP53, O(6)-methylguanine-deoxyribonucleic-acid-methyltransferase, CD44H, nestin, and Ki-67.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. In Situ Hybridization, Fluorescence. Intermediate Filament Proteins / genetics. Male. Middle Aged. Nerve Tissue Proteins / genetics. Nestin. Predictive Value of Tests. Retrospective Studies. Survival Rate. Treatment Outcome. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Young Adult

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19099201.001).
  • [ISSN] 1573-7373
  • [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 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


24. Volavsek M, Lamovec J, Popović M: Extraneural metastases of anaplastic oligodendroglial tumors. Pathol Res Pract; 2009;205(7):502-7
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extraneural metastases of anaplastic oligodendroglial tumors.
  • Fine needle aspiration biopsy (FNAB) of the cervical lymph node prior to neck dissection suggested a possible metastatic primitive neuroepithelial tumor.
  • It is important to bear this in mind, particularly in cases when the history of primary brain tumor is unavailable.
  • [MeSH-major] Astrocytoma / secondary. Brain Neoplasms / pathology. Femoral Neoplasms / secondary. Neoplasm Recurrence, Local. Oligodendroglia / pathology. Oligodendroglioma / secondary. Sacrum / pathology. Spinal Neoplasms / secondary
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols. Chemotherapy, Adjuvant. Cranial Irradiation. Craniotomy. Fatal Outcome. Female. Humans. Lymphatic Metastasis. Middle Aged. Radiotherapy, Adjuvant. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19410385.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


25. Zhang SK, Lu DH, Piao YS, Cai YN, Xu QZ: [Study of loss of heterozygosity in oligodendroglial tumors by real-time quantitative polymerase chain reaction-based microsatellite analysis]. Zhonghua Bing Li Xue Za Zhi; 2006 Dec;35(12):731-4
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study of loss of heterozygosity in oligodendroglial tumors by real-time quantitative polymerase chain reaction-based microsatellite analysis].
  • OBJECTIVE: To study the loss of heterozygosity (LOH) at chromosomes 1p or 19q in oligodendroglial tumors.
  • METHODS: Twenty-eight cases of oligodendroglial tumors were enrolled into the study.
  • Real-time quantitative polymerase chain reaction-based microsatellite analysis was performed on paraffin-embedded tumor tissues in order to study the status of chromosomes 1p and 19q.
  • RESULTS: Among the 28 cases of oligodendroglial tumors, 24 cases (85.7%) showed 1p LOH, while 18 cases (64.3%) showed 19q LOH and 17 cases (60.7%) showed LOH of both 1p and 19q.
  • CONCLUSIONS: Real-time quantitative polymerase chain reaction-based microsatellite analysis is a rapid and specific way in detecting LOH in paraffin-embedded tumor tissues.
  • LOH at 1p or 19q is present in majority of the oligodendroglial tumors studied.
  • [MeSH-major] Brain Neoplasms / genetics. Loss of Heterozygosity. Microsatellite Repeats. Oligodendroglioma / genetics. Polymerase Chain Reaction / methods
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. Male. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17374257.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


26. Kuo LT, Kuo KT, Lee MJ, Wei CC, Scaravilli F, Tsai JC, Tseng HM, Kuo MF, Tu YK: Correlation among pathology, genetic and epigenetic profiles, and clinical outcome in oligodendroglial tumors. Int J Cancer; 2009 Jun 15;124(12):2872-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation among pathology, genetic and epigenetic profiles, and clinical outcome in oligodendroglial tumors.
  • Recent studies have revealed a correlation between specific genetic changes, such as loss of chromosome 1p and 19q, and sensitivity of oligodendroglial neoplasm to radiotherapy and chemotherapy; epigenetic changes also play an important role in some tumors.
  • In this retrospective study, we analyzed chromosomal alterations in 17 loci and promoter methylation status of 8 tumor-related genes in 49 oligodendroglial tumors (29 WHO grade II and 11 WHO grade III oligodendrogliomas; 7 WHO grade II and 2 WHO grade III oligoastrocytomas) using quantitative microsatellite analysis and methylation-specific polymerase chain reaction and correlated this information with clinical data.
  • Promoter methylation was detected in p14, p15, p16, p53, p73, PTEN, MGMT and RASSF1A genes in 24.5%, 6.1%, 46.9%, 0%, 6.1%, 42.9%, 53.1% and 77.6% of tumors, respectively.
  • Our findings suggest that the frequent deletion and hypermethylation of tumor-related genes may represent a mechanism of tumor development and progression and emphasize the importance of defining new molecular markers for predicting prognosis, tumor recurrence and therapeutic response in cancer management.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Aberrations. Chromosomes, Human / genetics. Epigenesis, Genetic. Neoplasm Proteins / genetics. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Proliferation. Child. Child, Preschool. DNA Methylation. DNA Modification Methylases / genetics. DNA Modification Methylases / metabolism. DNA Repair Enzymes / genetics. DNA Repair Enzymes / metabolism. DNA, Neoplasm / genetics. Female. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Male. Microsatellite Repeats. Middle Aged. Neoplasm Staging. Polymerase Chain Reaction. Promoter Regions, Genetic / genetics. Retrospective Studies. Survival Rate. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood 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
  • [Copyright] Copyright 2008 UICC.
  • [ErratumIn] Int J Cancer. 2009 Sep 1;125(5):1241
  • (PMID = 19330828.001).
  • [ISSN] 1097-0215
  • [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, Neoplasm; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.3.2.19 / MIB1 ligase, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down


27. Hirose T, Ishizawa K, Shimada S: Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors. Neuropathology; 2010 Dec;30(6):586-96
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors.
  • To improve the diagnostic accuracy of oligodendroglial tumors and to find more convenient parameters that could predict the cytogenetic status, oligodendroglial and astrocytic tumors were cytogenetically and immunohistochemically investigated.
  • Materials included 22 oligodendroglial tumors (15 oligodendrogliomas and 7 oligoastrocytomas) and 20 astrocytic tumors.
  • Furthermore, TP53 mutation analyses were carried out on three oligodendroglial tumors showing p53 protein overexpression with a direct sequence analysis.
  • Our FISH studies demonstrated 1p loss in 73% of oligodendroglial tumors (80% oligodendrogliomas and 57% oligoastrocytomas) and in only 10% of astrocytic tumors.
  • There were no clear-cut morphologic differences between 1p-deleted and 1p-intact oligodendroglial tumors.
  • GFAP and Olig2 were expressed in most oligodendroglial and astrocytic tumors, and their cellular localization was almost independent of each other.
  • Overexpression of p53 was observed in five oligodendroglial tumors, all of which were 1p-intact.
  • In comparison, 16 oligodendroglial tumors with 1p deletion showed no overexpression of p53.
  • TP53 missense mutations were detected in three of the p53 overexpressed oligodendroglial tumors studied.
  • Our results suggest that 1p loss is almost specific to oligodendroglial tumors.
  • Although the prediction of 1p status based solely on the morphologic features seems to be difficult, the immunohistochemistry for p53 is a useful tool in that p53 overexpression is closely related to the 1p-intact status in oligodendroglial tumors.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Chromosomes, Human, Pair 1 / genetics. Oligodendroglioma / diagnosis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Female. Gene Deletion. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Nerve Tissue Proteins / biosynthesis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 Japanese Society of Neuropathology.
  • (PMID = 20408960.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


28. Ferrer-Luna R, Mata M, Núñez L, Calvar J, Dasí F, Arias E, Piquer J, Cerdá-Nicolás M, Taratuto AL, Sevlever G, Celda B, Martinetto H: Loss of heterozygosity at 1p-19q induces a global change in oligodendroglial tumor gene expression. J Neurooncol; 2009 Dec;95(3):343-354
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of heterozygosity at 1p-19q induces a global change in oligodendroglial tumor gene expression.
  • Oligodendroglial tumors presenting loss of heterozygosity (LOH) at 1p and 19q have been shown to be sensitive to chemotherapy, thus making 1p-19q status testing a key aspect in oligodendroglioma diagnosis and prognosis.
  • Twenty-nine tumor samples (19 oligodendrogliomas, 10 oligoastrocytomas) were analyzed in order to obtain a molecular profile identifying those bearing 1p-19q LOH.
  • Tumors with 1p-19q LOH overexpressed genes related to neurogenesis.
  • This molecular signature was validated by analyzing a set of ten tumor samples (three oligodendrogliomas, seven oligoastrocytomas); all ten samples were correctly assigned.
  • Tumors without LOH at 1p-19q exhibit the opposite characteristics, explaining their more aggressive behavior.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Gene Expression Regulation, Neoplastic. Loss of Heterozygosity. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child, Preschool. Chromosome Deletion. Cluster Analysis. Gene Expression Profiling. Humans. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction


29. Li KK, Pang JC, Chung NY, Ng YL, Chan NH, Zhou L, Poon WS, Ng HK: EMP3 overexpression is associated with oligodendroglial tumors retaining chromosome arms 1p and 19q. Int J Cancer; 2007 Feb 15;120(4):947-50
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EMP3 overexpression is associated with oligodendroglial tumors retaining chromosome arms 1p and 19q.
  • The epithelial membrane protein 3 (EMP3) gene located on chromosome 19q13 has been implicated as a candidate tumor suppressor gene (TSG) in neuroblastomas and gliomas.
  • The aim of this study was to investigate whether EMP3 is involved in oligodendroglial tumors (OTs), which frequently carry combined chromosomes 1p and 19q deletion.
  • Our results showed that 10 (18%) tumors had reduced EMP3 expression level compared to normal brains.
  • Six of these tumors carried chromosome 19q13 deletion but no statistical correlation was found between the 2 parameters.
  • Intriguingly, a similar proportion (11 of 57, 19%) of tumors displayed EMP3 overexpression, with 8 of them having transcript level >10-fold higher than normal brain.
  • All tumors except 3 showed aberrant methylation of EMP3 and no correlation was observed between transcript level and methylation status, suggesting that methylation alone does not mediate transcriptional down-regulation of EMP3 in OTs.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Membrane Glycoproteins / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / pathology. Child. CpG Islands. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

  • 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 = 17187361.001).
  • [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 / EMP3 protein, human; 0 / Membrane Glycoproteins
  •  go-up   go-down


30. Perry A, Burton SS, Fuller GN, Robinson CA, Palmer CA, Resch L, Bigio EH, Gujrati M, Rosenblum MK: Oligodendroglial neoplasms with ganglioglioma-like maturation: a diagnostic pitfall. Acta Neuropathol; 2010 Aug;120(2):237-52
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oligodendroglial neoplasms with ganglioglioma-like maturation: a diagnostic pitfall.
  • Although oligodendroglial neoplasms are traditionally considered purely glial, increasing evidence suggests that they are capable of neuronal or neurocytic differentiation.
  • Herein, we report seven examples where the primary differential diagnosis was a ganglioglioma with an oligodendroglial component.
  • In contrast to classic ganglioglioma, however, cases lacked eosinophilic granular bodies and CD34-positive tumor cells.
  • We conclude that GGLF represents yet another form of neuronal differentiation in oligodendroglial neoplasms.
  • [MeSH-major] Brain Neoplasms / diagnosis. Ganglioglioma / diagnosis. Oligodendroglioma / diagnosis
  • [MeSH-minor] Adult. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neurofilament Proteins / metabolism. Retrospective Studies

  • Genetic Alliance. consumer health - Ganglioglioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] Acta Neuropathol. 2005 Nov;110(5):520-2 [16222523.001]
  • [Cites] Neuropathol Appl Neurobiol. 2006 Oct;32(5):461-8 [16972880.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5419-26 [17135643.001]
  • [Cites] Arch Pathol Lab Med. 2007 Feb;131(2):242-51 [17284109.001]
  • [Cites] Neuro Oncol. 2007 Apr;9(2):124-34 [17259542.001]
  • [Cites] J Neurooncol. 2007 Apr;82(2):199-205 [17039400.001]
  • [Cites] Histopathology. 2007 Jun;50(7):887-96 [17543079.001]
  • [Cites] Semin Ultrasound CT MR. 2008 Feb;29(1):40-6 [18383906.001]
  • [Cites] Brain Pathol. 2008 Jul;18(3):360-9 [18371182.001]
  • [Cites] Brain Pathol. 2008 Jul;18(3):326-37 [18371186.001]
  • [Cites] Mol Cancer. 2008;7:41 [18492260.001]
  • [Cites] Cancer. 2008 Dec 15;113(12):3355-63 [18988291.001]
  • [Cites] J Neurooncol. 2009 Dec;95(3):343-54 [19597701.001]
  • [Cites] Neuro Oncol. 2009 Dec;11(6):737-46 [19224764.001]
  • [Cites] Glia. 2000 Feb 1;29(3):233-45 [10642750.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):636-45 [10653879.001]
  • [Cites] Pediatr Neurosurg. 2001 Jun;34(6):301-5 [11455230.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Oct;60(10):984-93 [11589429.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Apr 1;134(1):71-6 [11996800.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 May;61(5):403-12 [12025943.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Jul;61(7):575-84 [12125736.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Nov;61(11):947-55 [12430711.001]
  • [Cites] Front Biosci. 2003 Jan 1;8:a1-9 [12456321.001]
  • [Cites] Brain Pathol. 2004 Jan;14(1):34-42 [14997935.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Apr;63(4):314-22 [15099021.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):89-96 [15146346.001]
  • [Cites] Hum Pathol. 2004 Sep;35(9):1156-9 [15343519.001]
  • [Cites] Histopathology. 1990 Nov;17(5):439-41 [1706300.001]
  • [Cites] Am J Pathol. 1994 Nov;145(5):1175-90 [7977648.001]
  • [Cites] Neuroscience. 1996 Mar;71(2):601-11 [9053811.001]
  • [Cites] Cancer. 1997 Jan 1;79(1):127-31 [8988736.001]
  • [Cites] Acta Neuropathol. 1997 Nov;94(5):436-43 [9386775.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] Neuropathol Appl Neurobiol. 1998 Aug;24(4):302-8 [9775396.001]
  • [Cites] Acta Neuropathol. 1999 May;97(5):481-90 [10334485.001]
  • [Cites] Clin Neuropathol. 2005 Sep-Oct;24(5):225-9 [16167546.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]
  • (PMID = 20464403.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Neurofilament Proteins
  • [Other-IDs] NLM/ PMC2892612
  •  go-up   go-down


31. Pang JC, Li KK, Lau KM, Ng YL, Wong J, Chung NY, Li HM, Chui YL, Lui VW, Chen ZP, Chan DT, Poon WS, Wang Y, Mao Y, Zhou L, Ng HK: KIAA0495/PDAM is frequently downregulated in oligodendroglial tumors and its knockdown by siRNA induces cisplatin resistance in glioma cells. Brain Pathol; 2010 Nov;20(6):1021-32
SciCrunch. HGNC: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] KIAA0495/PDAM is frequently downregulated in oligodendroglial tumors and its knockdown by siRNA induces cisplatin resistance in glioma cells.
  • Co-deletion of chromosomes 1p and 19q is a common event in oligodendroglial tumors (OTs), suggesting the presence of OT-related genes.
  • A novel gene KIAA0495/p53-dependent apoptosis modulator (PDAM) was found frequently deregulated, with 37 of 58 (63.8%) OTs examined showing reduced expression compared with normal brain.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Oligodendroglioma / metabolism. RNA, Long Noncoding / physiology. RNA, Small Interfering / pharmacology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Child. Cisplatin / pharmacology. Down-Regulation / drug effects. Drug Interactions. Female. Glioma / pathology. Humans. Male. Middle Aged. Protein Transport / drug effects. Protein Transport / genetics. Thermosensing / genetics. Transfection. Young Adult

  • 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. CIS-DIAMINEDICHLOROPLATINUM .
  • 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
  • [Copyright] © 2010 The Authors; Brain Pathology © 2010 International Society of Neuropathology.
  • (PMID = 20477830.001).
  • [ISSN] 1750-3639
  • [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 / Antineoplastic Agents; 0 / RNA, Long Noncoding; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Proteins; 0 / long non-coding RNA KIAA0495, human; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


32. Vesper J, Graf E, Wille C, Tilgner J, Trippel M, Nikkhah G, Ostertag C: Retrospective analysis of treatment outcome in 315 patients with oligodendroglial brain tumors. BMC Neurol; 2009;9:33
Hazardous Substances Data Bank. PROCARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retrospective analysis of treatment outcome in 315 patients with oligodendroglial brain tumors.
  • Although chemotherapy with procarbazine, lomustine and vincristine (PCV) is considered to be well tolerated, side effects frequently lead to dose reduction or even discontinuation of treatment of oligodendroglial brain tumors.
  • Based on the updated histology data, patients were included in the study if they had at least one histological diagnosis of an oligodendroglial tumor.
  • Significant advantages in terms of overall survival after first diagnosis of oligodendroglial tumor (OS, n = 315) were found for patients < 50 y (p < 0.001), oligodendrogliomas versus oligoastrocytomas (p = 0.002), and WHO degrees II vs. degrees III (p < 0.001).
  • Younger age, lower tumor grade and histology of an oligodendroglioma were identified to be favorable prognostic factors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Lomustine / administration & dosage. Lomustine / therapeutic use. Male. Middle Aged. Procarbazine / administration & dosage. Procarbazine / therapeutic use. Prognosis. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage. Vincristine / therapeutic use

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • Hazardous Substances Data Bank. LOMUSTINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurology. 2000 Apr 11;54(7):1442-8 [10751254.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] Semin Radiat Oncol. 2001 Apr;11(2):145-51 [11285552.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):705-10 [11723377.001]
  • [Cites] Acta Neurochir (Wien). 2001 Dec;143(12):1195-203 [11810382.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Jan;61(1):58-63 [11829344.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Curr Treat Options Oncol. 2001 Dec;2(6):495-506 [12057095.001]
  • [Cites] Expert Rev Anticancer Ther. 2001 Dec;1(4):595-605 [12113092.001]
  • [Cites] J Neurooncol. 2002 Sep;59(3):231-7 [12241120.001]
  • [Cites] Neuro Oncol. 2003 Apr;5(2):128-38 [12672285.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2525-8 [12829671.001]
  • [Cites] Semin Oncol. 2003 Dec;30(6 Suppl 19):23-8 [14765381.001]
  • [Cites] Semin Oncol. 2004 Oct;31(5):645-52 [15497117.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1991 Oct;54(10):915-20 [1744647.001]
  • [Cites] J Clin Oncol. 1994 Oct;12(10):2013-21 [7931469.001]
  • [Cites] Eur J Cancer. 1994;30A(12):1809-15 [7880611.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1996 Sep;61(3):291-6 [8795601.001]
  • [Cites] Control Clin Trials. 1996 Aug;17(4):343-6 [8889347.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1998 May;64(5):581-7 [9598670.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] Neurosurg Rev. 1998;21(2-3):138-46 [9795948.001]
  • [Cites] Can J Neurol Sci. 1999 Feb;26(1):18-22 [10068802.001]
  • [Cites] Curr Opin Neurol. 2004 Dec;17(6):675-80 [15542975.001]
  • [Cites] J Mol Med (Berl). 2004 Oct;82(10):638-55 [15322700.001]
  • [Cites] Neurosurgery. 2005 Feb;56(2):257-65; discussion 257-65 [15670374.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1372-81 [16470609.001]
  • [Cites] Strahlenther Onkol. 2000 Jun;176(6):259-64 [10897252.001]
  • (PMID = 19604414.001).
  • [ISSN] 1471-2377
  • [Journal-full-title] BMC neurology
  • [ISO-abbreviation] BMC Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
  • [Other-IDs] NLM/ PMC2719586
  •  go-up   go-down


33. Wu A, Aldape K, Lang FF: High rate of deletion of chromosomes 1p and 19q in insular oligodendroglial tumors. J Neurooncol; 2010 Aug;99(1):57-64
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).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High rate of deletion of chromosomes 1p and 19q in insular oligodendroglial tumors.
  • It has been reported recently that oligodendroglial tumors arising in the insula rarely harbor co-deletions of chromosomes 1p and 19q, a molecular signature which is associated with a good prognosis and increased responsiveness to radiation and chemotherapy compared with tumors in which 1p and/or 19q is intact.
  • In the context of this claim, we analyzed a series of insular oligodendroglial tumors in order to determine the frequency of 1p/19q co-deletion in tumors arising in this region.
  • Seven of the eight tumors with co-deletion of 1p/19q were WHO grade II gliomas.
  • There were no statistical differences between tumors with 1p/19q co-deletion compared to those with 1p and/or 19q intact in terms of age, preoperative KPS, presenting symptoms, left versus right lateralization, tumor location (purely insular versus extension into frontal or temporal lobe), preoperative tumor size.
  • In contradistinction to previous reports, loss of 1p/19q occurs commonly in insular oligodendroglial tumors.
  • With respect to 1p/19q, insular gliomas do not appear to be distinct from gliomas arising elsewhere in the brain.

  • 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
  • [Cites] J Clin Oncol. 2000 Feb;18(3):636-45 [10653879.001]
  • [Cites] Cancer. 2006 Oct 15;107(8):1891-7 [16986124.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6713-5 [11559541.001]
  • [Cites] J Neurosurg. 2001 Oct;95(4):638-50 [11596959.001]
  • [Cites] Am J Pathol. 2002 Jul;161(1):313-9 [12107116.001]
  • [Cites] Cancer. 2004 Jun 15;100(12):2622-6 [15197805.001]
  • [Cites] Brain Res Brain Res Rev. 1996 Oct;22(3):229-44 [8957561.001]
  • [Cites] J Neurooncol. 1998 Mar;37(1):87-93 [9525843.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] Neurology. 2004 Dec 28;63(12):2360-2 [15623700.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1119-28 [15709179.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]
  • [Cites] Neurosurgery. 2005 Jul;57(1 Suppl):176-83; discussion 176-83 [15987586.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1468-77 [16088966.001]
  • [Cites] Neurosurg Focus. 2005 Nov;19(5):E15 [16398465.001]
  • [Cites] Clin Neuropathol. 2006 Jan-Feb;25(1):18-24 [16465770.001]
  • [Cites] Int J Cancer. 2006 Aug 15;119(4):792-800 [16550607.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):9852-61 [17047046.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 18;99(8):639-52 [17440165.001]
  • [Cites] Acta Neurobiol Exp (Wars). 2007;67(2):103-12 [17691218.001]
  • [Cites] J Neurooncol. 2008 Jul;88(3):293-8 [18345516.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jul 15;184(2):77-86 [18617055.001]
  • [Cites] J Neurooncol. 2009 Jan;91(1):1-5 [18726074.001]
  • [Cites] J Neurosurg. 2010 Jan;112(1):1-9 [19612970.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • (PMID = 20035368.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115729-04; United States / NCI NIH HHS / CA / P50CA127001; United States / NCI NIH HHS / CA / R01 CA115729; United States / NCI NIH HHS / CA / P50 CA127001; United States / NCI NIH HHS / CA / R01 CA115729-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS172388; NLM/ PMC2891585
  •  go-up   go-down


34. Idbaih A, Boisselier B, Marie Y, Sanson M, El Hallani S, Crinière E, Fourtassi M, Paris S, Carpentier C, Rousseau A, Mokhtari K, Combadière C, Laigle-Donadey F, Hoang-Xuan K, Delattre JY: Influence of MDM2 SNP309 alone or in combination with the TP53 R72P polymorphism in oligodendroglial tumors. Brain Res; 2008 Mar 10;1198:16-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of MDM2 SNP309 alone or in combination with the TP53 R72P polymorphism in oligodendroglial tumors.
  • This SNP has never been specifically investigated in a large series of oligodendroglial tumors.
  • In a comparison with 232 healthy controls, we retrospectively analyzed blood samples of 293 oligodendroglial tumor patients for MDM2 SNP309.
  • In addition, the TP53 R72P polymorphism and chromosome 1p/19q status, a major biomarker in oligodendroglial tumors, were investigated.
  • The frequencies of T/T, T/G, and G/G genotypes in patients and controls did not suggest an increased risk of oligodendroglial tumor formation correlating with MDM2 SNP309.
  • A borderline association was found between MDM2 SNP309 and overall survival (p=0.05), but in multivariate analysis, MDM2 SNP309 did not provide prognostic information complementary to age, tumor phenotype, grade, and 1p/19q status in oligodendroglial tumors.
  • Finally, MDM2 SNP309, alone or in combination with TP53 R72P, was not associated with oligodendroglial tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Genetic Predisposition to Disease / genetics. Oligodendroglioma / genetics. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins c-mdm2 / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Chromosomes, Human, Pair 1 / genetics. DNA Mutational Analysis. Female. Genetic Testing. Genotype. Humans. Male. Middle Aged. Phenotype. Prognosis. Retrospective Studies. Survival Rate

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18262501.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down


35. Ty AU, See SJ, Rao JP, Khoo JB, Wong MC: Oligodendroglial tumor chemotherapy using "decreased-dose-intensity" PCV: a Singapore experience. Neurology; 2006 Jan 24;66(2):247-9
Hazardous Substances Data Bank. PROCARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oligodendroglial tumor chemotherapy using "decreased-dose-intensity" PCV: a Singapore experience.
  • The authors propose "decreased-dose-intensity" PCV (procarbazine, lomustine [CCNU], and vincristine) chemotherapy for Asian patients with oligodendroglial tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Asian Continental Ancestry Group. Brain Neoplasms / drug therapy. Brain Neoplasms / ethnology. Oligodendroglioma / drug therapy. Oligodendroglioma / ethnology
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Dose-Response Relationship, Drug. Female. Humans. Lomustine / administration & dosage. Male. Procarbazine / administration & dosage. Survival Analysis. Vincristine / administration & dosage

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • Hazardous Substances Data Bank. LOMUSTINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16434664.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
  •  go-up   go-down


36. Rodriguez FJ, Scheithauer BW, Jenkins R, Burger PC, Rudzinskiy P, Vlodavsky E, Schooley A, Landolfi J: Gliosarcoma arising in oligodendroglial tumors ("oligosarcoma"): a clinicopathologic study. Am J Surg Pathol; 2007 Mar;31(3):351-62
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gliosarcoma arising in oligodendroglial tumors ("oligosarcoma"): a clinicopathologic study.
  • Gliosarcomas are morphologically biphasic tumors composed of glial and sarcomatous elements.
  • Only rare examples of gliosarcoma with oligodendroglial components have been reported.
  • Seven patients with oligodendroglial tumors and a sarcomatous component were identified.
  • At first resection, the tumors included grade II oligodendroglioma (n=3), grade III oligodendroglioma (n=1), grade II oligoastrocytoma (n=1), and grade III oligoastrocytoma (n=2).
  • The sarcomatous component developed in recurrent/progressive tumors in 6 cases but was a focal finding at first tumor resection in 1 and included fibrosarcoma (n=5), leiomyosarcoma (n=1), or pleomorphic myogenic sarcoma (n=1).
  • Rhabdoid change was a focal finding in the sarcomatous component of 1 tumor.
  • Gliosarcomas with oligodendroglial elements are rare.
  • [MeSH-major] Brain Neoplasms / pathology. Gliosarcoma / pathology. Neoplasms, Second Primary / pathology. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Brain / surgery. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Combined Modality Therapy. Fatal Outcome. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging

  • Genetic Alliance. consumer health - Gliosarcoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17325476.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


37. Sepulveda Sanchez JM, Martinez Montero JC, Diez-Lobato R, Hernandez-Lain A, Cabello A, Ramos A, Gonzalez Leon P, Ricoy Campo JR: Classification of oligodendroglial tumors based on histopathology criteria is a significant predictor of survival--clinical, radiological and pathologic long-term follow-up analysis. Clin Neuropathol; 2009 Jan-Feb;28(1):11-20
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification of oligodendroglial tumors based on histopathology criteria is a significant predictor of survival--clinical, radiological and pathologic long-term follow-up analysis.
  • BACKGROUND: The clinical course of oligodendroglial tumors is variable and there is a lack of consensus with regard to precisely diagnose which minimal criteria are required to make a diagnosis of a high-grade oligodendrial tumor.
  • The aims of the present study are to assess pathologic factors with prognostic significance, in addiction to clinical and neuroradiologic variables, in an attempt to identify reproducible histological parameters that are useful for classification of oligodendroglial tumors.
  • METHODS: 80 oligodendroglial tumors diagnosed between 1977 and 2004 were analyzed.
  • To make a diagnosis of anaplastic tumor we used reproducible parameters: endothelial proliferation, high cellularity, increased mitotic activity and necrosis.
  • CONCLUSIONS: Clear cut histopathological criteria (endothelial proliferation, high cellularity, mitotic activity and necrosis) allow to establish different oligodendroglial tumor entities with distinct survival outcome.
  • [MeSH-major] Brain Neoplasms / classification. Brain Neoplasms / pathology. Oligodendroglioma / classification. Oligodendroglioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Clin Neuropathol. 2009 Mar-Apr;28(2):150
  • (PMID = 19216215.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  •  go-up   go-down


38. Tanaka Y, Yokoo H, Komori T, Makita Y, Ishizawa T, Hirose T, Ebato M, Shibahara J, Tsukayama C, Shibuya M, Nakazato Y: A distinct pattern of Olig2-positive cellular distribution in papillary glioneuronal tumors: a manifestation of the oligodendroglial phenotype? Acta Neuropathol; 2005 Jul;110(1):39-47
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A distinct pattern of Olig2-positive cellular distribution in papillary glioneuronal tumors: a manifestation of the oligodendroglial phenotype?
  • Mixed neuronal-glial tumors of the central nervous system display a wide spectrum of differentiation.
  • Among them, the papillary glioneuronal tumor (PGNT) is characterized by pseudopapillary structures composed of astroglial cells covering hyalinized vessels, and by neurocytic, ganglioid and ganglion cells.
  • This study disclosed an additional cellular component of PGNT that is characterized by Olig2 positivity, suggestive of oligodendroglial phenotype, and the results also encourage us to investigate oligodendroglial participation in various glioneuronal tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Glioma / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytes / metabolism. Astrocytes / pathology. Basic Helix-Loop-Helix Transcription Factors. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Neurons / metabolism. Neurons / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15906048.001).
  • [ISSN] 0001-6322
  • [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] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human
  •  go-up   go-down


39. Sherman JH, Prevedello DM, Shah L, Raghavan P, Pouratian N, Starke RM, Lopes MB, Shaffrey ME, Schiff D: MR imaging characteristics of oligodendroglial tumors with assessment of 1p/19q deletion status. Acta Neurochir (Wien); 2010 Nov;152(11):1827-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MR imaging characteristics of oligodendroglial tumors with assessment of 1p/19q deletion status.
  • Effective treatment of patients with brain tumors requires accurate diagnostic techniques.
  • MR imaging can be used to help differentiate between low- and high-grade tumors.
  • METHODS: Using the clinical database at the University of Virginia Neuro-Oncology Center, we identified adult patients with grade II and III oligodendroglial tumors who underwent treatment from 2002 to 2007.
  • Age at diagnosis, gender, tumor grade, chromosomal deletion status, duration of follow-up, and MR imaging characteristics were analyzed; the latter was read by a blinded neuroradiologist.
  • The greatest cross-sectional area (mean) of the tumor measured 23.4 cm(2) for patients with the co-deletion and 31.7 cm(2) for patients with intact alleles (p = 0.008).
  • In addition, inner table thinning was noted directly adjacent to seven tumors with intact 1p and 19q alleles and in no tumors with the 1p/19q co-deletion (p = 0.020).
  • Amongst patients with pure oligodendrogliomas, those with 1p/19q co-deletion had tumors more often confined to a single lobe as compared with those patients without the co-deletion (p = 0.023).
  • Finally, tumors with intact alleles were more often found in the temporal lobe (45.0%) as compared with co-deleted tumors (22.7%) (p = 0.011).
  • While imaging will never replace definitive tissue diagnosis, imaging characteristics such as tumor size, location, and overlying skull thinning can assist clinicians in assessing patients with oligodendroglial tumors prior to surgical or medical intervention.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Gene Deletion. Genetic Predisposition to Disease / genetics. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. DNA Mutational Analysis / methods. Disease Progression. Female. Genetic Testing / methods. Humans. Male

  • MedlinePlus Health Information. consumer health - 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
  • (PMID = 20711790.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
  •  go-up   go-down


40. Häyry V, Tynninen O, Haapasalo HK, Wölfer J, Paulus W, Hasselblatt M, Sariola H, Paetau A, Sarna S, Niemelä M, Wartiovaara K, Nupponen NN: Stem cell protein BMI-1 is an independent marker for poor prognosis in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2008 Oct;34(5):555-63
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell protein BMI-1 is an independent marker for poor prognosis in oligodendroglial tumours.
  • METHODS: Tumour samples were collected from 305 adult patients treated for primary grades 2-4 gliomas between 1980 and 2006 in Finland and Germany.
  • CONCLUSIONS: BMI-1 is found in all histological types of gliomas and the relative protein expression of BMI-1 is a novel independent prognostic marker in oligodendroglial tumours.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Glioma / metabolism. Nuclear Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Female. Gene Expression. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Polycomb Repressive Complex 1. Proto-Oncogene Proteins c-mdm2 / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18346113.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Polycomb Repressive Complex 1; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down


41. Stockhammer F, von Deimling A, Synowitz M, Blechschmidt C, van Landeghem FK: Expression of glucose transporter 1 is associated with loss of heterozygosity of chromosome 1p in oligodendroglial tumors WHO grade II. J Mol Histol; 2008 Oct;39(5):553-60
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of glucose transporter 1 is associated with loss of heterozygosity of chromosome 1p in oligodendroglial tumors WHO grade II.
  • Objective Oligodendroglial tumors with a loss of heterozygosity of 1p (LOH1p) appear to have a better prognosis than oligodendrogliomas without LOH.
  • Previously, we reported glucose uptake in low-grade oligodendroglial tumors to be related to LOH 1p status.
  • Results Confocal microscopy depicted immunoreaction for GLUT-1, -3 and -12 in the cytoplasm of the tumor cells.
  • GLUT-1 expression in tumors with LOH 1p was significantly lower than in tumors with wild type 1p status (P = 0.0017).
  • Conclusion Expression of GLUT-1 is significantly reduced in low-grade oligodendroglial tumors harboring LOH 1p.
  • [MeSH-major] Brain Neoplasms / metabolism. Chromosomes, Human, Pair 1 / metabolism. Glioma / metabolism. Glucose Transporter Type 1 / biosynthesis. Loss of Heterozygosity
  • [MeSH-minor] Adult. Aged. Female. Gene Expression Regulation, Neoplastic / genetics. Glucose Transport Proteins, Facilitative / biosynthesis. Glucose Transport Proteins, Facilitative / genetics. Glucose Transporter Type 3 / biosynthesis. Glucose Transporter Type 3 / genetics. Humans. Male. Microscopy, Confocal / methods. Middle Aged. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics

  • MedlinePlus Health Information. consumer health - 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
  • (PMID = 18726700.001).
  • [ISSN] 1567-2379
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glucose Transport Proteins, Facilitative; 0 / Glucose Transporter Type 1; 0 / Glucose Transporter Type 3; 0 / SLC2A1 protein, human; 0 / SLC2A12 protein, human; 0 / SLC2A3 protein, human; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


42. Gan HK, Rosenthal MA, Dowling A, Kalnins R, Algar E, Wong N, Benson A, Woods AM, Cher L: A phase II trial of primary temozolomide in patients with grade III oligodendroglial brain tumors. Neuro Oncol; 2010 May;12(5):500-7
Hazardous Substances Data Bank. DACARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II trial of primary temozolomide in patients with grade III oligodendroglial brain tumors.
  • Glial tumors with oligodendroglial components are considered chemo-responsive.
  • These data add to the growing body of data showing that primary chemotherapy may be an acceptable alternative to radiotherapy for patients with gliomas containing oligodendroglial histology.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Oligodendroglioma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Disease-Free Survival. Female. Gene Deletion. Humans. Kaplan-Meier Estimate. Loss of Heterozygosity. Male. Middle Aged. Tumor Suppressor Proteins / genetics. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1997 Apr 1;79(7):1381-93 [9083161.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]
  • [Cites] J Neurooncol. 2006 Sep;79(2):153-7 [16855865.001]
  • [Cites] Eur J Cancer. 2006 Oct;42(15):2499-503 [16914310.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4746-53 [16954518.001]
  • [Cites] Arch Pathol Lab Med. 2007 Feb;131(2):242-51 [17284109.001]
  • [Cites] Nucleic Acids Res. 2007;35(6):e41 [17289753.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Jun;66(3):262-72 [18272388.001]
  • [Cites] J Clin Oncol. 2008 Sep 1;26(25):4189-99 [18757334.001]
  • [Cites] J Neurooncol. 2009 Mar;92(1):57-63 [19011763.001]
  • [Cites] Neuro Oncol. 2009 Apr;11(2):167-75 [18779504.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Aug;60(8):808-16 [11487055.001]
  • [Cites] Int J Cancer. 2005 Jan 20;113(3):379-85 [15455350.001]
  • (PMID = 20406900.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC2940620
  •  go-up   go-down


43. Gresner SM, Rieske P, Wozniak K, Piaskowski S, Jaskolski DJ, Skowronski W, Golanska E, Sikorska B, Liberski PP: Molecular analysis of chromosome 1, 10 and 19 abnormalities in human oligodendroglial tumors: relationship between frequency of LOH grade, age and gender. Clin Neuropathol; 2006 Jan-Feb;25(1):18-24
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular analysis of chromosome 1, 10 and 19 abnormalities in human oligodendroglial tumors: relationship between frequency of LOH grade, age and gender.
  • BACKGROUND: Loss of heterozygosity (LOH) on 1p and 19q is observed in most oligodendroglial tumors.
  • LOH on 10q appears to be less common in these tumors as compared to other gliomas.
  • PATIENTS AND METHODS: We reviewed 14 patients with oligodendroglial tumors (10 low-grade and 4 anaplastic oligodendroglioma) to evaluate the frequency of LOH on 1p, 10q and 19q and correlate it with tumor grade and patients' age and gender; 5 loci on 1p and 5 on 19q as well as 4 on 10q were analyzed for LOH using PCR techniques.
  • RESULTS: LOH on 1p together with 19q was detected in 6 tumors, 1 tumor showed deletion of 19q accompanied with deletion on 10q.
  • No association between LOH on 1p nor 19q and tumor grade or patients' gender was found.
  • CONCLUSION: Our study provides several clinically interesting findings and further supports the hypothesis of chromosome 1p and 19q involvement in the oligodendroglial cancerogenesis.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosome Aberrations. DNA, Neoplasm / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Age Factors. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Sex Factors

  • Genetic Alliance. consumer health - Chromosome 10.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16465770.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


44. Shukla B, Agarwal S, Suri V, Pathak P, Sharma MC, Gupta D, Sharma BS, Suri A, Halder A, Sarkar C: Assessment of 1p/19q status by fluorescence in situ hybridization assay: A comparative study in oligodendroglial, mixed oligoastrocytic and astrocytic tumors. Neurol India; 2009 Sep-Oct;57(5):559-66
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of 1p/19q status by fluorescence in situ hybridization assay: A comparative study in oligodendroglial, mixed oligoastrocytic and astrocytic tumors.
  • Majority of oligodendrogliomas (85%; 17/20) and oligodendroglial areas in mixed oligoastrocytomas (77.7%; 7/9) showed a membranous lace-like immunopositivity with EGFR.
  • CONCLUSION: Loss of 1p/19q is strongly associated with oligodendroglial phenotype, while astrocytic tumors are more likely to show p53 over-expression. p53 expression and 1p/19q status appear to be mutually exclusive.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 19. In Situ Hybridization, Fluorescence / methods. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Receptor, Epidermal Growth Factor / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / metabolism. Young Adult

  • MedlinePlus Health Information. consumer health - 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 = 19934553.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


45. Scheie D, Andresen PA, Cvancarova M, Bø AS, Helseth E, Skullerud K, Beiske K: Fluorescence in situ hybridization (FISH) on touch preparations: a reliable method for detecting loss of heterozygosity at 1p and 19q in oligodendroglial tumors. Am J Surg Pathol; 2006 Jul;30(7):828-37
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluorescence in situ hybridization (FISH) on touch preparations: a reliable method for detecting loss of heterozygosity at 1p and 19q in oligodendroglial tumors.
  • Combined loss of heterozygosity (LOH) on 1p and 19q is reported in 50% to 90% of oligodendroglial tumors and has emerged as a strong and favorable prognostic factor.
  • The aim of this study was to evaluate the reliability of FISH to predict LOH at 1p and 19q when performed on touch preparations from 40 oligodendroglial tumors, even if the majority of the nuclei showed chromosomal imbalance.
  • Under these conditions, even a dominant population of nuclei showing FISH-imbalance represented an LOH status in the tumor cells.
  • [MeSH-minor] Adult. Aged. Cell Count. DNA, Neoplasm / analysis. Humans. Middle Aged. Polymerase Chain Reaction. Reproducibility of Results

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16819324.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


46. Hartmann C, Meyer J, Balss J, Capper D, Mueller W, Christians A, Felsberg J, Wolter M, Mawrin C, Wick W, Weller M, Herold-Mende C, Unterberg A, Jeuken JW, Wesseling P, Reifenberger G, von Deimling A: Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas. Acta Neuropathol; 2009 Oct;118(4):469-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas.
  • IDH2 encoding mitochondrial NADP+-dependent isocitrate dehydrogenase is also mutated in these tumors, albeit at much lower frequencies.
  • Preliminary data suggest an importance of IDH1 mutation for prognosis showing that patients with anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas harboring IDH1 mutations seem to fare much better than patients without this mutation in their tumors.
  • We report on an inverse association of IDH1 and IDH2 mutations in these gliomas and a non-random distribution of the mutation types within the tumor entities.
  • IDH1 mutations of the R132C type are strongly associated with astrocytoma, while IDH2 mutations predominantly occur in oligodendroglial tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Cell Differentiation. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Mutation. Prognosis. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - 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
  • (PMID = 19554337.001).
  • [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
  •  go-up   go-down


47. Takei H, Yogeswaren ST, Wong KK, Mehta V, Chintagumpala M, Dauser RC, Lau CC, Adesina AM: Expression of oligodendroglial differentiation markers in pilocytic astrocytomas identifies two clinical subsets and shows a significant correlation with proliferation index and progression free survival. J Neurooncol; 2008 Jan;86(2):183-90
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of oligodendroglial differentiation markers in pilocytic astrocytomas identifies two clinical subsets and shows a significant correlation with proliferation index and progression free survival.
  • We present here the pattern of expression of oligodendroglial differentiation markers (ODMs) in PAs by immunohistochemistry and their correlation with PI and PFS.

  • 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 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 = 17690840.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA120534
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Myelin Basic Protein; 0 / Nerve Tissue Proteins; 0 / OLIG1 protein, human; 0 / OLIG2 protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  •  go-up   go-down


48. Seol HJ, Kim JE, Wang KC, Kim SK, Seo JS, Park SH, Jung HW: The pattern of gene expression and possible relation of steroidogenic genes in oligodendroglial tumors. Int J Oncol; 2009 Jan;34(1):181-90
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pattern of gene expression and possible relation of steroidogenic genes in oligodendroglial tumors.
  • StAR is expressed at a very low level in the white matter of the normal human brain, but is highly expressed in several brain neoplasms including oligodendroglioma (OD).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / genetics. Gene Expression Profiling. Oligodendroglioma / genetics. Steroids / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / metabolism. Brain / pathology. Child. Child, Preschool. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Oligonucleotide Array Sequence Analysis. Phosphoproteins / genetics. Phosphoproteins / metabolism. RNA, Neoplasm. Transcription, Genetic. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19082489.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Phosphoproteins; 0 / RNA, Neoplasm; 0 / Steroids; 0 / steroidogenic acute regulatory protein
  •  go-up   go-down


49. Stege EM, Kros JM, de Bruin HG, Enting RH, van Heuvel I, Looijenga LH, van der Rijt CD, Smitt PA, van den Bent MJ: Successful treatment of low-grade oligodendroglial tumors with a chemotherapy regimen of procarbazine, lomustine, and vincristine. Cancer; 2005 Feb 15;103(4):802-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of low-grade oligodendroglial tumors with a chemotherapy regimen of procarbazine, lomustine, and vincristine.
  • BACKGROUND: Anaplastic oligodendroglioma (OD) tumors, especially those with the combined loss of the short arm of chromosome 1 (1p) and the long arm of chromosome 19 (19q), are sensitive to chemotherapy.
  • METHODS: Two groups of patients were studied: newly diagnosed patients with large OD and mixed oligoastrocytomas (OA) and patients with recurrent OD and OA after radiotherapy who still showed nonenhancing tumors.
  • RESULTS: Three of five patients with recurrent tumors responded.
  • Several patients showed a signficant clinical improvement despite only a modest improvement of the tumor on the MRI scans.
  • CONCLUSIONS: Newly diagnosed patients with OD tumors, with or without loss of 1p/19q, responded to PCV chemotherapy.
  • Up-front chemotherapy may be indicated especially for patients with large tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lomustine / therapeutic use. Magnetic Resonance Imaging. Male. Middle Aged. Polymerase Chain Reaction. Procarbazine / therapeutic use. Retrospective Studies. Tumor Suppressor Protein p53 / genetics. Vincristine / therapeutic use

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LOMUSTINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. PROCARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • (PMID = 15637687.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
  •  go-up   go-down


50. Jeon YK, Park K, Park CK, Paek SH, Jung HW, Park SH: Chromosome 1p and 19q status and p53 and p16 expression patterns as prognostic indicators of oligodendroglial tumors: a clinicopathological study using fluorescence in situ hybridization. Neuropathology; 2007 Feb;27(1):10-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 1p and 19q status and p53 and p16 expression patterns as prognostic indicators of oligodendroglial tumors: a clinicopathological study using fluorescence in situ hybridization.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Genes, p16 / physiology. Genes, p53 / physiology. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Female. Gene Expression. Gene Expression Profiling. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Prognosis. Survival Analysis. Tissue Array Analysis. Tumor Suppressor Protein p53 / genetics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17319279.001).
  • [ISSN] 0919-6544
  • [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 / Tumor Suppressor Protein p53
  •  go-up   go-down


51. van den Bent MJ, Dubbink HJ, Marie Y, Brandes AA, Taphoorn MJ, Wesseling P, Frenay M, Tijssen CC, Lacombe D, Idbaih A, van Marion R, Kros JM, Dinjens WN, Gorlia T, Sanson M: IDH1 and IDH2 mutations are prognostic but not predictive for outcome in anaplastic oligodendroglial tumors: a report of the European Organization for Research and Treatment of Cancer Brain Tumor Group. Clin Cancer Res; 2010 Mar 1;16(5):1597-604
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH1 and IDH2 mutations are prognostic but not predictive for outcome in anaplastic oligodendroglial tumors: a report of the European Organization for Research and Treatment of Cancer Brain Tumor Group.
  • [MeSH-major] Brain Neoplasms / genetics. Isocitrate Dehydrogenase / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Disease-Free Survival. Female. Genes, erbB-1. Humans. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Lomustine / therapeutic use. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Procarbazine / therapeutic use. Prognosis. Promoter Regions, Genetic. Radiotherapy. Treatment Outcome. Tumor Suppressor Proteins / genetics. Vincristine / therapeutic use. Young Adult


52. Li NY, Zhou XJ, Jin XZ, Meng K, Ma HH, Zheng XG, Jiang SJ, Sun GQ: [A clinicopathologic study of dysembryoplstic neuroepithelial tumor]. Zhonghua Bing Li Xue Za Zhi; 2005 Sep;34(9):561-5
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A clinicopathologic study of dysembryoplstic neuroepithelial tumor].
  • OBJECTIVE To study the clinicopathologic features, radiologic findings, treatment modalities and prognosis of dysembryoplastic neuroepithelial tumor (DNT).
  • On magnetic resonance imaging (MRI) study, the tumor was hypodense on T1 and hyperdense on T2.
  • Ten cases were treated by complete surgical excision and the remaining 8 tumors were partially excised.
  • None of the cases showed tumor recurrence after operation.
  • Histologically, all tumors demonstrated a multinodular architecture and were intracortical in location, sometimes with extension into the white matter.
  • The tumor was formed by an admixture of oligodendrocyte-like cells, mature neurons and astrocytes, with obvious microcystic changes.
  • Electron microscopy showed early neuronal, astrocytic and oligodendroglial differentiation of the oligodendrocyte-like cells.
  • CONCLUSIONS: DNT is a benign tumor (corresponding to WHO grade I) that can be cured by surgical excision, despite sometimes incomplete tumor removal.
  • [MeSH-major] Brain Neoplasms / pathology. Cerebral Cortex / pathology. Neoplasms, Neuroepithelial / pathology. Oligodendroglia / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neurofilament Proteins / metabolism. S100 Proteins / metabolism. Survival Rate. Synaptophysin / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16468305.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Synaptophysin
  •  go-up   go-down


53. Lavon I, Refael M, Zelikovitch B, Shalom E, Siegal T: Serum DNA can define tumor-specific genetic and epigenetic markers in gliomas of various grades. Neuro Oncol; 2010 Feb;12(2):173-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum DNA can define tumor-specific genetic and epigenetic markers in gliomas of various grades.
  • We evaluated whether cell-free circulating DNA can be used as a noninvasive approach for detection of genetic/epigenetic alterations in brain tumors during the course of the disease.
  • Paired tumor-serum samples from 70 patients with either high-grade astrocytomas (n = 41) or oligodendrogliomas of various grades were analyzed.
  • DNA was extracted from whole blood, serum, and paraffin-embedded tumor sections.
  • LOH and/or methylation that could identify DNA as tumor-specific was found in 80.5% of astrocytic tumors and in all oligodendrogliomas.
  • Statistically significant tumor-serum concordance was found for MGMT methylation in both astrocytic tumors (83%; P < .001) and oligodendroglial tumors (72%; P < .003) and for LOH of 10q (79%; P < .002) and 1p (62%; P < .03) in oligodendrogliomas.
  • We conclude that serum DNA in glial tumors is informative for both LOH and aberrant gene promoter methylation analysis during the course of the disease.
  • The sensitivity is moderate and specificity is high for both low- and high-grade tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. DNA / blood. Glioma / genetics
  • [MeSH-minor] Adult. Aged. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Epigenesis, Genetic. Female. Humans. Loss of Heterozygosity. Male. Microsatellite Repeats. Middle Aged. PTEN Phosphohydrolase / genetics. Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Suppressor Proteins / genetics. Young Adult

  • 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
  • [Cites] N Engl J Med. 2000 Nov 9;343(19):1350-4 [11070098.001]
  • [Cites] Brain Pathol. 2009 Apr;19(2):279-92 [18616639.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1659-65 [11245480.001]
  • [Cites] Nucleic Acids Res. 2001 Jul 1;29(13):E65-5 [11433041.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):371-5 [11809682.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1461-8 [12684420.001]
  • [Cites] Clin Chem. 2003 Jun;49(6 Pt 1):1028-9 [12766024.001]
  • [Cites] Rocz Akad Med Bialymst. 2003;48:34-41 [14737938.001]
  • [Cites] Pharm Res. 2004 Jul;21(7):1223-8 [15290863.001]
  • [Cites] Oncology. 1989;46(5):318-22 [2779946.001]
  • [Cites] Pancreas. 1998 Jul;17(1):89-97 [9667526.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):67-70 [9892187.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1219-25 [15709192.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] Lung Cancer. 2005 Jul;49(1):1-12 [15949585.001]
  • [Cites] Immunol Lett. 2005 Oct 15;101(1):32-40 [15979158.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 8;102(45):16368-73 [16258065.001]
  • [Cites] Cancer Invest. 2006 Feb;24(1):35-40 [16466990.001]
  • [Cites] Br J Cancer. 2006 May 22;94(10):1492-5 [16641902.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4270-6 [16963729.001]
  • [Cites] Ann N Y Acad Sci. 2006 Sep;1075:299-307 [17108224.001]
  • [Cites] Ann N Y Acad Sci. 2006 Sep;1075:328-33 [17108228.001]
  • [Cites] Oncogene. 2007 Jan 25;26(4):583-93 [16909125.001]
  • [Cites] Arch Pathol Lab Med. 2007 Feb;131(2):242-51 [17284109.001]
  • [Cites] Br J Cancer. 2007 Mar 12;96(5):681-5 [17311021.001]
  • [Cites] Pathology. 2007 Apr;39(2):197-207 [17454749.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4545-9 [17510378.001]
  • [Cites] Bioessays. 2007 Jul;29(7):654-67 [17563084.001]
  • [Cites] Nature. 2008 Apr 3;452(7187):548-52 [18385728.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Jun;66(3):262-72 [18272388.001]
  • [Cites] J Mol Diagn. 2008 Jul;10(4):332-7 [18556773.001]
  • [Cites] BJU Int. 2008 Jul;102(2):253-8 [18336598.001]
  • [Cites] Clin Chem. 2008 Sep;54(9):1528-36 [18653827.001]
  • [Cites] Nat Med. 2008 Sep;14(9):985-90 [18670422.001]
  • [Cites] Clin Chem. 2009 Mar;55(3):559-67 [19131636.001]
  • [Cites] Lung Cancer. 2009 Apr;64(1):92-7 [18804892.001]
  • [Cites] Transfusion. 2001 Feb;41(2):276-82 [11239235.001]
  • (PMID = 20150384.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Proteins; 9007-49-2 / DNA; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC2940579
  •  go-up   go-down


54. Rhee W, Ray S, Yokoo H, Hoane ME, Lee CC, Mikheev AM, Horner PJ, Rostomily RC: Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology. Glia; 2009 Apr 1;57(5):510-23
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology.
  • The capacity of adult human glial progenitor cells (AGPs), to proliferate and undergo multipotent differentiation, positions them as ideal candidate cells of origin for human gliomas.
  • To investigate this potential role we identified AGPs as mitotically active Olig2 cells in nonneoplastic adult human brain and gliomas.
  • Extrapolating from a mean Olig2/Mib-1 labeling index (LI) of 52% and total cell number of 100 billion, we estimated the overall prevalence of mitotic Olig2 AGPs in nonneoplastic human brain parenchyma at 10 million.
  • The vast majority of mitotic cells in Grade II and Grade III gliomas of all histologic subtypes expressed Olig2 (mean LI 75%) but rarely S100B (LI 0.6%), identifying the Olig2 cell as a distinct contributor to the proliferating cell population of human gliomas of both oligodendroglial and astrocytic lineages.
  • The novel framework provided by this quantitative and comparative analysis supports future studies to examine the histogenetic role of Olig2 AGPs in adult gliomas, their potential contribution to the tumor stroma and the molecular role of Olig2 in glioma pathogenesis.

  • Genetic Alliance. consumer health - Glioma.
  • 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] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18837053.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007144; United States / NINDS NIH HHS / NS / T32 NS007144-25; United States / NINDS NIH HHS / NS / T32 NS007144-28; United States / NINDS NIH HHS / NS / T32 NS 0007144
  • [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 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / MIB-1 antibody; 0 / Nerve Growth Factors; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human
  • [Other-IDs] NLM/ NIHMS77469; NLM/ PMC4415884
  •  go-up   go-down


55. Weller M: [Chemotherapy for brain tumors in adult patients]. Nervenarzt; 2008 Feb;79(2):231-41
Zurich Open Access Repository and Archive. Full text from .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chemotherapy for brain tumors in adult patients].
  • Chemotherapy has become a third major treatment option for patients with brain tumors, in addition to surgery and radiotherapy.
  • Outside such clinical trials chemotherapy is used in addition to radiotherapy, e.g., in anaplastic astrocytoma, medulloblastoma or germ cell tumors, or as an alternative to radiotherapy, e.g., in anaplastic oligodendroglial tumors or low-grade gliomas.
  • In contrast, there is no established role for chemotherapy in other tumors such as ependymomas, meningiomas or neurinomas.
  • Primary cerebral lymphomas are probably the only brain tumors which can be cured by chemotherapy alone and only by chemotherapy.
  • The chemotherapy of brain metastases follows the recommendations for the respective primary tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Combined Modality Therapy. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Genetic Markers / genetics. Humans. Prognosis. Promoter Regions, Genetic / genetics. Topotecan / adverse effects. Topotecan / therapeutic use. Tumor Suppressor Proteins / genetics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Topotecan .
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurooncol. 2005 Feb;71(3):271-6 [15735916.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):44-55; discussion 55-6 [12182434.001]
  • [Cites] Neurologist. 2006 Jul;12(4):179-87 [16832237.001]
  • [Cites] Curr Treat Options Neurol. 2006 Jul;8(4):346-57 [16942677.001]
  • [Cites] Nervenarzt. 2003 Dec;74(12):1139-49 [14994756.001]
  • [Cites] J Clin Oncol. 2003 Sep 1;21(17):3276-84 [12947063.001]
  • [Cites] J Neurol. 2005 Mar;252(3):291-9 [16189725.001]
  • [Cites] Cancer. 2005 Jul 1;104(1):143-8 [15912507.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3357-61 [17664483.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] Acta Neurochir (Wien). 2006 Mar;148(3):269-75; discussion 275 [16482400.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):997-1003 [15758010.001]
  • [Cites] Hematol Oncol Clin North Am. 2006 Dec;20(6):1287-95 [17113463.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):987-96 [15758009.001]
  • (PMID = 18253773.001).
  • [ISSN] 0028-2804
  • [Journal-full-title] Der Nervenarzt
  • [ISO-abbreviation] Nervenarzt
  • [Language] ger
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Genetic Markers; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 7M7YKX2N15 / Topotecan; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; YF1K15M17Y / temozolomide
  •  go-up   go-down


56. Abou-Ghazal M, Yang DS, Qiao W, Reina-Ortiz C, Wei J, Kong LY, Fuller GN, Hiraoka N, Priebe W, Sawaya R, Heimberger AB: The incidence, correlation with tumor-infiltrating inflammation, and prognosis of phosphorylated STAT3 expression in human gliomas. Clin Cancer Res; 2008 Dec 15;14(24):8228-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The incidence, correlation with tumor-infiltrating inflammation, and prognosis of phosphorylated STAT3 expression in human gliomas.
  • RESULTS: We did not detect p-STAT3 expression in normal brain tissues or low-grade astrocytomas.
  • We observed significant differences in the incidence of p-STAT3 expression between the different grades of astrocytomas and different pathologic glioma types. p-STAT3 expression was associated with the population of tumor-infiltrating immune cells but not with that of T regulatory cells.
  • CONCLUSIONS: p-STAT3 expression is common within gliomas of both the astrocytic and oligodendroglial lineages and portends poor survival in patients with anaplastic astrocytomas. p-STAT3 expression differs significantly between gliomas of different pathologic types and grades and correlated with the degree of immune infiltration.

  • 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] Cancer Res. 2002 Jun 15;62(12):3351-5 [12067972.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5423-34 [17000676.001]
  • [Cites] J Immunol. 2002 Sep 1;169(5):2253-63 [12193690.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1270-9 [12649187.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4138-43 [12640143.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3692-9 [14506160.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7443-50 [14612544.001]
  • [Cites] Nat Rev Cancer. 2004 Feb;4(2):97-105 [14964307.001]
  • [Cites] Anticancer Res. 2004 Jan-Feb;24(1):37-42 [15015573.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1682-8 [15117990.001]
  • [Cites] Lab Invest. 2004 Aug;84(8):941-51 [15184909.001]
  • [Cites] Nat Med. 2004 Sep;10(9):942-9 [15322536.001]
  • [Cites] J Clin Invest. 2004 Sep;114(5):720-8 [15343391.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 3;321(4):828-34 [15358102.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Ann Neurol. 1978 Sep;4(3):219-24 [718133.001]
  • [Cites] J Neurosurg. 1984 Jun;60(6):1138-47 [6374063.001]
  • [Cites] Endocrinology. 1995 Mar;136(3):897-902 [7867598.001]
  • [Cites] Stroke. 1995 Aug;26(8):1393-8 [7631343.001]
  • [Cites] EMBO J. 1998 Feb 16;17(4):1006-18 [9463379.001]
  • [Cites] Immunity. 1999 Jan;10(1):39-49 [10023769.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):267-72 [15671555.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1053-65 [15558012.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):970-9 [15592503.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8288-94 [16322287.001]
  • [Cites] Nat Med. 2005 Dec;11(12):1314-21 [16288283.001]
  • [Cites] Int J Biol Markers. 2006 Jul-Sep;21(3):175-83 [17013800.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Dec;65(12):1181-8 [17146292.001]
  • [Cites] Nat Rev Immunol. 2007 Jan;7(1):41-51 [17186030.001]
  • [Cites] J Clin Pathol. 2007 Feb;60(2):173-9 [17264243.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):902-11 [17289884.001]
  • [Cites] Lung Cancer. 2007 Mar;55(3):349-55 [17161498.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1362-6 [17332277.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2075-81 [17404089.001]
  • [Cites] Oncogene. 2007 Apr 12;26(17):2435-44 [17043651.001]
  • [Cites] J Immunother. 2007 Feb-Mar;30(2):131-9 [17471161.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7391-6 [17463090.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):642-8 [16901975.001]
  • [Cites] Clin Cancer Res. 2007 Jun 15;13(12):3559-67 [17575219.001]
  • [Cites] J Clin Oncol. 2007 Jun 20;25(18):2586-93 [17577038.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9630-6 [17942891.001]
  • [Cites] Clin Cancer Res. 2008 Aug 15;14(16):5166-72 [18698034.001]
  • [Cites] Clin Cancer Res. 2008 Sep 15;14(18):5759-68 [18794085.001]
  • [Cites] J Neurotrauma. 2001 Mar;18(3):351-9 [11284554.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1386-93 [15746037.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1462-6 [15746047.001]
  • [Cites] World J Gastroenterol. 2005 Jun 14;11(22):3385-91 [15948243.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9589-94 [15976028.001]
  • [Cites] J Clin Pathol. 2005 Aug;58(8):833-8 [16049285.001]
  • [Cites] Gynecol Oncol. 2005 Sep;98(3):446-52 [16005944.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18538-43 [16344461.001]
  • [Cites] Ai Zheng. 2006 Mar;25(3):269-74 [16536977.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3188-96 [16540670.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3355-60 [16740757.001]
  • [Cites] Neuro Oncol. 2006 Jul;8(3):261-79 [16775224.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1571-9 [16645171.001]
  • [Cites] J Urol. 2002 Aug;168(2):762-5 [12131365.001]
  • (PMID = 19088040.001).
  • [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 / CA120813-01A1; United States / NCI NIH HHS / CA / R01 CA120813; 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 / STAT3 Transcription Factor; 0 / STAT3 protein, human
  • [Other-IDs] NLM/ NIHMS78715; NLM/ PMC2605668
  •  go-up   go-down


57. Maiuri F, Del Basso De Caro M, Siciliano A, Peca C, Vergara P, Mariniello G, Pettinato G: Expression of growth factors in brain tumors: correlation with tumor grade, recurrence and survival. Clin Neuropathol; 2010 Mar-Apr;29(2):109-14
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of growth factors in brain tumors: correlation with tumor grade, recurrence and survival.
  • OBJECTIVE: The aim of this study is to evaluate the correlation between the expression of some growth factors (GFs) and the tumor grade, recurrence and survival of brain glial and ependymal tumors.
  • MATERIAL AND METHODS: The expression of vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR), tenascine, transforming growth factor (TGFbeta), isomeres, platelet-derived growth factor (PDGF) and p53 was studied in 40 primary brain tumors, both low-grade and high-grade, including astrocytomas, oligodendrogliomas, glioblastomas and ependymomas.
  • The same GFs were also studied in 46 specimens of recurrent tumors from the same patients.
  • The positivity and intensity of the immunohistochemical expression were correlated with the tumor grade, the interval and type of recurrence, and the survival.
  • RESULTS: The expression of all GFs, excepting TGFbeta1, TGFbetaRI and tenascine, was found to be correlated with the tumor grade in all tumors of both astroglial and oligodendroglial origin, whereas ependymomas showed significant differences only for EGFR.
  • Low-grade (Grade II) tumors recurring as anaplastic (Grade III) forms showed GF expression rather similar to initially high-grade gliomas and significantly higher than that of low-grade (Grade II) tumors in both initial surgery and recurrence.
  • Besides, low-grade (Grade II) tumors recurring as low-grade showed significantly longer median recurrence time (5.4 vs. 3.5 years) and better median survival (8.3 vs. 5.4 years) than those recurring as anaplastic forms (WHO III).
  • CONCLUSION: The immunohistochemical study of expression of VEGF, EGFR, TGFbeta2, TGFbeta3, PDGF and p53 in all low-grade (Grade II) brain gliomas at the first operation may help to differentiate cases with slower evolution and longer survival from those with higher potential of anaplastic transformation.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Brain Neoplasms / pathology. Intercellular Signaling Peptides and Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Middle Aged. Neoplasm Recurrence, Local / metabolism. Prognosis. Young Adult

  • 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 = 20175962.001).
  • [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; 0 / Intercellular Signaling Peptides and Proteins
  •  go-up   go-down


58. Chen L, Xu QZ, Piao YS, Zhang GJ, Yu T, Yang XP, Yang H, Lu DH: [Dysembryoplastic neuroepithelial tumor: a clinicopathologic and immunohistochemical study]. Zhonghua Bing Li Xue Za Zhi; 2007 Aug;36(8):524-8
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Dysembryoplastic neuroepithelial tumor: a clinicopathologic and immunohistochemical study].
  • OBJECTIVE: To study the clinicopathologic features, immunophenotype and histogenesis of dysembryoplastic neuroepithelial tumor (DNT).
  • Histologically, the tumor consisted of a heterogeneous admixture of neuronal and glial cells (including 1 simple form case, 8 complex form cases and 5 non-specific form cases).
  • Immunohistochemically, the oligodendroglial-like cells expressed Olig2.
  • No tumor recurrence was detected.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Brain Neoplasms / pathology. Malformations of Cortical Development / pathology. Neoplasms, Neuroepithelial / pathology. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Anticonvulsants / therapeutic use. Child. Child, Preschool. Epilepsy / drug therapy. Epilepsy / etiology. Female. Follow-Up Studies. Humans. Infant. Intermediate Filament Proteins / metabolism. Male. Microtubule-Associated Proteins / metabolism. Nestin. Oligodendroglia / pathology. Retrospective Studies. Young Adult

  • Genetic Alliance. consumer health - Dysembryoplastic Neuroepithelial Tumor.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17980099.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Intermediate Filament Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / OLIG2 protein, human
  •  go-up   go-down


59. 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
The Lens. Cited by Patents in .

  • [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.
  • Taken together, our study provides a set of interesting novel candidate genes that may play important roles in the pathogenesis of oligodendroglial tumors.
  • [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
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA, Complementary / genetics. Down-Regulation. Female. Humans. Male. Middle Aged. Transcription, Genetic / genetics. Up-Regulation

  • 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 .
  • [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
  •  go-up   go-down


60. Kordes U, Hagel C: Expression of SOX9 and SOX10 in central neuroepithelial tumor. J Neurooncol; 2006 Nov;80(2):151-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of SOX9 and SOX10 in central neuroepithelial tumor.
  • We have examined the pattern of expression for SOX9 and SOX10 in primary brain tumors by immunohistochemistry.
  • Pediatric and adult high grade tumors display strong nuclear staining for both SOX9 and SOX10 (astrocytic, oligodendroglial and primitive neuroectodermal tumors).
  • [MeSH-minor] Adolescent. Adult. Astrocytes / metabolism. Cell Nucleus / pathology. Child. Child, Preschool. Gene Expression Regulation, Neoplastic / genetics. Gliosis / pathology. Humans. Immunohistochemistry. Oligodendroglia / metabolism. Paraffin Embedding. SOX9 Transcription Factor. SOXE Transcription Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16791471.001).
  • [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] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / SOX10 protein, human; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; 0 / SOXE Transcription Factors; 0 / Transcription Factors
  •  go-up   go-down


61. Barbashina V, Salazar P, Ladanyi M, Rosenblum MK, Edgar MA: Glioneuronal tumor with neuropil-like islands (GTNI): a report of 8 cases with chromosome 1p/19q deletion analysis. Am J Surg Pathol; 2007 Aug;31(8):1196-202
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioneuronal tumor with neuropil-like islands (GTNI): a report of 8 cases with chromosome 1p/19q deletion analysis.
  • Glioneuronal tumor with neuropil-like islands (GTNI) is a rare neoplasm harboring circumscribed loci of neuronal differentiation and diffusely infiltrating astroglial and oligodendrocytelike components.
  • All tumors showed characteristic histologic features and immunoprofile.
  • One primary tumor displayed frankly malignant histology with frequent mitoses, microvascular proliferation, and necrosis.
  • This tumor progressed within months of the initial resection.
  • Three other tumors (2 low-grade and 1 showing only focal microvascular proliferation) recurred at 2 years, 3 years, and 1 year, respectively.
  • No evidence of 1p/19q losses was found in 7 of 8 tumors.
  • One tumor demonstrated small interstitial deletions at 1p36 (at D1S1612 and D1S513, but not at D1S548 or D1S1592) and a small interstitial deletion at 19q13 (at D19S219 and D19S412, but not at PLA2G4C).
  • The lack of large, whole-arm 1p/19q losses (such as those found in oligodendroglial tumors), aberrant p53 expression, and the predominance of astroglial components may indicate a biologic relationship of the GTNI to diffuse astrocytoma.
  • Although GTNI shares some morphologic features with recently reported cases of oligodendroglioma with neurocytic differentiation, the 2 tumors appear different at the molecular genetic level.
  • [MeSH-major] Brain Neoplasms / pathology. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Ganglioglioma / pathology. Neuropil / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Combined Modality Therapy. DNA, Neoplasm / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Recurrence, Local. Synaptophysin / analysis

  • Genetic Alliance. consumer health - Chromosome 8 Deletion.
  • 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 = 17667543.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Synaptophysin
  •  go-up   go-down


62. Chen Z, Ma L, Lou X, Zhou Z: Diagnostic value of minimum apparent diffusion coefficient values in prediction of neuroepithelial tumor grading. J Magn Reson Imaging; 2010 Jun;31(6):1331-8
MedlinePlus Health Information. consumer health - MRI Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic value of minimum apparent diffusion coefficient values in prediction of neuroepithelial tumor grading.
  • PURPOSE: To retrospectively evaluate the diagnostic accuracy of diffusion weighted image (DWI) in the prediction of neuroepithelial tumors grading, and to appraise the apparent diffusion coefficient (ADC) value of neuroepithelial tumors with histologic findings as a reference standard.
  • MATERIALS AND METHODS: ADC values in 110 patients with pathologically proved neuroepithelial tumors, including 77 astrocytic tumors, 16 oligodendroglial tumors, 11 oligoastrocytic tumors, and 6 ependymal tumors, were investigated retrospectively.
  • The minimum ADC (MinADC) value of tumors was measured postoperatively on ADC maps, avoiding cystic, necrotic, or hemorrhagic components.
  • The area under the ROC curve (AUC) was 0.809, and the cutoff MinADC value of 0.900 x 10(-3) mm(2)/s for the differentiation between high and low grade neuroepithelial tumors provided the best combination of sensitivity (85.4%) and specificity (71.0%).
  • CONCLUSION: MinADC value may be a simple and effective optional tool for the prediction of neuroepithelial tumor grading.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diffusion. Female. Humans. Ki-67 Antigen / biosynthesis. Male. Middle Aged. ROC Curve. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Magn Reson Imaging. 2011 Mar;33(3):755; author reply 756 [21563262.001]
  • (PMID = 20512884.001).
  • [ISSN] 1522-2586
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen
  •  go-up   go-down


63. Ichimura K, Pearson DM, Kocialkowski S, Bäcklund LM, Chan R, Jones DT, Collins VP: IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas. Neuro Oncol; 2009 Aug;11(4):341-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas.
  • We screened exon 4 of the gene isocitrate dehydrogenase 1 (NADP+), soluble (IDH1) for mutations in 596 primary intracranial tumors of all major types.
  • Codon 132 mutation was seen in 54% of astrocytomas and 65% of oligodendroglial tumors but in only 6% of glioblastomas (3% of primary and 50% of secondary glioblastomas).
  • There were no mutations in any other type of tumor studied.
  • While mutations in the tumor protein p53 gene (TP53) and total 1p/19q deletions were mutually exclusive, IDH1 mutations were strongly correlated with these genetic abnormalities.
  • The data indicate that IDH1 mutation combined with either TP53 mutation or total 1p/19q loss is a frequent and early change in the majority of oligodendroglial tumors, diffuse astrocytomas, anaplastic astrocytomas, and secondary glioblastomas but not in primary glioblastomas.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Isocitrate Dehydrogenase / genetics. Mutation / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Comparative Genomic Hybridization. Exons / genetics. Genotype. Humans. Loss of Heterozygosity. Prognosis. Tumor Suppressor Protein p53 / genetics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cell lines described in this publication .
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neuropathol Exp Neurol. 1999 Nov;58(11):1170-83 [10560660.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):30527-33 [10521434.001]
  • [Cites] Cell Growth Differ. 2000 Jul;11(7):373-84 [10939591.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):839-45 [11309331.001]
  • [Cites] Int J Biochem Cell Biol. 2002 Feb;34(2):148-57 [11809417.001]
  • [Cites] Free Radic Biol Med. 2002 Jun 1;32(11):1185-96 [12031902.001]
  • [Cites] Free Radic Res. 2003 Mar;37(3):309-16 [12688426.001]
  • [Cites] J Biol Chem. 2004 Aug 6;279(32):33946-57 [15173171.001]
  • [Cites] Biochemistry. 1997 Nov 4;36(44):13743-7 [9354646.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Oct;58(10):1041-50 [10515227.001]
  • [Cites] Acta Neuropathol. 2005 Jan;109(1):93-108 [15685439.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Jun;65(6):549-61 [16783165.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):9852-61 [17047046.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Nov;65(11):1049-58 [17086101.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Jun;4(6):362-74 [17534392.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8673-7 [18974108.001]
  • [Cites] Acta Neuropathol. 2008 Dec;116(6):597-602 [18985363.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):417-24 [10667596.001]
  • (PMID = 19435942.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 1.1.1.41 / Isocitrate Dehydrogenase
  • [Other-IDs] NLM/ PMC2743214; NLM/ UKMS28703
  •  go-up   go-down


64. Yao Y, Tang X, Li S, Mao Y, Zhou L: Brain tumor stem cells: view from cell proliferation. Surg Neurol; 2009 Mar;71(3):274-9
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain tumor stem cells: view from cell proliferation.
  • A small population of TSCs, which form neurospheres and possess the capacity for self-renewal, has been recently identified in adult and pediatric brain tumors.
  • They differentiate into phenotypically diverse populations, including neuronal, astrocytic, and oligodendroglial cells in vitro and recapitulate original tumors in vivo.
  • The understanding of brain TSCs has been greatly advanced by the knowledge of cell proliferation, which contributes to initiate and sustain the malignant phenotype.
  • In this article, the authors summarized the evidence of the presence of TSCs in human brain tumors and emphasized the significance of the proliferative status of TSCs.
  • Finally, the preliminary evidence that TSCs in malignant brain tumors have more proliferative capacity than stem/progenitor cells in benign brain tumors was discussed.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19249579.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 40
  •  go-up   go-down


65. Barbashina V, Salazar P, Holland EC, Rosenblum MK, Ladanyi M: Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene. Clin Cancer Res; 2005 Feb 1;11(3):1119-28
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene.
  • Because most 1p deletions in gliomas involve almost the entire chromosome arm, narrowing the region of the putative tumor suppressor gene has been difficult.
  • EXPERIMENTAL DESIGN: Among 205 consecutive cases of glioma studied for 1p loss of heterozygosity (LOH), 112 tumors were evaluated for both 1p and 19q LOH using at least three polymorphic markers on 1p and 19q each.
  • The latter group included both low-grade tumors (oligodendroglioma, diffuse astrocytoma, and "oligoastrocytoma") and high-grade tumors (anaplastic oligodendrogliomas, anaplastic astrocytomas, anaplastic oligoastrocytomas).
  • Tumors with small segmental 1p losses (defined as LOH at some loci with retention of heterozygosity at other loci) were studied using a more extensive panel of markers to define the 1p MDR.
  • In contrast, no astrocytomas and only 6 of 30 (20%) oligoastrocytic tumors had combined 1p/19q loss.
  • Eleven tumors (6 oligodendrogliomas or having oligodendroglial components, 5 purely astrocytic) with small segmental 1p losses underwent further detailed LOH mapping.
  • All informative tumors in the oligodendroglial group and 2 of 3 informative astrocytomas showed LOH at 1p36.23, with a 150-kb MDR located between D1S2694 and D1S2666, entirely within the CAMTA1 transcription factor gene.
  • CAMTA1 is normally expressed predominantly in non-neoplastic adult brain tissue.
  • Relative to the latter, the expression level of CAMTA1 was low in oligodendroglial tumors and was further halved in cases with 1p deletion compared with those without 1p deletion (Mann-Whitney, P = 0.03).
  • CONCLUSIONS: Our data confirm the strong association of combined 1p/19q loss with classic oligodendroglioma histology and identify a very small segment of 1p36 located within CAMTA1 that was deleted in all oligodendroglial tumors with 1p LOH.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioma / genetics. Loss of Heterozygosity
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Calcium-Binding Proteins / genetics. Chromosome Deletion. Chromosome Mapping. Expressed Sequence Tags. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Microsatellite Repeats. Mutation. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators / genetics

  • 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 = 15709179.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CAMTA1 protein, human; 0 / Calcium-Binding Proteins; 0 / Trans-Activators
  •  go-up   go-down


66. Majumdar K, Radotra BD, Vasishta RK, Pathak A: Platelet-derived growth factor expression correlates with tumor grade and proliferative activity in human oligodendrogliomas. Surg Neurol; 2009 Jul;72(1):54-60
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet-derived growth factor expression correlates with tumor grade and proliferative activity in human oligodendrogliomas.
  • BACKGROUND: For the last one and a half decade, it has been found that platelet-derived growth factor (PDGF) promotes glial tumor growth through autocrine and paracrine loops, by expression of PDGFalpha receptor (PDGFRalpha) on glioma cells and PDGFbeta receptor (PDGFRbeta) on proliferating endothelial cells.
  • However, studies on oligodendrogliomas, correlating expression of PDGF and its receptor with tumor grade and proliferative activity, through MIB-1 labeling index (LI) are relatively few as compared to astroglial counterpart.
  • METHODS: Formalin-fixed paraffin-embedded tissues from 55 cases of oligodendrogliomas (34 World Health Organization [WHO] grade II and 21 WHO grade III tumors) were subjected to immunohistochemistry.
  • The PDGF expression scores had a positive correlation with MIB-1 LI, irrespective of tumor grade (Pearson's correlation coefficient, r = 0.566; P < .001).
  • However, there was no significant difference of PDGFRalpha expression between 2 grades of tumors.
  • CONCLUSIONS: The results of this study showed that MIB-1 LI is a rapid and cost-effective modality for predicting tumor grade in oligodendrogliomas.
  • Immunohistochemistry for PDGF was found to be useful in differentiating various grades of oligodendroglioma, and therefore, it may be involved in tumor cell proliferation and malignant transformation.
  • Platelet-derived growth factor receptor alpha, although expressed in oligodendroglial neoplasms, was not found to be useful in predicting tumor grade.
  • [MeSH-major] Antibodies, Antinuclear / metabolism. Antibodies, Monoclonal / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. Platelet-Derived Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Cost-Benefit Analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry / economics. Immunohistochemistry / methods. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Sensitivity and Specificity. Time Factors. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19559929.001).
  • [ISSN] 1879-3339
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / MIB-1 antibody; 0 / Platelet-Derived Growth Factor
  •  go-up   go-down


67. Jeuken JW, van der Maazen RW, Wesseling P: Molecular diagnostics as a tool to personalize treatment in adult glioma patients. Technol Cancer Res Treat; 2006 Jun;5(3):215-29
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular diagnostics as a tool to personalize treatment in adult glioma patients.
  • Gliomas, the most frequent primary brain tumors in humans, form a heterogeneous group, encompassing many different histological types and malignancy grades.
  • The major representatives in this subgroup are the diffuse astrocytic, oligodendroglial, and mixed oligo-astrocytic tumors.
  • After summarizing the most relevant genetic aberrations and pathways in these tumors detected up till now, this review will discuss the clinical relevance of this information.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioma / genetics. Molecular Diagnostic Techniques
  • [MeSH-minor] Cell Cycle Proteins / genetics. DNA Methylation. DNA Repair. Gene Dosage. Humans. Neovascularization, Pathologic. Receptor Protein-Tyrosine Kinases / genetics. Retinoblastoma Protein / genetics. Tumor Suppressor Protein p53 / genetics

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16700618.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 94
  •  go-up   go-down


68. Fontaine D, Vandenbos F, Lebrun C, Paquis V, Frenay M: [Diagnostic and prognostic values of 1p and 19q deletions in adult gliomas: critical review of the literature and implications in daily clinical practice]. Rev Neurol (Paris); 2008 Jun-Jul;164(6-7):595-604
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnostic and prognostic values of 1p and 19q deletions in adult gliomas: critical review of the literature and implications in daily clinical practice].
  • In grade 3 oligodendroglial tumors, the probability of responding to chemotherapy, and the duration of response, were higher when codeletions were present.
  • This suggests that, in these tumors, the presence of codeletion is a strong argument in favor of adjuvant chemotherapy.
  • Oligodendroglial tumors with 1p deletion or 1p19q codeletion seemed to have a better prognosis, as five-year survival rates were 50% higher than in tumors without deletion.
  • (1) higher chemosensitivity, (2) tumor location more frequently in the frontal lobe, leading to better resection and lower risk of neurological deficit, (3) slower growth rate, (4) higher risk of epilepsy, leading to an early detection.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioma / genetics. Glioma / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18565359.001).
  • [ISSN] 0035-3787
  • [Journal-full-title] Revue neurologique
  • [ISO-abbreviation] Rev. Neurol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 63
  •  go-up   go-down


69. Yakut T, Gutenberg A, Bekar A, Egeli U, Gunawan B, Ercan I, Tolunay S, Doygun M, Schulten HJ: Correlation of chromosomal imbalances by comparative genomic hybridization and expression of EGFR, PTEN, p53, and MIB-1 in diffuse gliomas. Oncol Rep; 2007 May;17(5):1037-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The most frequent imbalances in oligodendroglial tumors including the oligoastrocytic case were, in decreasing order of frequency, +7q, -1p, and -4q and in astrocytomas +7q, -10q, +7p, -9p, -10p, +20q, and +20p.
  • In addition, p53 overexpression correlated positively with +7q and negatively with -1p in the oligodendroglial group whereas EGFR overexpression correlated positively with -1p in the oligodendroglial and positively with +7p and -10p in the astrocytic group.
  • Collectively, these results contribute to the increasing clinical relevance of assessing tumor biological markers in gliomas.
  • [MeSH-major] Chromosome Aberrations. Glioma / genetics. PTEN Phosphohydrolase / biosynthesis. Receptor, Epidermal Growth Factor / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis. Ubiquitin-Protein Ligases / biosynthesis
  • [MeSH-minor] Adult. Aged. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Nucleic Acid Hybridization / methods

  • 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 = 17390041.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MIB1 ligase, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


70. Ren XH, Cui XL, Lin S, Wang ZC: [The correlation between combining 1p/19q LOH and pathology in gliomas]. Zhonghua Yi Xue Za Zhi; 2010 Jul 6;90(25):1781-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Tumor samples from 127 glioma patients were collected.
  • RESULTS: The frequencies of combining 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 19.30%, 50.00% and 80.77% respectively.
  • The frequencies of combining 1p/19q LOH in oligoastrocytic and oligodendroglial tumors were higher than those in astrocytic tumors (P < 0.01) and the frequencies of combining 1p/19q LOH in oligodendroglial tumors was higher than those in oligoastrocytic tumors (P < 0.05).
  • The frequencies of 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 12.28%, 11.36 and 0 respectively.
  • It is significantly correlated with oligodendroglial component.
  • Combining 1p/19q LOH may be valuable in the diagnosis, treatment and prognostic prediction for glioma with oligodendroglial component.
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. Male. Middle Aged. Oligodendroglia / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20979900.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


71. Phi JH, Park SH, Kim SK, Paek SH, Kim JH, Lee YJ, Cho BK, Park CK, Lee DH, Wang KC: Sox2 expression in brain tumors: a reflection of the neuroglial differentiation pathway. Am J Surg Pathol; 2008 Jan;32(1):103-12
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sox2 expression in brain tumors: a reflection of the neuroglial differentiation pathway.
  • Moreover, it was recently found that brain tumors contain stem cells that resemble normal neuroglial stem cells in many respects.
  • This study was undertaken to describe Sox2 expression in various brain tumors, and to determine whether Sox2 expression is a universal feature of brain tumors, or whether its expression is limited to a specific lineage of brain tumors.
  • Sox2 immunohistochemistry was performed on 194 brain tumor tissues of various kinds.
  • Fetal and adult normal brain tissues obtained by autopsy and brain tissues of epilepsy patients with cortical dysplasia were used as controls.
  • Sox2 was found to be expressed in various glial tumors, including those with astroglial, oligodendroglial, and ependymal lineages, and in the glial components of mixed neuroglial tumors, regardless of pathologic grade.
  • In brain tumors of embryonal origin, supratentorial primitive neuroectodermal tumors showed robust Sox2 expression, whereas medulloblastomas and pineoblastomas did not.
  • The majority of Sox2-positive tumor cells coexpressed glial fibrillary acidic protein, and most Sox2-negative cells in medulloblastomas and pineoblastomas showed neuronal differentiation.
  • This study suggest that Sox2 may be a tumor marker of glial lineages rather than a universal brain tumor stem cell marker, because its expression pattern was found to correspond to differentiation pathways.
  • On the other hand, the aberrant coexpressions of Sox2 and of a neuronal marker were widely observed in glioblastomas, which reflects a disorganized differentiation pattern that characterizes highly malignant tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. HMGB Proteins / biosynthesis. Neuroglia / cytology. Neuroglia / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Brain / cytology. Brain / embryology. Brain / metabolism. Cell Differentiation. Cell Lineage. Fluorescent Antibody Technique. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. SOXB1 Transcription Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18162777.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / HMGB Proteins; 0 / RNA, Messenger; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors; 0 / Transcription Factors
  •  go-up   go-down


72. Frenel JS, Botti M, Loussouarn D, Campone M: [Prognostic and predictive factors for gliomas in adults]. Bull Cancer; 2009 Apr;96(4):357-67
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant gliomas are the most prevalent type of primary brain tumor in adults.
  • Because patients with a same histologic diagnosis have variable outcomes, there is a need to develop better prognostic markers to predict tumor behaviour and response to therapy.
  • For patients with low-grade gliomas, several clinical parameters affect prognosis and therapeutic options: histological type, tumor measurements, young age, performance status.
  • For high-grade tumors, prognostic and predictive molecular markers have been identified.
  • The combined loss of 1p and 19q is strongly correlated with the oligodendroglial phenotype and is associated with both chemotherapeutic response and prolonged overall survival in anaplastic (grade III) oligodendrogliomas treated with PCV chemotherapy and probably with temozolomide.
  • [MeSH-major] Brain Neoplasms. Glioma
  • [MeSH-minor] Adult. Age Factors. Biomarkers, Tumor / metabolism. Chromosome Deletion. Humans. PTEN Phosphohydrolase / metabolism. Predictive Value of Tests. Prognosis. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Treatment Outcome. Tumor Burden

  • 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 = 19357011.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 52
  •  go-up   go-down


73. Traiffort E, Ruat M, O'Regan S, Meunier FM: Molecular characterization of the family of choline transporter-like proteins and their splice variants. J Neurochem; 2005 Mar;92(5):1116-25
SciCrunch. HGNC: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In adult rat tissues, CTL2-4 mRNAs are mainly detected in peripheral tissues, while CTL1 is widely expressed throughout the nervous system.
  • In the developing brain, CTL1a is expressed in both neurones and oligodendroglial cells, whereas CTL1b is restricted to oligodendroglial cells.
  • [MeSH-minor] Amino Acid Sequence. Animals. Animals, Newborn. Blotting, Northern / methods. Brain / cytology. Brain / metabolism. Cell Line, Tumor. Choline / metabolism. Choline O-Acetyltransferase / metabolism. DNA / isolation & purification. Humans. In Situ Hybridization / methods. Male. Mice. Molecular Sequence Data. Myelin Basic Protein / metabolism. Neuroblastoma. Neurons / metabolism. Oligodendroglia / metabolism. Peripheral Nerves / metabolism. Phylogeny. Protein Isoforms. RNA / isolation & purification. RNA, Messenger. Rats. Rats, Wistar. Transfection / methods. Tritium / metabolism


74. Tejada S, Lobo MV, García-Villanueva M, Sacristán S, Pérez-Morgado MI, Salinas M, Martín ME: Eukaryotic initiation factors (eIF) 2alpha and 4E expression, localization, and phosphorylation in brain tumors. J Histochem Cytochem; 2009 May;57(5):503-12
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eukaryotic initiation factors (eIF) 2alpha and 4E expression, localization, and phosphorylation in brain tumors.
  • One or both of these factors are often overexpressed in several types of cancer cells; however, no data are available at present regarding eIF4E and eIF2alpha levels in brain tumors.
  • In this study, we analyzed the expression, subcellular localization and phosphorylation states of eIF4E and eIF2alpha in 64 brain tumors (26 meningiomas, 16 oligodendroglial tumors, and 22 astrocytomas) and investigated the correlation with the expression of MIB-1, p53, and cyclin D1 proteins as well.
  • There are significant differences in the phosphorylated eIF4E levels between the tumors studied, being the highest in meningiomas and the lowest in the oligodendroglial tumors.
  • Relative to subcellular localization, eIF4E is frequently found in the nucleus of the oligodendroglial tumors and rarely in the same compartment of the meningiomas, whereas eIF2alpha showed an inverse pattern.
  • The different expression, phosphorylation, or/and subcellular distribution of eIF2alpha and eIF4E within the brain types of tumors studied could indicate that different pathways are activated for promoting cell cycle proliferation, for instance, leading to increased cyclin D1 expression.
  • [MeSH-major] Brain Neoplasms / metabolism. Eukaryotic Initiation Factor-2 / metabolism. Eukaryotic Initiation Factor-4E / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Cyclin D1 / metabolism. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Phosphorylation. Tumor Suppressor Protein p53 / metabolism. Young Adult

  • 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
  • [Cites] Am J Pathol. 2000 Feb;156(2):425-32 [10666371.001]
  • [Cites] J Clin Neurosci. 2005 Feb;12(2):166-8 [15749420.001]
  • [Cites] Histochem J. 2000 Mar;32(3):139-50 [10841309.001]
  • [Cites] Pathol Res Pract. 2000;196(7):483-8 [10926326.001]
  • [Cites] Biochem J. 2000 Oct 15;351 Pt 2:327-34 [11023817.001]
  • [Cites] Cancer. 2001 Oct 15;92(8):2164-71 [11596034.001]
  • [Cites] Mol Cell. 2000 Nov;6(5):1099-108 [11106749.001]
  • [Cites] Cell. 2002 Feb 22;108(4):545-56 [11909525.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Apr;6(4):318-27 [15803138.001]
  • [Cites] J Cell Biol. 2005 Apr 25;169(2):245-56 [15837800.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2005 Jun;13(2):178-83 [15894932.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4215-24 [15961768.001]
  • [Cites] Cell Cycle. 2007 Jan 1;6(1):65-9 [17245113.001]
  • [Cites] Arch Pathol Lab Med. 2007 Feb;131(2):234-41 [17284108.001]
  • [Cites] J Clin Neurosci. 2007 Apr;14(4):355-8 [17240151.001]
  • [Cites] Nat Rev Genet. 2007 Jul;8(7):533-43 [17572691.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Genes Dev. 2007 Dec 15;21(24):3232-7 [18055695.001]
  • [Cites] Oncogene. 2008 Mar 6;27(11):1645-9 [17828301.001]
  • [Cites] Cell Cycle. 2008 Mar 1;7(5):553-5 [18256539.001]
  • [Cites] Cell Mol Neurobiol. 2008 Sep;28(6):907-13 [18379871.001]
  • [Cites] Differentiation. 2002 Mar;70(1):10-22 [11963652.001]
  • [Cites] Thyroid. 2001 Dec;11(12):1101-7 [12186496.001]
  • [Cites] Eur J Biochem. 2002 Nov;269(22):5350-9 [12423333.001]
  • [Cites] Oncogene. 2002 Dec 12;21(57):8741-8 [12483527.001]
  • [Cites] Oncogene. 2004 Apr 19;23(18):3189-99 [15094768.001]
  • [Cites] Oncogene. 2004 Apr 19;23(18):3230-47 [15094773.001]
  • [Cites] Pathol Int. 2004 Jun;54(6):387-91 [15144396.001]
  • [Cites] Cell Tissue Res. 2004 Jun;316(3):369-76 [15127288.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11269-74 [15277680.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Oct;5(10):827-35 [15459663.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Science. 1992 Sep 18;257(5077):1685-9 [1382315.001]
  • [Cites] Cancer Res. 1993 Jun 15;53(12):2736-9 [8504413.001]
  • [Cites] Cell. 1994 Nov 18;79(4):573-82 [7954824.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1065-70 [8577715.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4382-6 [8813130.001]
  • [Cites] Neuropathol Appl Neurobiol. 1996 Aug;22(4):311-6 [8875465.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Feb;56(2):180-5 [9034372.001]
  • [Cites] Acta Neuropathol. 1998 Feb;95(2):131-5 [9498046.001]
  • [Cites] Neuropathol Appl Neurobiol. 1998 Oct;24(5):381-8 [9821169.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Jan;31(1):1-23 [10216939.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Jan;31(1):73-86 [10216945.001]
  • [Cites] Am J Pathol. 1999 Jul;155(1):247-55 [10393856.001]
  • [Cites] Endocrinology. 2004 Dec;145(12):5439-47 [15331580.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8639-42 [15574771.001]
  • [Cites] Int J Biochem Cell Biol. 2000 Jun;32(6):633-42 [10785360.001]
  • (PMID = 19188486.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Eukaryotic Initiation Factor-2; 0 / Eukaryotic Initiation Factor-4E; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC2675073
  •  go-up   go-down


75. Schittenhelm J, Trautmann K, Tabatabai G, Hermann C, Meyermann R, Beschorner R: Comparative analysis of annexin-1 in neuroepithelial tumors shows altered expression with the grade of malignancy but is not associated with survival. Mod Pathol; 2009 Dec;22(12):1600-11
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative analysis of annexin-1 in neuroepithelial tumors shows altered expression with the grade of malignancy but is not associated with survival.
  • It is unclear how annexin-1 is expressed in various neuroepithelial tumors, and whether there is any association with tumor malignancy or survival.
  • We studied annexin-1 expression in 394 glial neoplasms of all grades of malignancy and 81 normal brain samples by immunohistochemistry using tissue microarrays.
  • In the normal human brain, the expression of annexin-1 is limited to ependymal cells and subependymal astrocytes, but is also upregulated in reactive astrocytes.
  • In addition, nuclear staining of annexin-1 in oligodendroglial tumor cells was significantly reduced (P=0.0002), which may be used as a diagnostic tool for differentiating between astrocytomas and oligodendrogliomas.
  • Although annexin-1 expression in ependymomas decreased with the grade of malignancy, diffuse astrocytomas showed a significant increase in cytoplasmic annexin-1-positive tumor cells.
  • Thus, annexin-1 upregulation in astrocytomas may contribute to tumor progression and its expression profile is similar to its substrate, EGFR, suggesting a possible regulation thereof.
  • [MeSH-major] Annexin A1 / analysis. Biomarkers, Tumor / analysis. Brain Neoplasms / chemistry. Glioma / chemistry
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytoma / chemistry. Blotting, Western. Cell Nucleus / chemistry. Child. Child, Preschool. Ependymoma / chemistry. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Logistic Models. Male. Middle Aged. Neoplasm Staging. Oligodendroglioma / chemistry. Prognosis. Receptor, Epidermal Growth Factor / analysis. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Time Factors. Tissue Array Analysis. Young Adult

  • 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 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 = 19767728.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A1; 0 / Biomarkers, Tumor; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


76. Kunitz A, Wolter M, van den Boom J, Felsberg J, Tews B, Hahn M, Benner A, Sabel M, Lichter P, Reifenberger G, von Deimling A, Hartmann C: DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas. Brain Pathol; 2007 Oct;17(4):363-70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Allelic losses on 19q are found in the majority of oligodendroglial tumors and approximately one-third of diffuse astrocytomas.
  • However, the tumor suppressor genes (TSG) on 19q are still elusive.
  • In oligodendroglial tumors, we found that aberrant methylation in the 5'-region of EMP3 was significantly associated with reduced mRNA expression and LOH 19q.
  • Our data corroborate that oligodendroglial and astrocytic gliomas often show EMP3 hypermethylation and aberrant expression.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. Membrane Glycoproteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / physiopathology. Gene Expression Profiling. Gene Silencing / physiology. Genetic Predisposition to Disease / genetics. Humans. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / physiopathology. Oligonucleotide Array Sequence Analysis

  • 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 = 17610521.001).
  • [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 / EMP3 protein, human; 0 / Membrane Glycoproteins
  •  go-up   go-down


77. Lavon I, Zrihan D, Zelikovitch B, Fellig Y, Fuchs D, Soffer D, Siegal T: Longitudinal assessment of genetic and epigenetic markers in oligodendrogliomas. Clin Cancer Res; 2007 Mar 1;13(5):1429-37
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Because little is known about the evolution of genetic and epigenetic changes that occur during tumor progression in oligodendrogliomas, we evaluated these changes in paired early and progressive oligodendrogliomas.
  • RESULTS: In early tumors, 60.8% were of low grade compared with only 17% low-grade tumors at recurrence.
  • Of 17 early tumors described as pure oligodendrogliomas, 76.5% remained in this lineage, regardless of their grade, whereas others changed to astrocytic tumors.
  • Oligoastrocytic tumors had a significantly higher tendency to transform to astrocytic tumors.
  • All pure oligodendrogliomas with 1p/19q codeletions remained phenotypically unchanged, unlike mixed tumors with codeletions, of which 83% changed their cell lineage.
  • Of tumors with early 1p deletion, 80% remained oligodendroglial at progression, whereas 75% of tumors with an intact 1p changed to astrocytic phenotype.
  • 10q loss was uncommon in both early and progressive tumors.
  • The proportional gain in methylation at progression was 31% for tumors with early 1p deletion, unlike tumors with an intact 1p, which had an 87.5% gain of methylation at progression.
  • CONCLUSIONS: Pure oligodendrogliomas with 1p/19q deletion tend to retain their cell phenotype and genetic profile unlike tumors with no deletions or mixed histology.
  • MGMT promoter methylation is more pronounced at tumor progression, particularly in tumors with an intact 1p.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Epigenesis, Genetic. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Female. Humans. Immunohistochemistry. Male. Microsatellite Repeats. Middle Aged. Phenotype. Polymerase Chain Reaction. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17332285.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down


78. Cui XL, Zhao ZG, Ren XH, Sui DL, Chu JS, Tang K, Zeng C, Lin S: [Characteristics of combining loss of heterozygosity of 1p/19q in glioma]. Zhonghua Wai Ke Za Zhi; 2010 Jun 1;48(11):852-5
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The status of 1p and 19q of 138 glioma specimen from January 2009 to December 2009 was evaluated by Fluorescence in situ hybridization (FISH) method, and the frequencies of combining LOH of 1p/19q were compared between different pathologies, brain sub-regions, genders and ages.
  • RESULTS: The frequencies of combined LOH of 1p and 19q of oligodendroglial (81.3%) and oligo astrocytic tumors (55.8%) were significantly higher than that of astrocytic tumor (22.2%) (P < 0.01), and the frequency of oligodendroglial tumor was significantly higher than that of oligo astrocytic tumor (P < 0.05).
  • CONCLUSION: Combining LOH of 1p and 19q has significant correlation with the pathologies and brain sub-regions.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Loss of Heterozygosity
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Humans. Male. Middle Aged. Young Adult

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21163056.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


79. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EXPERIMENTAL DESIGN: We measured the incidence of Tregs in 135 glial tumors (including all pathologic types) in a glioma microarray using immunohistochemical analysis.
  • Results were categorized according to the total number of Tregs within the tumors.
  • 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.
  • The presence of Tregs within GBMs did not alter the median survival in patients from whom the tumors were obtained.
  • 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
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunohistochemistry. Incidence. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. T-Lymphocyte Subsets / immunology. Tissue Array Analysis

  • 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 = 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
  •  go-up   go-down


80. Barnett JA, Urbauer DL, Murray GI, Fuller GN, Heimberger AB: Cytochrome P450 1B1 expression in glial cell tumors: an immunotherapeutic target. Clin Cancer Res; 2007 Jun 15;13(12):3559-67
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytochrome P450 1B1 expression in glial cell tumors: an immunotherapeutic target.
  • EXPERIMENTAL DESIGN: We studied the frequency and extent of CYP1B1 expression by immunohistochemical analysis in 269 glial tumors (including all major pathologic types) on a tissue microarray.
  • RESULTS: Overall, increased CYP1B1 expression in glial tumors was associated with decreased patient survival time (P < 0.0014 for both percentage and intensity of staining).
  • A significant difference existed in percentage and intensity of staining between astrocytic and oligodendroglial tumors (P = 0.0002 and 0.0003, respectively), between grades of tumors (P < 0.0001 and 0.0079), and between pathologic types of tumors (P < 0.0001 and 0.0339).
  • Paradoxically, within specific tumor pathologies, there was a trend toward increased survival as CYP1B1 expression increased.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cytochrome P-450 Enzyme System / biosynthesis. Gene Expression. Glioma / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Aryl Hydrocarbon Hydroxylases. Child. Child, Preschool. Cytochrome P-450 CYP1B1. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Tissue Array Analysis

  • 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 = 17575219.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1B1
  •  go-up   go-down


81. Phi JH, Park SH, Chung CK, Wang KC, Cho BK, Kim SK: Atypical cell clusters expressing both neuronal and oligodendrocytic markers: novel histological pattern of glioneuronal tumors? Pathol Int; 2009 Oct;59(10):735-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical cell clusters expressing both neuronal and oligodendrocytic markers: novel histological pattern of glioneuronal tumors?
  • Glioneuronal tumors are a group of brain tumors that consist of both neuronal and glial cells.
  • The spectrum of glioneuronal tumors is currently expanding, and many atypical glioneuronal tumors require further characterization.
  • Two patients are described who had an atypical glioneuronal tumor with peculiar pathological features.
  • One patient was a 7-year-old girl with a tumor in the right cerebellar hemisphere.
  • The other was a 37-year-old man with a tumor in the spinal cord.
  • Although the clinical features (age at diagnosis, tumor location, and recurrence) were very different in these patients, the tumors had a characteristic common feature of atypical cell clusters.
  • Intriguingly, the tumor cells in the clusters expressed both neuronal and oligodendroglial markers, indicating aberrant differentiation.
  • Furthermore, the cluster-forming cells had modest proliferative indices and CD133 expression, indicating their role in the growth of the tumor.
  • It is believed that these atypical cell clusters are a novel pattern of differentiation of glioneuronal tumors and that they need further investigation.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cerebellar Neoplasms / pathology. Ganglioglioma / pathology. Neurons / pathology. Oligodendroglia / pathology. Spinal Neoplasms / pathology
  • [MeSH-minor] Adult. Child. Disease-Free Survival. Female. Humans. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19788619.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


82. Meng Y, Kujas M, Marie Y, Paris S, Thillet J, Delattre JY, Carpentier AF: Expression of TLR9 within human glioblastoma. J Neurooncol; 2008 May;88(1):19-25
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • No significant relationships between TLR9 expression and age, sex, tumor location, lymphocytes infiltration, oligodendroglial components or survival were found.
  • TLR9 is unlikely to be expressed by tumor cells as no TLR9 expression was detected in pure human GBM xenografts.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Toll-Like Receptor 9 / biosynthesis. Toll-Like Receptor 9 / genetics
  • [MeSH-minor] Adult. Aged. Animals. Female. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Karnofsky Performance Status. Lymphocytes / pathology. Male. Mice. Mice, Nude. Middle Aged. Neoplasm Transplantation. Neurosurgical Procedures. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival

  • Genetic Alliance. consumer health - Glioblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18253698.001).
  • [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] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Toll-Like Receptor 9
  •  go-up   go-down


83. Seiz M, Tuettenberg J, Meyer J, Essig M, Schmieder K, Mawrin C, von Deimling A, Hartmann C: Detection of IDH1 mutations in gliomatosis cerebri, but only in tumors with additional solid component: evidence for molecular subtypes. Acta Neuropathol; 2010 Aug;120(2):261-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of IDH1 mutations in gliomatosis cerebri, but only in tumors with additional solid component: evidence for molecular subtypes.
  • The current WHO classification of brain tumors defines gliomatosis cerebri (GC) as an extensively infiltrating astrocytic glioma involving at least three cerebral lobes.
  • Recent reports showed IDH1 mutations in astrocytic and oligodendroglial tumors WHO grades II and III and in secondary glioblastomas with a frequency of up to 90%, whereas IDH1 mutations occurred in only 5% of primary glioblastomas.
  • We identified IDH1 mutations in 10/24 (42%) cases, which also included a solid tumor portion (type 2 GC), but not in 11 "classical" cases without solid tumor mass (type 1 GC).
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Isocitrate Dehydrogenase / genetics. Mutation / genetics. Neoplasms, Neuroepithelial / genetics. Neoplasms, Neuroepithelial / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Arginine / genetics. Astrocytoma / secondary. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Mutational Analysis. Female. Histidine / genetics. Humans. In Situ Hybridization, Fluorescence / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Oligodendroglioma / secondary. Polymorphism, Single Nucleotide / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism


84. Gonzalez-Perez O, Romero-Rodriguez R, Soriano-Navarro M, Garcia-Verdugo JM, Alvarez-Buylla A: Epidermal growth factor induces the progeny of subventricular zone type B cells to migrate and differentiate into oligodendrocytes. Stem Cells; 2009 Aug;27(8):2032-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • New neurons and oligodendrocytes are continuously produced in the subventricular zone (SVZ) of adult mammalian brains.
  • However, the fate of cells derived from adult neural stem cells after EGF stimulation remains unknown.
  • This work indicates that EGF infusion can greatly expand the number of progenitors derived from the SVZ primary progenitors which migrate and differentiate into oligodendroglial cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3675-85 [9851974.001]
  • [Cites] Glia. 1999 Mar;26(1):84-91 [10088675.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Mol Cell Neurosci. 2004 Dec;27(4):453-65 [15555923.001]
  • [Cites] Glia. 2005 May;50(3):212-22 [15712210.001]
  • [Cites] Neuron. 2005 Mar 24;45(6):873-86 [15797549.001]
  • [Cites] J Neurol Sci. 2005 Jun 15;233(1-2):117-9 [15896808.001]
  • [Cites] Glia. 2005 Aug 1;51(2):81-97 [15782413.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4694-9 [17360586.001]
  • [Cites] J Cereb Blood Flow Metab. 2007 May;27(5):983-97 [16985505.001]
  • [Cites] Nat Neurosci. 2007 Aug;10(8):990-1002 [17618276.001]
  • [Cites] Dev Neurobiol. 2008 Feb 1;68(2):223-36 [18000828.001]
  • [Cites] J Neurosci. 2008 Jan 23;28(4):914-22 [18216199.001]
  • [Cites] Cell Stem Cell. 2008 Sep 11;3(3):265-78 [18786414.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):328-33 [19104058.001]
  • [Cites] Cell. 2002 Apr 5;109(1):75-86 [11955448.001]
  • [Cites] NeuroRx. 2004 Oct;1(4):472-81 [15717048.001]
  • [Cites] J Neurosci. 2005 Aug 10;25(32):7289-98 [16093378.001]
  • [Cites] Nat Neurosci. 2005 Jul;8(7):865-72 [15951811.001]
  • [Cites] Trends Neurosci. 2005 Dec;28(12):677-83 [16213602.001]
  • [Cites] J Neurosci. 2005 Nov 30;25(48):11092-106 [16319309.001]
  • [Cites] J Anat. 2005 Dec;207(6):695-706 [16367797.001]
  • [Cites] Stem Cells. 2006 Apr;24(4):1001-10 [16253982.001]
  • [Cites] Dev Biol. 2006 May 15;293(2):358-69 [16581057.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 16;103(20):7853-8 [16682644.001]
  • [Cites] Transpl Int. 2006 Jul;19(7):539-48 [16764632.001]
  • [Cites] Neurol Res. 2006 Jul;28(5):513-7 [16808881.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] J Neurosci. 2006 Jul 26;26(30):7907-18 [16870736.001]
  • [Cites] Neuroscientist. 2007 Feb;13(1):62-76 [17229976.001]
  • [Cites] Neuron. 2007 Feb 15;53(4):503-17 [17296553.001]
  • [Cites] Nat Neurosci. 2007 Mar;10(3):321-30 [17293857.001]
  • [Cites] Eur J Neurosci. 1999 Dec;11(12):4357-66 [10594662.001]
  • [Cites] Neuron. 2000 Feb;25(2):317-29 [10719888.001]
  • [Cites] Neuron. 2000 Feb;25(2):331-43 [10719889.001]
  • [Cites] Cell Transplant. 2000 Mar-Apr;9(2):289-94 [10811401.001]
  • [Cites] Nature. 2000 May 11;405(6783):187-91 [10821275.001]
  • [Cites] Mech Dev. 2000 Dec;99(1-2):143-8 [11091082.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14686-91 [11121069.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] Lancet. 2001 Jul 28;358(9278):298-300 [11498220.001]
  • [Cites] Neuron. 2001 Sep 13;31(5):791-807 [11567617.001]
  • [Cites] Development. 2001 Nov;128(21):4203-16 [11684657.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Curr Biol. 2002 Jul 9;12(13):1157-63 [12121626.001]
  • [Cites] Trends Neurosci. 2002 Aug;25(8):417-22 [12127759.001]
  • [Cites] Mol Cell Neurosci. 2002 Jul;20(3):390-403 [12139917.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13211-6 [12235363.001]
  • [Cites] Neuron. 2002 Dec 19;36(6):1021-34 [12495619.001]
  • [Cites] J Neurosci. 2003 Apr 15;23(8):3385-93 [12716946.001]
  • [Cites] J Neurocytol. 2002 Jul-Aug;31(6-7):437-55 [14501215.001]
  • [Cites] J Neurocytol. 2002 Jul-Aug;31(6-7):469-80 [14501217.001]
  • [Cites] J Neurocytol. 2002 Jul-Aug;31(6-7):497-505 [14501219.001]
  • [Cites] J Neurocytol. 2002 Jul-Aug;31(6-7):551-65 [14501223.001]
  • [Cites] Mol Cell Neurosci. 2004 Apr;25(4):664-78 [15080895.001]
  • [Cites] Nat Rev Neurosci. 2004 May;5(5):409-19 [15100723.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 May;63(5):499-509 [15198128.001]
  • [Cites] Glia. 2004 Oct;48(1):64-75 [15326616.001]
  • [Cites] J Comp Neurol. 1969 Dec;137(4):433-57 [5361244.001]
  • [Cites] J Neurosci. 1987 Sep;7(9):2737-44 [3305800.001]
  • [Cites] Glia. 1988;1(3):184-90 [2852171.001]
  • [Cites] Neuron. 1990 Nov;5(5):603-14 [2171589.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] J Neurosci. 1993 Apr;13(4):1730-50 [8463848.001]
  • [Cites] Development. 1993 Feb;117(2):525-33 [8330523.001]
  • [Cites] Neuron. 1993 Nov;11(5):951-66 [8240816.001]
  • [Cites] J Neurosci. 1994 Mar;14(3 Pt 1):1030-7 [8120611.001]
  • [Cites] Science. 1994 May 20;264(5162):1145-8 [8178174.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5359-63 [8202493.001]
  • [Cites] J Neurosci. 1996 Apr 15;16(8):2649-58 [8786441.001]
  • [Cites] Glia. 1996 May;17(1):39-51 [8723841.001]
  • [Cites] J Neurosci Res. 1996 Feb 1;43(3):299-314 [8714519.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14895-900 [8962152.001]
  • [Cites] J Neurosci Res. 1997 Mar 1;47(5):455-70 [9067855.001]
  • [Cites] J Neurosci. 1997 Aug 1;17(15):5820-9 [9221780.001]
  • [Cites] Neuron. 1997 Aug;19(2):251-67 [9292717.001]
  • [Cites] Exp Neurol. 1997 Sep;147(1):84-95 [9294405.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1218-23 [9448312.001]
  • [Cites] J Neurosci. 1998 Oct 1;18(19):7869-80 [9742155.001]
  • [ErratumIn] Stem Cells. 2009 Dec;27(12):3122
  • (PMID = 19544429.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD 32116; United States / NICHD NIH HHS / HD / R37 HD032116-15; United States / NICHD NIH HHS / HD / R37 HD032116; United States / NICHD NIH HHS / HD / R01 HD032116; United States / NICHD NIH HHS / HD / R37 HD032116-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 62229-50-9 / Epidermal Growth Factor
  • [Other-IDs] NLM/ NIHMS366814; NLM/ PMC3346259
  •  go-up   go-down


85. Schulz R, Vogel T, Dressel R, Krieglstein K: TGF-beta superfamily members, ActivinA and TGF-beta1, induce apoptosis in oligodendrocytes by different pathways. Cell Tissue Res; 2008 Dec;334(3):327-38
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Apoptotic functions of TGF-betas, in contrast to those of the activins, are well documented in the developing and adult nervous system.
  • In this study, we show, for the first time, an apoptotic function of ActivinA in the nervous system, i.e. in oligodendroglial progenitor cells.
  • Using the oligodendroglial cell line OLI-neu, we show that ActivinA acts autonomously, without cooperating with TGF-beta.
  • [MeSH-minor] Animals. Apoptosis Inducing Factor / pharmacology. Apoptosis Regulatory Proteins. Caspases / metabolism. Cell Nucleus / drug effects. Cell Nucleus / metabolism. DNA Fragmentation / drug effects. Mice. Mitochondria / drug effects. Mitochondria / metabolism. Protein Transport / drug effects. Smad Proteins / metabolism. Stem Cells / cytology. Stem Cells / drug effects. Tumor Suppressor Proteins / metabolism. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism

  • 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 = 19002501.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Apoptosis Inducing Factor; 0 / Apoptosis Regulatory Proteins; 0 / PUMA protein, mouse; 0 / Smad Proteins; 0 / Transforming Growth Factor beta1; 0 / Tumor Suppressor Proteins; 0 / activin A; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 104625-48-1 / Activins; EC 3.4.22.- / Caspases
  •  go-up   go-down


86. Huang L, Jiang T, Yuan F, Li GL, Cui Y, Liu EZ, Wang ZC: Correlation of chromosomes 1p and 19q status and expressions of O6-methylguanine DNA methyltransferase (MGMT), p53 and Ki-67 in diffuse gliomas of World Health Organization (WHO) grades II and III: a clinicopathological study. Neuropathol Appl Neurobiol; 2009 Aug;35(4):367-79
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Loss of heterozygosity (LOH) on 1p, combined LOH on 1p and 19q, low MGMT expression and high Ki-67 expression were associated with oligodendroglial tumours, whereas high p53 expression was associated with astrocytic and mixed tumours.
  • LOH on 1p and low MGMT expression were associated with grade II oligodendroglial tumours, whereas high expressions of p53 and Ki-67 were associated with grade III oligodendroglial tumours.
  • LOH on 1p and LOH on 19q were associated with nontemporal oligodendroglial tumours.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Glioma / genetics. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Astrocytoma / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Child. Female. Gene Expression. Humans. Loss of Heterozygosity. Male. Middle Aged. Neoplasm Staging. Oligodendroglioma / genetics. Oligodendroglioma / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19019173.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down


87. Guillaudeau A, Durand K, Pommepuy I, Robert S, Chaunavel A, Lacorre S, DeArmas R, Bourtoumieux S, El Demery M, Moreau JJ, Labrousse F: Determination of EGFR status in gliomas: usefulness of immunohistochemistry and fluorescent in situ hybridization. Appl Immunohistochem Mol Morphol; 2009 May;17(3):220-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fluorescent in situ hybridization (FISH) and immunohistochemistry (IHC) techniques were used to assess EGFR gene amplification and protein abundance in a series of 35 gliomas, including World Health Organization (WHO) grade I, II, and III astrocytomas (AI, AII, AIII), grade II and III tumors with oligodendroglial component (OII, OIII) and grade IV glioblastomas (GBs).
  • EGFR gene amplification was found in one-third of the tumors studied.
  • It was frequent in GB and OIII but was never found in AI, AII, AIII, and OII tumors.
  • IHC and FISH provided similar findings for grade of tumor, despite the fact that, in contrast to the FISH gene amplification, EGFR protein was overexpressed in AIII and in GB.
  • EGFR gene amplification was never observed in tumors not containing EGFR protein: therefore FISH is unnecessary when IHC shows no EGFR protein expression.
  • EGFR gene amplification seems to be restricted to high-grade tumors, WHO grade IV astrocytomas, and grade III oligodendroglial tumors.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood 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 = 19391220.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


88. Kaloshi G, Mokhtari K, Carpentier C, Taillibert S, Lejeune J, Marie Y, Delattre JY, Godbout R, Sanson M: FABP7 expression in glioblastomas: relation to prognosis, invasion and EGFR status. J Neurooncol; 2007 Sep;84(3):245-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • FABP7 expression has been analysed in a series of 123 glioblastomas (68 pure GBM, 55 GBMO, i.e. with oligodendroglial component).
  • Nuclear expression of FABP7 was more specifically related to EGFR amplification and more invasive tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Carrier Proteins / biosynthesis. Glioblastoma / pathology. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Gene Amplification. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Invasiveness / pathology. Prognosis. Protein Transport / 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17415524.001).
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / FABP7 protein, human; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


89. Günther HS, Schmidt NO, Phillips HS, Kemming D, Kharbanda S, Soriano R, Modrusan Z, Meissner H, Westphal M, Lamszus K: Glioblastoma-derived stem cell-enriched cultures form distinct subgroups according to molecular and phenotypic criteria. Oncogene; 2008 May 1;27(20):2897-909
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor cells with stem cell-like properties can be cultured from human glioblastomas by using conditions that select for the expansion of neural stem cells.
  • They showed a multipotent differentiation profile along neuronal, astroglial and oligodendroglial lineages, grew spherically in vitro, expressed CD133 and formed highly invasive tumors in vivo.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Neoplastic Stem Cells / classification. Neoplastic Stem Cells / metabolism. Phenotype
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Culture Techniques. Cell Line, Tumor. Female. Gene Expression Profiling. Humans. Male. Mice. Mice, Nude. Middle Aged. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18037961.001).
  • [ISSN] 1476-5594
  • [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
  •  go-up   go-down


90. Cassoni P, Senetta R, Castellano I, Ortolan E, Bosco M, Magnani I, Ducati A: Caveolin-1 expression is variably displayed in astroglial-derived tumors and absent in oligodendrogliomas: concrete premises for a new reliable diagnostic marker in gliomas. Am J Surg Pathol; 2007 May;31(5):760-9
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caveolin-1 expression is variably displayed in astroglial-derived tumors and absent in oligodendrogliomas: concrete premises for a new reliable diagnostic marker in gliomas.
  • The distribution of caveolae within the normal brain and in brain tumors is controversial.
  • In the present study, we describe the expression of caveolin-1 (cav-1) in 64 brain tumors of different grade, of either astroglial or oligodendroglial origin.
  • All studied astrocitomas of any grade (from II to IV) were cav-1 positive, displaying staining patterns and intensity specifically associated to the different tumor grades.
  • In contrast to astroglial tumors, the striking totality of grade II oligodendrogliomas and the large majority of grade III were lacking cav-1 expression.
  • In conclusion, among astroglial tumors cav-1 expression varies in distribution, pattern, and intensity specifically according to tumor types and grades.
  • The association between tumor progression and a more structured membranous pattern of cav-1 expression could suggest the hypothesis of a neoplastic shift towards a mesenchymal phenotype, whose behavioral and biologic significance worth further studies.
  • [MeSH-major] Astrocytes / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Caveolin 1 / metabolism. Glioblastoma / metabolism. Oligodendroglioma / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Count. Cell Line, Tumor. Cell Separation. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Disease Progression. Flow Cytometry. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17460461.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Caveolin 1
  •  go-up   go-down


91. Hata N, Shono T, Mizoguchi M, Matsumoto K, Guan Y, Nagata S, Hayashi K, Iwaki T, Sasaki T: Loss of heterozygosity analysis in an anaplastic oligodendroglioma arising after radiation therapy. Neurol Res; 2007 Oct;29(7):723-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE AND IMPORTANCE: Oligodendroglial tumors rarely occur after radiation therapy.
  • CLINICAL PRESENTATION AND INTERVENTION: A 41-year-old man who had received radiation therapy for a tumor of the suprasellar and pineal regions 31 years previously, presented with headache and progressive right hemiparesis.
  • Total removal of the tumor was performed through left frontoparietal craniotomy, and the histologic diagnosis was anaplastic oligodendroglioma.
  • Based on the genetic analysis, this tumor was considered to be sensitive to chemotherapy.
  • However, tumor recurrence was detected only 3 months after the surgery.
  • Despite additional radiochemotherapy, the tumor aggressively increased in size and the patient died with multiple recurrent tumors 1 year after surgery.
  • The significance of 1p and 19q LOH in radiation-induced oligodendroglial tumors might differ from that in spontaneous counterparts.
  • [MeSH-major] Brain Neoplasms / genetics. Cell Transformation, Neoplastic / genetics. Frontal Lobe / pathology. Loss of Heterozygosity / genetics. Neoplasms, Radiation-Induced / genetics. Oligodendroglioma / genetics. Radiotherapy / adverse effects
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 19 / genetics. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Microsatellite Repeats / genetics. Neoplasm Recurrence, Local. Predictive Value of Tests. Treatment Failure


92. Takeuchi H, Kubota T, Kitai R, Matsuda K, Hashimoto N, Sato K: Chromosome 1p and 19q deletions in malignant glioneuronal tumors with oligodendroglioma-like component. J Neurooncol; 2009 Jan;91(1):33-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 1p and 19q deletions in malignant glioneuronal tumors with oligodendroglioma-like component.
  • Malignant glioneuronal tumors (MGNT) are suggested to be a new entity of glioma defined morphologically as any malignant glioma showing immunohistoichemical evidence of neuronal differentiation.
  • We encountered seven cases of MGNT with oligodendroglioma-like component and investigated alternations of chromosome 1p and 19q in these tumors.
  • Immunohistochemical study of these tumors was performed using neuronal markers (synaptophysin, neurofilament, beta-tubulin, chromogranin A and NeuN), astrocytic marker (GFAP) and Ki-67.
  • We undertook a molecular cytogenetic study of tumor specimens obtained from seven patients using fluorescence in situ hybridization (FISH) with DNA probes mapping to chromosome 1p36, 1q25, 19p13 and 19q13.
  • Histologically, these tumors resembled anaplastic oligodendroglioma.
  • Immunohistochemically, tumor cells were immunoreactive for synaptophysin (7/7), neurofilament (6/7), beta-tubulin (5/7), chromogranin A (4/7), NeuN (2/7) and GFAP (7/7).
  • 1p and 19q deletions were present in MGNT, especially those with oligodendroglial components.
  • We suggest that the oligodendroglial-like feature was associated with not only 1p or 19q loss but also differentiation along neuronal cell lines as a factor of favorable prognosis in glial tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Oligodendroglioma / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Nerve Tissue Proteins / metabolism. Oligodendroglia / metabolism. Oligodendroglia / pathology

  • Genetic Alliance. consumer health - Oligodendroglioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18781279.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins
  •  go-up   go-down


93. French PJ, Swagemakers SM, Nagel JH, Kouwenhoven MC, Brouwer E, van der Spek P, Luider TM, Kros JM, van den Bent MJ, Sillevis Smitt PA: Gene expression profiles associated with treatment response in oligodendrogliomas. Cancer Res; 2005 Dec 15;65(24):11335-44
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Oligodendrogliomas are a specific subtype of brain tumor of which the majority responds favorably to chemotherapy.
  • In this study, we made use of expression profiling to identify chemosensitive oligodendroglial tumors.
  • Correlation of expression profiles to the tumors' response to treatment identified 16 differentially expressed probe sets.
  • Because transcripts associated with chemotherapeutic response were identified independent of common chromosomal aberrations, expression profiling may be used as an alternative approach to the tumors' 1p status to identify chemosensitive oligodendroglial tumors.
  • The observation that many genes are differentially expressed between long and short survivors indicates that the genetic background of the tumor is an important factor in determining the prognosis of the patient.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA, Neoplasm / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Survival Rate. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16357140.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


94. Durand KS, Guillaudeau A, Weinbreck N, DeArmas R, Robert S, Chaunavel A, Pommepuy I, Bourthoumieu S, Caire F, Sturtz FG, Labrousse FJ: 1p19q LOH patterns and expression of p53 and Olig2 in gliomas: relation with histological types and prognosis. Mod Pathol; 2010 Apr;23(4):619-28
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In glial tumors, the loss of heterozygosity of the 1p and 19q chromosomal arms is thought to be a marker of good prognosis in oligodendroglial tumors.
  • However, 1p and 19q loss of heterozygosity may be telomeric, interstitial, centromeric or affect the whole arm of the chromosome and the associations between these different patterns and tumor type, other molecular markers and patient prognosis remain unclear.
  • We identified five different 1p19q loss of heterozygosity patterns among the tumors studied and found that loss of heterozygosity over the whole 1p arm was associated with loss of heterozygosity over the whole 19q arm in 90% of cases.
  • 1p19q whole loss was also significantly associated with Olig2 overexpression, but was never observed in tumors overexpressing p53 protein.
  • We also found that, among patients with contrast-enhancing tumors, those with 1p19q whole loss tended to survive for longer.
  • In combination with classical histological and immunohistochemical data, 1p19q status determination provides pertinent information useful for (1) discriminating between histological types of gliomas and (2) identifying a subgroup of tumors that are associated with a better prognosis.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioma / genetics. Nerve Tissue Proteins / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Loss of Heterozygosity. Male. Microsatellite Repeats. Middle Aged. Polymerase Chain Reaction. Prognosis. Receptor, Epidermal Growth Factor / genetics

  • MedlinePlus Health Information. consumer health - 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 = 20081802.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


95. Roessler K, Gatterbauer B, Becherer A, Paul M, Kletter K, Prayer D, Hoeftberger R, Hainfellner J, Asenbaum S, Knosp E: Surgical target selection in cerebral glioma surgery: linking methionine (MET) PET image fusion and neuronavigation. Minim Invasive Neurosurg; 2007 Oct;50(5):273-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The objective of this study was to investigate the histological correlate of (11)C-methionine (MET) PET uptake of brain gliomas by image fusion for navigated surgery.
  • RESULTS: MET PET tumor uptake was detected in 26 of 27 patients (96.3%).
  • The quantitative MET tumor standardized uptake value (SUV) ratio was significantly higher in malignant gliomas and oligodendrogliomas than in low-grade gliomas (2.76/2.62 vs. 1.67, p=0.03).
  • Focal uptake corresponded to malignant glioma histology in 66.7%, and uniform global uptake to oligodendroglial histology in 72.7%.
  • In oligodendrogliomas, global MET uptake constituted 81.5% (range 53.8-135%) of the MRI T(1) tumor volume on average and was limited to the MRI FLAIR tumor volume in 86% (7/8) of patients.
  • CONCLUSION: MET PET image fusion may facilitate the targeting of anaplastic foci in homogeneous MRI non-enhancing gliomas for biopsy, may identify oligodendroglial histology preoperatively as well as characterize biologically active tumor volumes within MRI T(1)/FLAIR tumor areas of candidate patients for resection.
  • [MeSH-major] Brain Neoplasms / radionuclide imaging. Brain Neoplasms / surgery. Glioma / radionuclide imaging. Glioma / surgery. Neuronavigation / methods. Positron-Emission Tomography / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Carbon Radioisotopes. Child. Diagnosis, Differential. Female. Humans. Image Processing, Computer-Assisted / instrumentation. Image Processing, Computer-Assisted / methods. Male. Methionine / metabolism. Middle Aged. Oligodendroglioma / pathology. Oligodendroglioma / radionuclide imaging. Oligodendroglioma / surgery. Predictive Value of Tests. Preoperative Care / instrumentation. Preoperative Care / methods. Sensitivity and Specificity

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • Hazardous Substances Data Bank. (L)-Methionine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18058643.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; AE28F7PNPL / Methionine
  •  go-up   go-down


96. Kapoor GS, Gocke TA, Chawla S, Whitmore RG, Nabavizadeh A, Krejza J, Lopinto J, Plaum J, Maloney-Wilensky E, Poptani H, Melhem ER, Judy KD, O'Rourke DM: Magnetic resonance perfusion-weighted imaging defines angiogenic subtypes of oligodendroglioma according to 1p19q and EGFR status. J Neurooncol; 2009 May;92(3):373-86
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have recently shown that magnetic resonance perfusion-weighted imaging (MR-PWI) may be useful in predicting the histopathological grade or cytogenetic type of oligodendroglial neoplasms.
  • MR-PWI allows noninvasive determination of relative tumor blood volume (rTBV), which may reflect the degree of neoplastic angiogenesis and metabolism.
  • The present study was aimed to correlate rTBV to the angiogenic markers and EGFR expression in oligodendroglial tumors with 1p/19q LOH or 1p LOH (Group 1) and 1p19q intact alleles or 19q LOH (Group 2), respectively.
  • However, the differences between Group 1 and Group 2 were not significant in grade III tumors.
  • Probe-based real-time RT-PCR analyses showed that 12% of Group 2 high-grade tumors with intact 1p19q exhibited dramatic EGFR overexpression (designated EGFR-high).
  • Group 1 tumors showed significantly higher rTBV than Group 2 tumors, independent of the EGFR-high subtype.
  • Real-time RT-PCR analyses showed increased expression of VEGF, CD31 and CD105 in Group 1 tumors as compared to Group 2 tumors, excluding the EGFR-high subtype.
  • Therefore, the combined use of extensive molecular profiling and advanced MR imaging modalities may improve the accuracy of tumor grading, provide prognostic information, and has the potential to influence treatment decisions.
  • [MeSH-major] Brain Neoplasms / diagnosis. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Neovascularization, Pathologic / diagnosis. Oligodendroglioma / diagnosis. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Female. Humans. In Situ Hybridization, Fluorescence. Loss of Heterozygosity. Magnetic Resonance Angiography. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Oligodendroglioma.
  • MedlinePlus Health Information. consumer health - 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
  • (PMID = 19357963.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA-90586
  • [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 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


97. Mut M, Güler-Tezel G, Lopes MB, Bilginer B, Ziyal I, Ozcan OE: Challenging diagnosis: oligodendroglioma versus extraventricular neurocytoma. Clin Neuropathol; 2005 Sep-Oct;24(5):225-9
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • He presented with intratumoral hemorrhage and he underwent radical resection of tumor in 2003.
  • Histopathological examination of the recurrent tumor showed anaplastic progression with confusing immunohistochemical (IHC) results; the tumor was positive for NeuN and synaptophysin staining.
  • The question arisen was whether the recurrent tumor was an oligodendroglioma with neuronal differentiation or an extraventricular neurocytoma initially misdiagnosed as oligodendroglioma.
  • Current diagnostic methods of oligodendroglial tumors are discussed in context of differentiating oligodendrogliomas from other clear cell neoplasms of CNS, especially from extraventricular neurocytomas.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Neurocytoma / pathology. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging. Male. Nerve Tissue Proteins / biosynthesis. Synaptophysin / biosynthesis

  • Genetic Alliance. consumer health - Oligodendroglioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16167546.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / Synaptophysin
  •  go-up   go-down


98. Khayal IS, Nelson SJ: Characterization of low-grade gliomas using RGB color maps derived from ADC histograms. J Magn Reson Imaging; 2009 Jul;30(1):209-13
Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Color maps of oligodendroglial tumor regions were generally visualized in pink, while color maps of astrocytic tumor regions showed various shades of blue.
  • CONCLUSION: This technique allows for the visualization of biologically different regions within the whole tumor mass, which may aid in directing image-guided biopsies.
  • This can be used to ensure that the biopsy is directed to regions that can more accurately define the dominant tumor characteristics.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Brain Mapping / methods. Contrast Media. Diffusion Magnetic Resonance Imaging / methods. Echo-Planar Imaging / methods. Female. Gadolinium. Humans. Image Enhancement / methods. Image Processing, Computer-Assisted / methods. Imaging, Three-Dimensional / methods. Male. Middle Aged. 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
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19557741.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; AU0V1LM3JT / Gadolinium
  •  go-up   go-down


99. Stockhammer F, Thomale UW, Plotkin M, Hartmann C, Von Deimling A: Association between fluorine-18-labeled fluorodeoxyglucose uptake and 1p and 19q loss of heterozygosity in World Health Organization Grade II gliomas. J Neurosurg; 2007 Apr;106(4):633-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECT: Oligodendroglial tumors harboring combined 1p and 19q loss (1p/19q LOH) are characterized by a favorable prognosis and response to chemotherapy and radiotherapy, but detection of 1p/19q LOH relies on postoperative procedures.
  • The authors investigated the potential of fluorine-18-labeled fluorodeoxyglucose (FDG) uptake in positron emission tomography (PET) to predict 1p/19q LOH preoperatively in tumors whose appearance on initial magnetic resonance images was consistent with that of low-grade glioma.
  • METHODS: The study population comprised 25 patients who had undergone preoperative FDG-PET followed by tumor resection.
  • All tumor specimens were graded according to the World Health Organization (WHO) classification system.
  • Raised glucose utilization within the tumor was seen in the six of eight WHO Grade II gliomas with 1p/19q LOH and in none of the WHO Grade II gliomas without this genetic alteration (p = 0.003).
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / radionuclide imaging. Glioma / genetics. Glioma / radionuclide imaging. Loss of Heterozygosity. Positron-Emission Tomography
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Fluorodeoxyglucose F18. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. Predictive Value of Tests. Radiopharmaceuticals. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17432715.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


100. Derlon JM, Cabal P, Blaizot X, Borha A, Chapon F: [Metabolic imaging for supratentorial oligodendrogliomas]. Neurochirurgie; 2005 Sep;51(3-4 Pt 2):309-22
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Only a few publications have yet reported its use in oligodendroglial tumors.
  • These findings and partial results obtained in ongoing work, suggest some preliminary conclusions: 11C-MET (L-methyl-methionine) is a more appropriate tracer than 18F-FDG (fluoro-deoxy-glucose), in terms of both specificity and sensitivity, for the assessment of patients with this category of tumor.
  • PET/MET allows differentiation between grade II and grade III oligodendrogliomas; better targeting for stereotactic biopsy; more accurate assessment of the post-operative residual tumor; identification of progression from low-grade to anaplastic grade during the disease course; differentiation between recurrence and a post-radiation processes.
  • [MeSH-major] Brain. Oligodendroglioma / metabolism. Positron-Emission Tomography. Supratentorial Neoplasms / metabolism
  • [MeSH-minor] Adult. Amino Acids / metabolism. Female. Glucose / metabolism. Glycolysis. Humans. Imaging, Three-Dimensional. Magnetic Resonance Imaging. Male. Methionine / analogs & derivatives. Methionine / pharmacokinetics. Radioactive Tracers. Tomography, X-Ray Computed

  • Hazardous Substances Data Bank. GLUCOSE .
  • Hazardous Substances Data Bank. (L)-Methionine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16292175.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Radioactive Tracers; AE28F7PNPL / Methionine; BN630929UL / methionine methyl ester; IY9XDZ35W2 / Glucose
  •  go-up   go-down






Advertisement