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[Title] Phase II trial of preirradiation and concurrent temozolomide in patients with newly diagnosed anaplastic oligodendrogliomas and mixed anaplastic oligoastrocytomas: RTOG BR0131.

The primary objectives of this phase II study were to evaluate the use of preirradiation temozolomide followed by concurrent temozolomide and radiotherapy (RT) in patients with newly diagnosed anaplastic oligodendroglioma (AO) and mixed anaplastic oligoastrocytoma (MOA).

Tumor tissue was analyzed for the presence of chromosomal deletions on 1p and 19q and for MGMT-promoter methylation.

The worst nonhematological toxicity was grade 4 in three patients (8%).

There were no grade 4 nonhematological toxicities during the concurrent chemotherapy and RT.

[MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Astrocytoma / therapy. Brain Neoplasms / therapy. Dacarbazine / analogs & derivatives. Neoplasm Recurrence, Local / therapy. Oligodendroglioma / therapy

[MeSH-minor] Adolescent. Adult. Aged. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Combined Modality Therapy. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Dose Fractionation. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Promoter Regions, Genetic. Survival Rate. Treatment Outcome. Tumor Suppressor Proteins / genetics. Young Adult

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(PMID = 18779504.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 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/ PMC2718988

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anaplastic oligodendrogliomas with 1p19q codeletion have a proneural gene expression profile.

BACKGROUND: In high grade gliomas, 1p19q codeletion and EGFR amplification are mutually exclusive and predictive of dramatically different outcomes.

We performed a microarray gene expression study of four high grade gliomas with 1p19q codeletion and nine with EGFR amplification, identified by CGH-array.

One of the most striking differences was the expression of normal brain genes by oligodendrogliomas with 1p19q codeletion.

Immunohistochemical study of the most differentially expressed neuronal gene, alpha-internexin, clearly differentiated the two groups of gliomas, with 1p19q codeletion gliomas showing specific staining in tumor cells.

CONCLUSION: These findings provide evidence for neuronal differentiation in oligodendrogliomas with 1p19q codeletion and support the hypothesis that the cell of origin for gliomas with 1p19q codeletion could be a bi-potential progenitor cell, able to give rise to both neurons and oligodendrocytes.

[MeSH-major] Chromosome Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Neurons / metabolism. Oligodendroglioma / genetics

[MeSH-minor] Cluster Analysis. Genes, Neoplasm. Genome, Human / genetics. Humans. Immunohistochemistry. Intermediate Filament Proteins / metabolism. Neoplastic Stem Cells / pathology. Receptor, Epidermal Growth Factor / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18492260.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / alpha-internexin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

[Other-IDs] NLM/ PMC2415112

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Gene amplification is a poor prognostic factor in anaplastic oligodendrogliomas.

Prognostic-genomic correlations testing simultaneously all these amplified genes have never been conducted in anaplastic oligodendrogliomas.

A set of 38 genes that have been reported to be amplified in gliomas and investigated as the main targets of amplicons were studied in a series of 52 anaplastic oligodendrogliomas using bacterial artificial chromosome-array based comparative genomic hybridization and quantitative polymerase chain reaction.

Among the 38 target genes, 15 were found to be amplified in at least one tumor.

Overall, 27% of anaplastic oligodendrogliomas exhibited at least one gene amplification.

The most frequently amplified genes were epidermal growth factor receptor (EGFR) and cyclin-dependent kinase 4/sarcoma amplified sequence (CDK4/SAS) in 17% and 8% of anaplastic oligodendrogliomas, respectively.

In uni- and multivariate analyses, gene amplification was a negative prognostic factor for progression-free survival and overall survival in anaplastic oligodendrogliomas, providing complementary information to the classic prognostic factors identified in anaplastic oligodendrogliomas (extent of surgery, KPS, and chromosome arms 1p/19q status).

[MeSH-major] Brain Neoplasms / genetics. Gene Amplification. Oligodendroglioma / genetics

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(PMID = 18544654.001).

[ISSN] 1522-8517

[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

[Other-IDs] NLM/ PMC2666226

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Large clinical studies have provided important information on the impact of chemotherapy for anaplastic oligodendrogliomas in the upfront setting.

Investigations are also under way to clarify the role of chemotherapy for low-grade gliomas.

This review article summarises the recent developments and approaches in the use of chemotherapy to treat adult patients with astrocytomas and oligodendrogliomas.

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(PMID = 17549285.001).

[ISSN] 0304-4602

[Journal-full-title] Annals of the Academy of Medicine, Singapore

[ISO-abbreviation] Ann. Acad. Med. Singap.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Singapore

[Number-of-references] 37

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adjuvant treatment of anaplastic oligodendrogliomas and oligoastrocytomas.

Outcomes analyzed include overall survival (OS), progression-free survival (PFS), and treatment toxicity greater than or equal to grade 3.

Based on the differences in patient selection with respect to the definition of AO (2 versus 3 high risk anaplastic features) and sequence of treatment (RT and chemotherapy), the results from the two RCTs were not able to be considered for meta-analysis.

Tumors with 1p and 19q co-deletions are associated with better OS and may indicate a more chemo-responsive tumor.

[MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy

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[UpdateIn] Cochrane Database Syst Rev. 2014;5:CD007104 [24833028.001]

(PMID = 18425979.001).

[ISSN] 1469-493X

[Journal-full-title] The Cochrane database of systematic reviews

[ISO-abbreviation] Cochrane Database Syst Rev

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 11

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cognition and quality of life after chemotherapy plus radiotherapy (RT) vs. RT for pure and mixed anaplastic oligodendrogliomas: radiation therapy oncology group trial 9402.

PURPOSE: Radiation Therapy Oncology Group 9402 compared procarbazine, lomustine, and vincristine (PCV) chemotherapy plus radiation therapy (PCV + RT) vs. RT alone for anaplastic oligodendroglioma.

For those who died, MMSE scores remained stable initially, whereas B-QOL slowly declined; both declined rapidly in the last year of life and similarly between arms.

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[Copyright] (c) 2010 Elsevier Inc. All rights reserved.

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(PMID = 19783377.001).

[ISSN] 1879-355X

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U10 CA037422-15; None / None / / U10 CA021661-30; United States / NCI NIH HHS / CA / U10 CA021661-31S1; United States / NCI NIH HHS / CA / U10 CA021661-27S2; None / None / / U10 CA021661-28S1; United States / NCI NIH HHS / CA / U10 CA021661-25; United States / NCI NIH HHS / CA / U10 CA037422-12; None / None / / U10 CA021661-27; United States / NCI NIH HHS / CA / U10 CA021661-28S1; United States / NCI NIH HHS / CA / U10 CA037422-19; None / None / / U10 CA021661-32S2; United States / NCI NIH HHS / CA / U10 CA021661-28; None / None / / U10 CA037422-19; None / None / / U10 CA037422-16; None / None / / U10 CA021661-25; United States / NCI NIH HHS / CA / U10 CA021661-32S4; United States / NCI NIH HHS / CA / U10 CA037422-20; United States / NCI NIH HHS / CA / U10 CA037422-22S1; United States / NCI NIH HHS / CA / U10 CA021661-32S1; None / None / / U10 CA037422-22; United States / NCI NIH HHS / CA / U10 CA021661-31; United States / NCI NIH HHS / CA / U10 CA021661-32; None / None / / U10 CA037422-15; None / None / / U10 CA021661-24; None / None / / U10 CA021661-27S1; United States / NCI NIH HHS / CA / U10 CA037422-18; None / None / / U10 CA021661-28; None / None / / U10 CA021661-32S3; None / None / / U10 CA021661-32S4; United States / NCI NIH HHS / CA / U10 CA021661-30; United States / NCI NIH HHS / CA / U10 CA037422-16; United States / NCI NIH HHS / CA / U10 CA037422-17; United States / NCI NIH HHS / CA / U10 CA021661-32S3; United States / NCI NIH HHS / CA / U10 CA021661-32S2; None / None / / U10 CA037422-21; United States / NCI NIH HHS / CA / U10 CA037422-21; None / None / / U10 CA021661-24S1; None / None / / U10 CA037422-17; None / None / / U10 CA021661-29; None / None / / U10 CA037422-12; None / None / / U10 CA021661-31S1; None / None / / U10 CA037422-14; None / None / / U10 CA021661-32; United States / NCI NIH HHS / CA / U10 CA037422-14; None / None / / U10 CA037422-22S1; United States / NCI NIH HHS / CA / U10 CA037422-21S1; None / None / / U10 CA037422-20; None / None / / U10 CA021661-31; None / None / / U10 CA021661-27S2; United States / NCI NIH HHS / CA / U10 CA021661-24; United States / NCI NIH HHS / CA / U10 CA021661-26; United States / NCI NIH HHS / CA / U10 CA021661-27S1; United States / NCI NIH HHS / CA / U10 CA021661-27; United States / NCI NIH HHS / CA / U10 CA021661-24S1; United States / NCI NIH HHS / CA / U10 CA037422-22; United States / NCI NIH HHS / CA / U10 CA037422-13; None / None / / U10 CA037422-13; None / None / / U10 CA037422-18; United States / NCI NIH HHS / CA / U10 CA021661-29; None / None / / U10 CA037422-21S1; None / None / / U10 CA021661-26; None / None / / U10 CA021661-32S1

[Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine

[Other-IDs] NLM/ NIHMS123692; NLM/ PMC2878934

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Polysomy for chromosomes 1 and 19 predicts earlier recurrence in anaplastic oligodendrogliomas with concurrent 1p/19q loss.

PURPOSE: Loss of chromosome arms 1p and 19q is a molecular feature of oligodendroglial tumors characterized by responsiveness to chemotherapy and a favorable prognosis.

EXPERIMENTAL DESIGN: We analyzed 64 anaplastic oligodendrogliomas with 1p/19q loss or maintenance diagnosed at Massachusetts General Hospital and Brigham and Women's Hospital from 1996 to 2005; fluorescence in situ hybridization for 1p/19q and Ki-67 immunohistochemistry was done.

In agreement with previous studies, the group of anaplastic oligodendrogliomas with 1p/19q loss had significantly better progression-free survival and overall survival than anaplastic oligodendrogliomas with 1p/19q maintenance (P = 0.0009 and P < 0.0003, respectively).

Among anaplastic oligodendrogliomas with 1p/19q loss, those with polysomy showed shorter progression-free survival than those with 1p/19q loss without polysomy (P = 0.0048).

CONCLUSION: The presence of polysomy in anaplastic oligodendrogliomas with deletion of 1p/19q is a marker of earlier recurrence.

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(PMID = 19808867.001).

[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 / CA057683-16; United States / NCI NIH HHS / CA / R01 CA057683; United States / NCI NIH HHS / CA / R01 CA057683-16

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ NIHMS160000; NLM/ PMC2818514

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] YKL-40 is a differential diagnostic marker for histologic subtypes of high-grade gliomas.

PURPOSE AND EXPERIMENTAL DESIGN: In modern neuro-oncology, no variable affects therapeutic decisions and prognostic estimation more than tumor classification.

We showed recently that class prediction models, based on gene expression profiles, classify diagnostically challenging malignant gliomas in a manner that better correlates with clinical outcome than standard pathology.

In the present study, we used immunohistochemistry to investigate YKL-40 protein expression in independent sets of glioblastomas and anaplastic oligodendrogliomas to determine whether this single marker can aid classification of these high-grade gliomas.

RESULTS AND CONCLUSIONS: Glioblastomas show strikingly more YKL-40 expression than anaplastic oligodendrogliomas.

Only 2 of 37 glioblastomas showed completely negative YKL-40 staining in both tumor cells and extracellular matrix, whereas 18 of 29 anaplastic oligodendrogliomas were completely negative in non-microgemistocytic tumor cells and extracellular matrix.

Tumor cell staining intensity was also markedly different: 84% of glioblastomas showed strong staining intensities of 2+ or 3+ whereas 76% of anaplastic oligodendrogliomas either did not stain or stained at only 1+.

YKL-40 staining provided a better class distinction of glioblastoma versus anaplastic oligodendroglioma than glial fibrillary acidic protein, the current standard immunohistochemical marker used to distinguish diagnostically challenging gliomas.

Moreover, a combination of YKL-40 and glial fibrillary acidic protein immunohistochemistry afforded even greater diagnostic accuracy in anaplastic oligodendrogliomas.

[MeSH-major] Biomarkers, Tumor / metabolism. Glioblastoma / diagnosis. Glioblastoma / metabolism. Glycoproteins / metabolism. Oligodendroglioma / diagnosis. Oligodendroglioma / metabolism

[MeSH-minor] Adipokines. Autoantigens / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Diagnosis, Differential. Glial Fibrillary Acidic Protein / analysis. Humans. Immunoenzyme Techniques. Lectins. Neoplasm Staging. Prognosis

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(PMID = 15788675.001).

[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 / CA 57683

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Adipokines; 0 / Autoantigens; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Glycoproteins; 0 / Lectins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anaplastic oligodendrogliomas after treatment of acute lymphoblastic leukemia in children: report of 2 cases.

High-grade gliomas, meningiomas, and sarcomas are the most frequent neoplasms.

Secondary anaplastic oligodendrogliomas are exceedingly rare.

Five cases of pure anaplastic oligodendroglioma have been reported in the literature, and only 1 case was in a child after ALL treatment.

The authors present 2 cases of pediatric anaplastic oligodendroglioma after treatment of ALL.

[MeSH-major] Brain Neoplasms / etiology. Oligodendroglioma / etiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Radiotherapy / adverse effects

[MeSH-minor] Child. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Neoplasm Proteins / biosynthesis. Neurosurgical Procedures. Treatment Outcome

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(PMID = 20121367.001).

[ISSN] 1933-0715

[Journal-full-title] Journal of neurosurgery. Pediatrics

[ISO-abbreviation] J Neurosurg Pediatr

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic value of health-related quality-of-life data in predicting survival in patients with anaplastic oligodendrogliomas, from a phase III EORTC brain cancer group study.

PATIENTS AND METHODS: Baseline HRQOL scores (from the European Organisation for Research and Treatment of Cancer [EORTC] Quality of Life Questionnaire C30 and the EORTC Brain Cancer Module) were examined in 247 patients with anaplastic oligodendrogliomas to determine the relationship with overall survival by using Cox proportional hazards regression models.

[MeSH-major] Brain Neoplasms / mortality. Oligodendroglioma / mortality. Quality of Life

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(PMID = 18089867.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 5U10CA11488-30; United States / NCI NIH HHS / CA / 5U10CA11488-31; United States / NCI NIH HHS / CA / 5U10CA11488-32; United States / NCI NIH HHS / CA / 5U10CA11488-33; United States / NCI NIH HHS / CA / 5U10CA11488-34

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparative genomic hybridization pattern of non-anaplastic and anaplastic oligodendrogliomas--a meta-analysis.

Many oligodendrogliomas (ODG) have been investigated by comparative genomic hybridization (CGH).

To visualize characteristic aberration profiles of non-anaplastic in a comparison with anaplastic ODGs, we performed a meta-analysis of the CGH results of all 89 cases published so far.

The frequencies of each chromosomal band affected by a genetic imbalance were calculated for WHO grades II and III separately.

In non-anaplastic ODGs, -1p and -19q were the most prominent aberrations.

In anaplastic ODGs, +7, -4q, -9p, -10, and -15q emerged additionally.

Scrutinizing published putative progression markers of ODG, we found that only +7, -10, and -15q significantly correlated with a higher grade of malignancy.

Summing up, the expansion of the CGH results to the 850 GTG band resolution enabled a meta-analysis to visualize WHO grade-specific aberration profiles in ODG for the first time.

[MeSH-major] Chromosome Aberrations. Genetic Markers. Oligodendroglioma / classification. Oligodendroglioma / genetics

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(PMID = 16356658.001).

[ISSN] 0344-0338

[Journal-full-title] Pathology, research and practice

[ISO-abbreviation] Pathol. Res. Pract.

[Language] eng

[Publication-type] Journal Article; Meta-Analysis

[Publication-country] Germany

[Chemical-registry-number] 0 / Genetic Markers

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adjuvant procarbazine, lomustine, and vincristine improves progression-free survival but not overall survival in newly diagnosed anaplastic oligodendrogliomas and oligoastrocytomas: a randomized European Organisation for Research and Treatment of Cancer phase III trial.

PURPOSE: Anaplastic oligodendrogliomas are more responsive to chemotherapy than high-grade astrocytomas.

We investigated, in a multicenter randomized controlled trial, whether adjuvant procarbazine, lomustine, and vincristine (PCV) chemotherapy improves overall survival (OS) in newly diagnosed patients with anaplastic oligodendrogliomas or anaplastic oligoastrocytomas.

In the RT arm, 82% of patients with tumor progression received chemotherapy.

CONCLUSION: Adjuvant PCV chemotherapy does not prolong OS but does increase PFS in anaplastic oligodendroglioma.

Combined loss of 1p/19q identifies a favorable subgroup of oligodendroglial tumors.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy

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[CommentIn] Nat Clin Pract Oncol. 2007 Feb;4(2):78-9 [17228307.001]

[CommentIn] J Clin Oncol. 2006 Jun 20;24(18):2689-90 [16782906.001]

[CommentIn] Curr Neurol Neurosci Rep. 2007 May;7(3):189-90 [17488583.001]

[CommentIn] Nat Clin Pract Neurol. 2007 Jan;3(1):14-5 [17205067.001]

(PMID = 16782911.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; PCV protocol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Temozolomide treatment for newly diagnosed anaplastic oligodendrogliomas: a clinical efficacy trial.

PURPOSE: Chemotherapy with alkylating agents is of proven efficacy in recurrent anaplastic oligodendroglioma (AO) with reported response rates ranging between 50% and 70%.

This study evaluated the response and time to tumor progression of newly diagnosed AO initially treated with TMZ.

PATIENTS AND METHODS: Twenty patients with a median age of 47 (range: 26-65) received a median of 14 (range: 3-24) cycles of TMZ as their first modality of therapy following diagnosis of AO.

Treatment was given every 28 days for 5 days at a starting dose of 200 mg/m2/d and was continued for 24 cycles unless toxicity or tumor progression required withdrawal of TMZ.

The objective response rate was 75%, and median time to tumor progression was 24 months.

TMZ was well tolerated with only two events of grade 3/4 hematological toxicity.

[MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Oligodendroglioma / drug therapy

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[Cites] Expert Opin Pharmacother. 2004 Feb;5(2):295-306 [14996626.001]

[Cites] J Neurooncol. 2003 Nov;65(2):127-34 [14686732.001]

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(PMID = 16855865.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Factors affecting prognosis of patients with intracranial anaplastic oligodendrogliomas: a single institutional review of 70 patients.

Anaplastic oligodendroglioma (AO) is an uncommon intracranial tumor and prognosis is poor.

The patients younger than 50 years old and who received regular chemotherapy were likely to achieve a good outcome.

[MeSH-major] Brain Neoplasms / diagnosis. Oligodendroglioma / diagnosis

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[Cites] Surg Neurol. 2002 Aug;58(2):111-7; discussion 117 [12453646.001]

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[Cites] Oncogene. 2002 Jun 6;21(25):3961-8 [12037678.001]

(PMID = 20195700.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Chromosome 1p loss evaluation in anaplastic oligodendrogliomas.

The chromosome (chr) 1p deletion is a favorable biomarker in oligodendroglial tumors and is even more powerful a marker when combined with chr 19q loss.

To illustrate the usefulness of evaluating multiple loci, we here report two anaplastic oligodendrogliomas that were investigated using fluorescent in situ hybridization (FISH) and bacterial artificial chromosome (BAC)-array-based comparative genomic hybridization (aCGH).

[MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Nucleic Acid Hybridization / methods. Oligodendroglioma / genetics

[MeSH-minor] Biomarkers, Tumor / genetics. Chromosomes, Artificial, Bacterial. Humans. In Situ Hybridization, Fluorescence. Middle Aged

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(PMID = 18312547.001).

[ISSN] 0919-6544

[Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology

[ISO-abbreviation] Neuropathology

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Australia

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.

: e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.

METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.

The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.

Out of 80 cycles received there was no anemia; 5 (6%) grade 1, 8 (10%) grade 2, 2 (3%) grade 3 leucopenia; 1 (1%) grade 1, 2 (3%) grade 2, 1 (1%) grade 3, 1 (1%) grade 4 thrombocytopenia; 9 (11%) grade 1, 7 (9%) grade 2, 32 (40%) grade 3, and 11 (14%) grade 4 lymphopenia.

Study was terminated in 2 patients (one with grade 4 thrombocytopenia and the other with grade 4 hepatic toxicity).

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(PMID = 27962826.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Patterns in the care of oligodendrogliomas and oligoastrocytomas: A single center experience.

: e13034 Background: Although rare, oligodendrogliomas (ODs) and oligoastrocytomas (OAs) have established a unique identity due to their sensitivity to chemotherapy, especially if they exhibit combined loss of heterozygosity (LOH) of 1p and 19q.

RESULTS: 31 patients had low-grade tumors (either ODs or OAs) while 17 had high grade tumors (anaplastic ODs or anaplastic OAs).

Of the low grade tumors, 35% had combined 1p/19q LOH.

As for the high grade tumors, 47% had combined 1p/19q LOH.

At a mean of 29 months of follow up, eight patients had tumor progression while 12 died.

Median progression free survival (MPFS) for patients receiving chemotherapy was increased in patients with combined 1p/19q LOH, for both low-grade tumors (34 vs. 20 months) and high-grade tumors (14 vs. 8 months).

Also, significantly more patients with low-grade tumors and combined 1p/19q LOH were offered chemotherapy when compared to those without 1p/19q LOH (64% vs 20%, p = 0.04, Fisher exact).

However, in patients with high-grade tumors, knowledge of 1p/19q LOH did not significantly impact the choice to administer chemotherapy (88% vs. 67%, p = 0.67).

CONCLUSIONS: Patients with ODs/OAs and combined 1p/19q LOH who have been treated with chemotherapy demonstrate increased MPFS when compared with those without this genotype.

Despite this, determination of 1p/19q LOH significantly affects physician choice to offer chemotherapy only in patients with low-grade tumors, but not in those with high-grade tumors.

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(PMID = 27962862.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG).

METHODS: Eligibility included: adult patients with stable or recurrent MG (GBM, anaplastic astrocytoma [AA], anaplastic oligodendroglioma [AO]) previously treated with radiation therapy (RT) and with or without chemotherapy; interval of at least two weeks between prior RT, or four weeks between prior chemotherapy; Karnofsky ≥ 60%; and adequate hematologic, renal and liver function.

Dose-limiting toxicities were: deep venous thrombosis (1 grade 3); nausea and vomiting (1 grade 3); diarrhea (1 grade 3); elevated ALT (1 grade 3); elevated creatinine (1 grade 3); and fatigue (1 grade 3).

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(PMID = 27962751.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cognition and quality of life after chemotherapy plus radiotherapy (RT) vs. RT for pure and mixed anaplastic oligodendrogliomas: Radiation therapy oncology group trial 9402.

: e20519 Background: Radiation Therapy Oncology Group 9402 compared PCV chemotherapy plus radiation therapy (PCV+RT) versus RT alone for anaplastic oligodendroglioma.

For those who died, B-QOL scores declined slowly until the last year of life, then rapidly.

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(PMID = 27961031.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab.

Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.

It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.

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(PMID = 27964663.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In this study, the authors tested the presence of such mutations in 95 gliomas including glioblastomas, anaplastic oligodendrogliomas, and low-grade gliomas.

[MeSH-minor] Astrocytoma / drug therapy. Astrocytoma / enzymology. Astrocytoma / genetics. Carcinoma / drug therapy. Carcinoma / enzymology. Carcinoma / genetics. DNA Mutational Analysis. Drug Resistance, Neoplasm / genetics. Genetic Testing. Glioblastoma / drug therapy. Glioblastoma / enzymology. Glioblastoma / genetics. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Oligodendroglioma / drug therapy. Oligodendroglioma / enzymology. Oligodendroglioma / genetics. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Protein Structure, Tertiary / genetics. Quinazolines / pharmacology. Quinazolines / therapeutic use

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(PMID = 15851741.001).

[ISSN] 1526-632X

[Journal-full-title] Neurology

[ISO-abbreviation] Neurology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: Using immunohistochemistry to detect the expression of EGFR and PTEN and adopting confocal technology to verify their location in the specimens of 25 respectively glioblastoma multiformes, medulloblastomas, anaplastic oligodendrogliomas, and anaplastic ependymomas.

They were 36% and 8% in medulloblastomas, and 28% and 8% in anaplastic oligodendrogliomas, and 24% and 4% in anaplastic ependymomas.

PTEN mutation and EGFR overexpression are rare in medulloblastoma, anaplastic oligodendroglioma, and anaplastic ependymoma, so the EGFR or PTEN targeted antitumor approaches may be useful in glioblastoma multiformes but the other 3 tumors.

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(PMID = 17236582.001).

[ISSN] 1672-173X

[Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition

[ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.67 / PTEN Phosphohydrolase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Place of chemotherapy and radiotherapy in the management of oligodendrogliomas].

Twenty years ago, the discovery of the chemosensitivity of anaplastic oligodendrogliomas considerably boosted interest for these tumors.

In spite of difficulties for histological diagnosis, numerous studies on radiotherapy and chemotherapy for oligodendrogliomas appeared these last years.

For low grade oligodendrogliomas, radiotherapy delays the anaplastic transformation, but does not modify the overall survival; its indication has to be discussed particularly in the absence of clinical symptoms.

Chemotherapy seems to be effective for low grade oligodendrogliomas as well as anaplastic tumors.

However, phase III studies are necessary to clarify the contribution of chemotherapy for the treatment of low grade oligodendrogliomas, mainly in relation to radiotherapy.

In anaplastic oligodendrogliomas, in spite of the lack of phase III studies, radiotherapy seems to be effective.

[MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Oligodendroglioma / drug therapy. Oligodendroglioma / radiotherapy

[MeSH-minor] Combined Modality Therapy. Humans. Neoplasm Staging. Survival Rate

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(PMID = 16292180.001).

[ISSN] 0028-3770

[Journal-full-title] Neuro-Chirurgie

[ISO-abbreviation] Neurochirurgie

[Language] fre

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] France

[Number-of-references] 55

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

RESULTS: Our series included five pilocytic astrocytomas, seven oligodendrogliomas, and two glioblastomas.

Oligodendrogliomas frequently demonstrated an aspect of unilateral thalamic enlargement lacking or with slight contrast enhancement.

Anaplastic oligodendrogliomas and glioblastomas displayed a poor outcome, with a mean survival of 8 months after surgery.

CONCLUSION: Our series of pediatric thalamic gliomas clearly distinguishes pilocytic astrocytomas from anaplastic oligodendrogliomas regarding neuroimaging, pathology, and prognosis.

[MeSH-minor] Adolescent. Astrocytoma / diagnostic imaging. Astrocytoma / pathology. Astrocytoma / therapy. Child. Child, Preschool. Female. Glioblastoma / diagnostic imaging. Glioblastoma / pathology. Glioblastoma / therapy. Humans. Male. Oligodendroglioma / diagnostic imaging. Oligodendroglioma / pathology. Oligodendroglioma / therapy. Prognosis. Radiography. Survival Rate. Treatment Outcome

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(PMID = 16951965.001).

[ISSN] 0256-7040

[Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery

[ISO-abbreviation] Childs Nerv Syst

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The different glioma types are associated with distinct genetic aberrations, which may provide useful information for tumor classification as well as prediction of prognosis and response to therapy.

To facilitate the molecular classification of gliomas, we established a genomic microarray that consists of bacterial artificial chromosome (BAC) and P1-derived artificial chromosome (PAC) clones representing tumor suppressor genes, proto-oncogenes and chromosomal regions frequently gained or lost in gliomas.

Furthermore, molecular classification based on matrix CGH data closely paralleled histological classification and was able to distinguish with few exceptions between diffuse astrocytomas and oligodendrogliomas, anaplastic astrocytomas and anaplastic oligodendrogliomas, anaplastic oligodendrogliomas and glioblastomas, as well as primary and secondary glioblastomas.

[MeSH-major] Brain Neoplasms / classification. DNA, Neoplasm / analysis. Glioma / classification. Nucleic Acid Hybridization

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[Copyright] Copyright (c) 2005 Wiley-Liss, Inc.

(PMID = 15880582.001).

[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, Neoplasm

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase II trial of temozolomide (TMZ) followed by myeloablative chemotherapy with autologous peripheral blood progenitor cell rescue (APBPCR) for newly diagnosed anaplastic oligodendroglioma: An Oligodendroglioma Study Group trial.

: 2055 Background: Treatment of anaplastic oligodendroglioma (AO) and anaplastic oligoastrocytomas (AOA) is controversial.

Patients with surgical gross total resection who maintained response or patients who responded to temozolomide (CR or PR defined as >50% reduction in tumor) were eligible for myeloablative chemotherapy with thiotepa 250mg/m2/day for three days followed by busulfan 3.2mg/kg/day for three days, followed by APBPCR.

RESULTS: 19 patients (16 AO, 2 AOA, 1 low-grade oligodendroglioma with radiographic features suggestive of high-grade tumor) with a median age of 42 (28-56) and KPS of 90 (70-100) were enrolled.

2 of the 10 patients who underwent APBPCR recurred, one at 16.1 and one at 34.2 months.

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(PMID = 27964668.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[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.

In addition, we found that the cytosolic phospholipase A2 (PLA2G4C) gene at 19q13.3 demonstrated significantly lower expression in anaplastic oligodendrogliomas (WHO grade III) when compared to well-differentiated oligodendrogliomas (WHO grade II).

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

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[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular pathology of oligodendroglial tumors.

The term oligodendroglioma was created by Bailey, Cushing, and Bucy based on the observation that these tumors share morphological similarities with oligodendrocytes (Bailey and Cushing 1926; Bailey and Bucy 1929).

However, a convincing link between oligodendrocytes and oligodendrogliomas still needs to be shown.

Oligoastrocytomas or mixed gliomas are histologically defined by the presence of oligodendroglial and astrocytic components.

According to the WHO classification of brain tumors, oligodendroglial tumors are separated into oligodendrogliomas WHO grade II (OII), anaplastic oligodendrogliomas WHO grade III (OIII), oligoastrocytomas WHO grade II (OAII), anaplastic oligoastrocytomas WHO grade III (OAIII), and glioblastomas with oligodendroglioma component WHO grade IV (GBMo) (Louis et al. 2007).The perception of oligodendroglial tumors has changed in recent years.

The diagnosis of oligodendroglioma or oligoastrocytomas is made much more frequently than 10 years ago.

Treatment modalities have been advanced and novel concepts regarding the origin of oligodendroglial tumors have been developed.

This review focuses on recent developments with impact on the diagnosis and understanding of molecular mechanisms in oligodendroglial tumors.

[MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology

[MeSH-minor] Chromosome Aberrations. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Genotype. Humans. Immunohistochemistry. Mutation. Prognosis. Tumor Suppressor Proteins / genetics

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(PMID = 19322536.001).

[ISSN] 0080-0015

[Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer

[ISO-abbreviation] Recent Results Cancer Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Germany

[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

[Number-of-references] 172

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical significance of ABCA2' a possible molecular marker for oligodendrogliomas.

METHODS: To determine whether or not ABCA2 can distinguish oligodendrogliomas from astrocytic tumors, the authors investigated the expression of ABCA2 in a panel of 55 glioma tissues (13 oligodendrogliomas, nine anaplastic oligodendrogliomas, 12 anaplastic astrocytomas, and 21 glioblastomas) using real-time reverse-transcriptase polymerase chain reaction analysis, immunoblot analysis, and immunohistochemistry analysis.

The authors also compared the expression of Olig2, a recently identified marker for oligodendroglioma.

RESULTS: The relative expression level of ABCA2 messenger ribonucleic acid determined by real-time quantitative polymerase chain reaction is significantly higher (by a factor of five) in oligodendroglioma than in anaplastic astrocytoma or glioblastoma.

It was moderately increased in anaplastic oligodendrogliomas.

In immunohistochemical analysis, ABCA2 exhibited remarkable immunopositivity in 11 out of 13 oligodendrogliomas showing a granular pattern in the cytoplasm of tumor cells.

However, ABCA2 was completely negative in most anaplastic astrocytomas (75%) and glioblastomas (76%).

Anaplastic oligodendroglioma showed an intermediate pattern: strongly positive in two out of nine samples and negative in seven out of nine samples.

However, Olig2 was strongly positive in most anaplastic astrocytomas (83%) and glioblastomas (71%).

Although there was no difference in the detection of oligodendroglial tumors, the specificity (negative in astrocytic tumor) was significantly higher in ABCA2 than in Olig2.

CONCLUSION: These lines of evidence suggest that ABCA2 could be a molecular marker for oligodendroglioma.

[MeSH-major] ATP-Binding Cassette Transporters / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism. Oligodendroglioma / metabolism

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(PMID = 17415208.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / ABCA2 protein, human; 0 / ATP-Binding Cassette Transporters; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Among these, 30 rats had brain tumors, which were classified histologically as malignant glioma, anaplastic oligodendroglioma, and low-grade oligodendroglioma.

Six transgenic rats developed two different histologic types of brain tumor, which were considered to be of multiclonal origin, because of the lack of histological transitions.

Diffuse immunoreactivity for Olig2 and Nkx2.2 was observed in neoplastic cells in all seven anaplastic oligodendrogliomas and in all three low-grade oligodendrogliomas analyzed, but in none of 26 malignant gliomas.

Electron microscopy, carried out on four malignant gliomas and four anaplastic oligodendrogliomas, revealed the presence of intermediate filament bundles devoid of side arms, indicating glial differentiation.

The present study thus provides additional evidence that the brain tumors developing in S100beta-v-erbB transgenic rats are of glial origin, with or without oligodendroglial differentiation.

Reproducible development of three distinct histologic types of brain tumor in unique localizations may be explained by activation of the v-erbB transgene driven by the S100beta promoter in specific precursor cells during development of the brain.

[MeSH-minor] Animals. Basic Helix-Loop-Helix Transcription Factors / analysis. Female. Glial Fibrillary Acidic Protein / analysis. Glioma / chemistry. Glioma / ultrastructure. Homeodomain Proteins / analysis. Immunohistochemistry. Male. Microscopy, Electron. Nerve Tissue Proteins / analysis. Neuroglia / pathology. Oligodendroglioma / chemistry. Oligodendroglioma / ultrastructure. Rats. Rats, Transgenic. S100 Calcium Binding Protein beta Subunit. Transcription Factors / analysis

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(PMID = 18498286.001).

[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 / Homeodomain Proteins; 0 / Nerve Growth Factors; 0 / Nerve Tissue Proteins; 0 / Nkx-2.2 homedomain protein; 0 / Olig2 protein, rat; 0 / Oncogene Proteins v-erbB; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / Transcription Factors

   

[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.

RESULTS: Using CBTRUS data, the incidences (per 100,000 person-years) of oligodendrogliomas (APC = 4.7), mixed gliomas (APC = 3.9) and anaplastic oligodendrogliomas (APC = 12.5) have all increased over time, while the incidences of astrocytoma not otherwise specified (APC = -8.1) and fibrillary astrocytoma (APC = -2.1) have decreased.

Restricting the analyses to later years (1992-2004) using SEER data shows the incidence of oligodendrogliomas leveling off (APC = 0.5), while joinpoint analyses demonstrate a decreasing trend after 1998.

CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.

[MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology

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[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Health-related quality of life in patients treated for anaplastic oligodendroglioma with adjuvant chemotherapy: results of a European Organisation for Research and Treatment of Cancer randomized clinical trial.

PURPOSE: Little is known about the health-related quality of life (HRQOL) of patients treated for anaplastic oligodendrogliomas.

PATIENTS AND METHODS: Adult patients with anaplastic oligodendrogliomas received RT alone or RT plus PCV chemotherapy.

[MeSH-major] Brain Neoplasms / drug therapy. Oligodendroglioma / drug therapy. Quality of Life

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[CommentIn] J Clin Oncol. 2008 Apr 20;26(12):2061-2; author reply 2062 [18421064.001]

(PMID = 18089866.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 5U10CA11488-30; United States / NCI NIH HHS / CA / 5U10CA11488-31; United States / NCI NIH HHS / CA / 5U10CA11488-32; United States / NCI NIH HHS / CA / 5U10CA11488-33; United States / NCI NIH HHS / CA / 5U10CA11488-34

[Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anaplastic oligodendroglioma: a case report with characteristic cytologic features, including minigemistocytes.

BACKGROUND: Absolute criteria for grading oligodendrogliomas are somewhat poorly defined in contrast to those for grading astrocytic tumors, and cytologic features of anaplastic oligodendrogliomas have been poorly described.

Intraoperative smears of the tumor showed hypercellular, loosely cohesive cell clusters and single cells with nuclear pleomorphism, numerous apoptotic cells and no discernible fibrillary processes.

Cryostat sections showed cellular nests consisting of tumor cells with oval nuclei and clear cytoplasm.

These cells were proliferating in the finely reticulated vascular stroma, and the tumor had an infiltrative margin with areas of focal necrosis and numerous calcifications.

The diagnosis of anaplastic oligodendroglioma, World Health Organization grade 3, was made, and the results of fluorescence in situ hybridization (chromosome 1q deletion) supported the diagnosis.

CONCLUSION: Intraoperative diagnosis of anaplastic oligodendroglioma may not be easy but is possible with judicious consideration of several features: high cellularity, no fibrillary processes, nuclear atypia, pleomorphism, abundant apoptotic cells, occasional mitotic figures, coagulative necrosis, endothelial hyperplasia and characteristic conspicuous minigemistocytes.

[MeSH-major] Brain Neoplasms / pathology. Oligodendroglioma / pathology

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(PMID = 17718148.001).

[ISSN] 0001-5547

[Journal-full-title] Acta cytologica

[ISO-abbreviation] Acta Cytol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Long-term results of treatment in patients with oligodendrogliomas and oligoastrocytomas of the cerebral hemispheres].

BACKGROUND: the current approach to treating patients with cerebral oligodendrogliomas and oligoastrocytomas involves surgical treatment with the maximum tumor resection in reasonable ranges, by taking into account the anatomic and physiological availability, followed by chemo- and radiotherapy.

MATERIALS: the long-term results of treatment were analyzed in 80 patients with oligoglial tumors (oligodendrogliomas and oligoastrocytomas in 31 and 49 patients, respectively) treated at the A.L.

RESULTS: After complex therapy, the mean survival was 80.6 months in patients with oligodendrogliomas, 63.3 months in those with anaplastic oligoastrocytomas, and 42 months in those with anaplastic oligodendrogliomas.

[MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Oligodendroglioma / therapy

[MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Radiation Dosage

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(PMID = 18720725.001).

[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)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Significance and prospects of study on molecular alterations in oligodendrogliomas].

Oligodendroglial tumours represent a type of tumours in which molecular alterations may become a significant prognostic factor.

Oligodendrogliomas show distinct genetic alterations, allowing us to distinguish them from other types of gliomas.

Conversely, allelic loss on chromosome 10q, observed in many anaplastic oligodendrogliomas, predicts rather poor outcome.

The present paper is a compilation of the newest information on the characteristics of the genetic alterations related to the clinical course of oligodendrogliomas, which seems to be important for the proper diagnostics and selection of the appropriate methods of treatment.

[MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Loss of Heterozygosity / genetics. Oligodendroglioma / genetics

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(PMID = 17874342.001).

[ISSN] 0028-3843

[Journal-full-title] Neurologia i neurochirurgia polska

[ISO-abbreviation] Neurol. Neurochir. Pol.

[Language] pol

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Poland

[Number-of-references] 33

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Oligodendroglioma cell lines containing t(1;19)(q10;p10).

Investigating the biology of oligodendroglioma and its characteristic combined deletion of chromosomal arms 1p and 19q, mediated by an unbalanced translocation, t(1;19)(q10;p10), has been hampered by the lack of cell lines that harbor these traits.

We grew cells from 2 anaplastic oligodendrogliomas in serum-free conditions.

Serial propagation and expansion led to the establishment of permanent cell lines that maintained the genetic signature of the parent oligodendrogliomas and displayed features of brain tumor stem cells in vitro.

One line was established from a treatment-naïve tumor and the other from a temozolomide resistant recurrent tumor.

These lines may be important tools for understanding the biology of oligodendrogliomas and the function of their defining genetic traits.

[MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Oligodendroglioma / genetics

[MeSH-minor] Cell Line, Tumor. Humans. Translocation, Genetic / genetics

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(PMID = 20388696.001).

[ISSN] 1523-5866

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC2940664

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Univariate analysis was followed by multivariate analysis according to a Cox model. p14(ARF), p16(INK4A) and PTEN expressions, and 10p 10q23, 10q26 and 13q LOH for the entire cohort, hTERT expression for high-grade tumours, EGFR for glioblastomas, 10q26 LOH for grade III tumours and anaplastic oligodendrogliomas were found to be correlated with overall survival on univariate analysis and age and grade on multivariate analysis only.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Decision Making. Humans. Loss of Heterozygosity. Middle Aged. Multivariate Analysis. Prognosis. Promoter Regions, Genetic. Prospective Studies. Telomerase / genetics. Tumor Suppressor Proteins / genetics

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(PMID = 18506188.001).

[ISSN] 1532-1827

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 6.5.1.- / DNA Repair Enzymes

[Other-IDs] NLM/ PMC2410116

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here, we present for the first time a detailed analysis of the expression pattern of coronin-3 in human brain tumours and demonstrate that coronin-3 expression correlates with malignant phenotype in diffuse gliomas.

High-grade gliomas, such as anaplastic astrocytomas, anaplastic oligodendrogliomas, anaplastic oligoastrocytomas and glioblastomas, show high numbers of tumour cells positive for coronin-3, while diffuse low-grade gliomas, such as diffuse astrocytomas, oligodendrogliomas and oligoastrocytomas, exhibit low numbers of coronin-3-positive tumour cells.

In order to explore and verify a contribution of coronin-3 to the malignant phenotype of diffuse gliomas, we employed an efficient shRNA-mediated coronin-3 knockdown in U373 and A172 human glioblastoma cells.

Together, our findings demonstrate evidence for a contribution of coronin-3 expression in the malignant progression of diffuse gliomas.

[MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Microfilament Proteins / metabolism

[MeSH-minor] Astrocytes / metabolism. Cell Movement. Cell Proliferation. Extracellular Matrix / pathology. Humans. Matrix Metalloproteinases / metabolism. Neoplasm Invasiveness. Neoplasm Proteins / deficiency. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm Proteins / physiology. Tumor Cells, Cultured

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(PMID = 18189330.001).

[ISSN] 0022-3417

[Journal-full-title] The Journal of pathology

[ISO-abbreviation] J. Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Microfilament Proteins; 0 / Neoplasm Proteins; 145420-64-0 / coronin proteins; EC 3.4.24.- / Matrix Metalloproteinases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Imaging diagnosis and fundamental knowledge of common brain tumors in adults.

For instance, genetic analysis is important for differentiating oligodendroglial tumors from astrocytic tumors, and the gene mutation predicts response to chemotherapy for anaplastic oligodendrogliomas.

Background factors such as hormones, history of cranial irradiation, and medications influence oncogenesis, tumor growth, and tumor appearances as seen by imaging modalities.

A differential diagnosis with knowledge of the above may have some advantages over diagnoses based on imaging findings alone.

[MeSH-major] Brain Neoplasms / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed

[MeSH-minor] Adult. Glioma / diagnosis. Humans. Image Processing, Computer-Assisted. Japan / epidemiology. Meningioma / diagnosis. Neurilemmoma / diagnosis. Pituitary Neoplasms / diagnosis

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(PMID = 16958433.001).

[ISSN] 0288-2043

[Journal-full-title] Radiation medicine

[ISO-abbreviation] Radiat Med

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Japan

[Number-of-references] 31

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Pattern of care of high-grade gliomas].

[Transliterated title] Prise en charge des gliomes de haut grade.

High grade gliomas are the most frequent and malignant primary brain tumours in adults.

Prognosis depends on age, performance status and histological grade.

Associated with symptomatic treatments, surgery, radiotherapy and chemotherapy represent the main weapons of the specific multidisciplinary therapy of malignant gliomas.

Surgery is necessary for histological diagnosis.

In malignant gliomas, surgery may improve survival in case of complete removal, and debulking provides an improvement of the quality of life and a symptomatic relief.

Radiation therapy has been shown to improve survival in malignant glioma.

The place of chemotherapy is growing not only for anaplastic oligodendrogliomas, more chemosensitive (particularly when they harbor 1p19q codeletions), but also for glioblastomas patients, which have been shown to benefit from radiotherapy plus concomitant and adjuvant temozolomide.

[MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / therapeutic use. Adult. Age Factors. Aged. Anticonvulsants / therapeutic use. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Brain / pathology. Combined Modality Therapy. Dacarbazine / administration & dosage. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Epilepsy / prevention & control. Forecasting. Genetic Markers. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Humans. Magnetic Resonance Imaging. Neoplasm Recurrence, Local / drug therapy. Oligodendroglioma / drug therapy. Prognosis. Quality of Life. Radiotherapy Dosage. Randomized Controlled Trials as Topic. Survival Analysis. Thromboembolism / prevention & control. Time Factors. Tomography, X-Ray Computed

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(PMID = 17315503.001).

[ISSN] 0035-2640

[Journal-full-title] La Revue du praticien

[ISO-abbreviation] Rev Prat

[Language] fre

[Publication-type] Comparative Study; English Abstract; Journal Article; Review

[Publication-country] France

[Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anticonvulsants; 0 / Antineoplastic Agents, Alkylating; 0 / Genetic Markers; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide

[Number-of-references] 19

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The expression of Wilms' tumor gene WT1 protein was investigated immunohistochemically in 73 glial tumors, including 60 astrocytic tumors, eight oligodendroglial tumors, and five ependymal tumors.

Almost all glioblastomas, anaplastic astrocytomas, anaplastic ependymomas, and anaplastic oligodendrogliomas expressed high levels of WT1 protein.

Histological examination found that WT1 protein was strongly expressed in the anaplastic portions and areas with perivascular proliferation and high cellularity, implying that WT1 gene might be important in glial tumor cell proliferation.

This study indicates that many malignant glial tumors are good candidates for cancer immunotherapy targeting WT1 protein and that WT1 protein expression could be used as a proliferation marker in glial tumors.

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(PMID = 17457020.001).

[ISSN] 0470-8105

[Journal-full-title] Neurologia medico-chirurgica

[ISO-abbreviation] Neurol. Med. Chir. (Tokyo)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Ki-67 Antigen; 0 / WT1 Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We studied the status of chromosomes 1 and 19 in 363 astrocytic and oligodendroglial tumors.

Whereas the predominant pattern of copy number abnormality was a concurrent loss of the entire 1p and 19q regions (total 1p/19q loss) among oligodendroglial tumors and partial deletions of 1p and/or 19q in astrocytic tumors, a subset of apparently astrocytic tumors also had total 1p/19q loss.

The presence of total 1p/19q loss was associated with longer survival of patients with all types of adult gliomas independent of age and diagnosis (P = .041).

Novel regions of homozygous deletion, including a part of DPYD (1p21.3) or the KLK cluster (19q13.33), were observed in anaplastic oligodendrogliomas.

Thus, we show that the copy number abnormalities of 1p and 19q in human gliomas are complex and have distinct patterns that are prognostically predictive independent of age and pathological diagnosis.

[MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioma / diagnosis. Glioma / genetics

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(PMID = 20164239.001).

[ISSN] 1523-5866

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / /

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ PMC2940668

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analysis of EGFR overexpression, EGFR gene amplification and the EGFRvIII mutation in Portuguese high-grade gliomas.

BACKGROUND: Patients with malignant gliomas do not respond to any current therapy.

MATERIALS AND METHODS: EGFR overexpression, EGFRvIII mutation and EGFR amplification were determined by immunohistochemistry and chromogenic in situ hybridization (CISH) in 27 primary glioblastomas (GBM), 24 anaplastic oligodendrogliomas (AO) and four anaplastic oligoastrocytomas (AOA).

CONCLUSION: We characterized, for the first time, EGFR molecular alterations in Portuguese patients with malignant glioma and identified a subpopulation of patients presenting putative biomarkers for EGFR-based therapies.

[MeSH-minor] Adult. Aged. Female. Gene Amplification. Glioblastoma / genetics. Humans. Male. Middle Aged. Mutation. Oligodendroglioma / genetics. Portugal. Prognosis. Up-Regulation

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(PMID = 18507036.001).

[ISSN] 0250-7005

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In contrast, RTVP-1 and RTVP-1b showed similar patterns of expression in astrocytic tumors; highly expressed in glioblastomas as compared to normal brains, low-grade astrocytomas and anaplastic oligodendrogliomas.

[MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Nerve Tissue Proteins / biosynthesis. Nerve Tissue Proteins / genetics

[MeSH-minor] Alternative Splicing. Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Cell Movement. Cell Proliferation. Cloning, Molecular. Humans. Molecular Sequence Data. Protein Isoforms. Tissue Distribution

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(PMID = 17825796.001).

[ISSN] 0006-291X

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA-R21-96965; United States / NCI NIH HHS / CA / R24 CA095809

[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 / GLIPR1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Our studies show that IGFBP2 coexpression results in progression to a higher-grade glioma in platelet-derived growth factor beta (PDGFB)-driven tumors.

These anaplastic oligodendrogliomas are characterized by increased cellularity, vascular proliferation, small regions of necrosis, increased mitotic activity, and increased activation of the Akt pathway.

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(PMID = 17606927.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA098503; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA- 16672; United States / NCI NIH HHS / CA / R01 CA98503; United States / NIDDK NIH HHS / DK / 5 T90 DK070109-02; United States / NIDDK NIH HHS / DK / T90 DK070109

[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 / Insulin-Like Growth Factor Binding Protein 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / ras Proteins

[Other-IDs] NLM/ PMC1913900

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Retrospective analysis of outcomes among more than 1,000 patients with newly diagnosed anaplastic oligodendroglial tumors.

: 2014 Background: Treatment of anaplastic oligodendroglial tumors is controversial.

METHODS: We retrospectively identified adults with newly diagnosed anaplastic oligodendroglioma (AO) or oligo-astrocytoma (AOA) seen at 17 medical centers from 1981-2007 exclusive of phase III or bone marrow transplant trials.

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(PMID = 27964586.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Can tumor contrast enhancement be used as a criterion for differentiating tumor grades of oligodendrogliomas?

BACKGROUND AND PURPOSE: The association of high-grade oligodendrogliomas with tumor contrast material enhancement on MR images has been reported.

Some authors have even used contrast enhancement as a criterion for their oligodendroglioma grading system.

The purpose of our study was to evaluate if tumor contrast enhancement is a specific finding for anaplastic oligodendroglioma.

METHODS: Pretreatment MR images of 24 oligodendrogliomas were reviewed retrospectively, and findings were compared with the histologic grade.

The presence or absence and the pattern of tumor contrast enhancement were evaluated qualitatively.

A contrast enhancement ratio (CER), a quantitative criterion, was calculated to assess the difference in degree of enhancement between the low-grade and anaplastic tumors.

Tumor grade was diagnosed at pathologic examination according to the World Health Organization classification system.

RESULTS: Contrast enhancement was noted in nine (56%) of 16 low-grade tumors and in five (62%) of eight anaplastic tumors.

The CERs were 2.12-40.88 (mean, 20.08) in low-grade tumors and were 3.20-62.52 (mean, 28.73) in anaplastic tumors (P > .05).

CONCLUSION: Tumor contrast enhancement was not statistically significantly different between the tumor groups.

We believe that the presence or absence of tumor contrast enhancement is not a specific finding for simply discriminating low-grade from anaplastic oligodendrogliomas.

[MeSH-major] Brain Neoplasms / pathology. Magnetic Resonance Imaging. Oligodendroglioma / pathology

[MeSH-minor] Adolescent. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies

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(PMID = 15814921.001).

[ISSN] 0195-6108

[Journal-full-title] AJNR. American journal of neuroradiology

[ISO-abbreviation] AJNR Am J Neuroradiol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Survival analysis of presumptive prognostic markers among oligodendrogliomas.

BACKGROUND: Allelic losses of 1p and 19q arms correlate with the oligodendroglial phenotype as well as with sensitivity to radiotherapy and chemotherapy.

Furthermore, the DNA repair gene, methylguanine methyltransferase (MGMT), is diminished in 80% of oligodendroglial tumors and represents a possible mechanism for this therapeutic sensitivity.

However, the authors questioned the relevance of genetic testing and measuring MGMT levels in tumors that were diagnostic of oligodendroglioma.

METHODS: The authors performed a retrospective analysis of 1p, 19q, 9p21, TP53, and MGMT status in 46 patients with oligodendrogliomas to address any relations that may exist among these markers with regard to progression-free survival (PFS) and total survival.

RESULTS: The authors found that survival among patients with light microscopically diagnosed oligodendroglial tumors demonstrating LOH of 1p and 19q trended toward statistical significance (P = 0.102 and P = 0.058, respectively).

9p21 LOH was significant as a predictor of PFS only among anaplastic oligodendrogliomas in this cohort (P = 0.033).

Low-level MGMT labeling index (LI) (< 20%) was noted in 86% of all oligodendroglial tumors.

MGMT levels were decreased in a majority of oligodendrogliomas.

[MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. O(6)-Methylguanine-DNA Methyltransferase / analysis. Oligodendroglioma / mortality. Tumor Suppressor Protein p53 / analysis

[MeSH-minor] Chromosomes, Human / genetics. Cohort Studies. Disease-Free Survival. Humans. In Situ Hybridization. Loss of Heterozygosity. Neoplasm Proteins. Prognosis. Retrospective Studies. Survival Rate

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[Copyright] Copyright 2005 American Cancer Society

(PMID = 16116609.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 1P50 CA108786; United States / NCI NIH HHS / CA / 5R01 CA43722

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Real-time quantitative PCR analysis of gene dosages reveals gene amplification in low-grade oligodendrogliomas.

Proto-oncogene amplification is an important alteration that is present in about 45% to 50% of high-grade human gliomas.

We studied this mechanism in 8 genes (cyclin-dependent kinase-4 [CDK4], MDM2, MDM4, renin-angiotensin system-1, ELF3, GAC1, human epidermal growth factor receptor-2, and platelet-derived growth factor receptor-A gene) in a series of 40 oligodendrogliomas (World Health Organization (WHO) grade II, 21; WHO grade III, 13; and WHO grade II-III oligoastrocytomas, 6) using real-time quantitative polymerase chain reaction.

By histopathologic grade, 67% of grade II oligodendrogliomas (14/21), 46% of grade III anaplastic oligodendrogliomas (6/13), and 50% of mixed oligoastrocytomas (3/6) were positive for amplification of at least 1 gene.

Our findings demonstrate gene amplification in low-grade samples indicating that it is an important alteration in the early steps of oligodendroglioma development and, therefore, might be considered a molecular mechanism leading to malignant progression toward anaplastic forms.

[MeSH-major] Brain Neoplasms / genetics. Gene Amplification. Gene Dosage. Oligodendroglioma / genetics. Proto-Oncogenes / genetics. Reverse Transcriptase Polymerase Chain Reaction

[MeSH-minor] Biomarkers, Tumor / analysis. Humans

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(PMID = 15899783.001).

[ISSN] 0002-9173

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

CONTEXT: Deletions on chromosomes 1p and 19q have been shown to correlate with prognosis and chemosensitivity in anaplastic oligodendrogliomas.

OBJECTIVE: The purpose of this study was to identify patients with GBM who had evidence of 1p or 19q deletions by fluorescence in situ hybridization, and correlate these results with clinical findings and survival.

RESULT: Seventeen (5.1%) patients (9 males; mean age at diagnosis=61 y, range: 35 to 84 y) were found to have 1p deletions; 8 patients (47.1%) received chemotherapy and 13 patients received radiation therapy.

A control group of 20 patients (13 males; mean=60 y, range: 40 to 80 y) was selected, 8 patients (40%) of who received chemotherapy and 12 patients were known to have had radiation therapy.

In contrast to anaplastic oligodendrogliomas, 1p and 19q deletions alone were not found to improve survival of patients with GBM; however, when adjusted for age, sex, and chemotherapy, 19q deletions seem to negatively impact survival.

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(PMID = 19602970.001).

[ISSN] 1533-4058

[Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM

[ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Retrospective review of prognostic factors, including 1p19q deletion, in low-grade oligodendrogliomas and a review of recent published works.

The purpose of the present study was to investigate potential prognostic factors in low-grade oligodendrogliomas (LGOs), particularly 1p19q deletion, due to its proven prognostic significance in anaplastic oligodendrogliomas.

We carried out a retrospective review of patients with a histological diagnosis of LGO between 1990 and 2000 in Auckland and Wellington, New Zealand.

Univariate analysis of potential prognostic factors including 1p19q status, age, tumour size, tumour crossing midline, tumour enhancement, extent of surgery and seizures at diagnosis was carried out.

[MeSH-major] Brain Neoplasms. Oligodendroglioma

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(PMID = 19624298.001).

[ISSN] 1754-9485

[Journal-full-title] Journal of medical imaging and radiation oncology

[ISO-abbreviation] J Med Imaging Radiat Oncol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Australia

[Number-of-references] 30

   

[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.

PURPOSE: Allelic loss at 1p is seen in 70% to 85% of oligodendrogliomas (typically in association with 19q allelic loss) and 20-30% of astrocytomas.

Because most 1p deletions in gliomas involve almost the entire chromosome arm, narrowing the region of the putative tumor suppressor gene has been difficult.

The latter group included both low-grade tumors (oligodendroglioma, diffuse astrocytoma, and "oligoastrocytoma") and high-grade tumors (anaplastic oligodendrogliomas, anaplastic astrocytomas, anaplastic oligoastrocytomas).

RESULTS: Allelic losses on 1p and 19q, either separately or combined, were more common in classic oligodendrogliomas than in either astrocytomas or oligoastrocytomas (P < 0.0001).

Classic oligodendrogliomas showed 1p loss in 35 of 42 (83%) cases, 19q loss in 28 of 39 (72%), and these were combined in 27 of 39 (69%) cases.

There was no significant difference in 1p/19q LOH status between low-grade and anaplastic oligodendrogliomas.

Although rare, 1p deletions were more often segmental in astrocytomas (5 of 6, 83%) than in oligodendrogliomas (3 of 35, 9%; P = 0.006).

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.

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-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

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(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cyclooxygenase-2 expression in astrocytes and microglia in human oligodendroglioma and astrocytoma.

For this purpose we employed dual immunohistochemistry for cox-2 and GFAP (astrocyte) or LCA-MAC (microglia-macrophage) in archival formalin-fixed, paraffin embedded human tissue diagnosed as oligodendroglioma and/or astrocytoma.

The results showed that cox-2 immunoreactivity is up-regulated in the neurons according to the tumor grade.

Most of the cox-2 immunoreactive glia were GFAP-positive in anaplastic oligodendrogliomas and at lesser extend in glioblastomas.

It may be speculated that the induction of cox-2 in microglia may contribute to the deleterious effects of prostanoids in cerebral edema formation during the progression of oligodendrogliomas.

[MeSH-major] Astrocytes / enzymology. Astrocytoma / enzymology. Cyclooxygenase 2 / metabolism. Microglia / enzymology. Oligodendroglioma / enzymology

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(PMID = 20052522.001).

[ISSN] 1567-2387

[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 / Glial Fibrillary Acidic Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 3.1.3.48 / Antigens, CD45

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Current strategies in treatment of oligodendroglioma: evolution of molecular signatures of response.

Oligodendroglioma frequently (> or = 70%) responds to radiation and chemotherapy, and is the first CNS neoplasm in which a genetic signature (1p and 19q deletion) has been associated with outcome within the context of large clinical trials.

Current translational investigations focus on deletions or mutations of potential tumor suppressor genes, epigenetic alterations, amplification or mutation of growth factor and regulatory genes, and characterization of signaling events and regulatory protein expression.

The most compelling data has involved 1p and 19q loss, which is observed in over 50% of anaplastic oligodendrogliomas.

In two randomized phase III trials (Radiation Therapy Oncology Group 9402 and European Organisation for Research and Treatment of Cancer 26951), the addition of neoadjuvant or adjuvant procarbazine, lomustine, and vincristine (PCV; respectively) to radiotherapy did not produce superior survival as compared with radiotherapy alone.

However, it is unclear whether these deletions represent surrogate markers of a favorable biologic tumor behavior, or are predictive of outcome after specific treatment.

Future phase III trials are evaluating other chemotherapeutic and targeted agents, including temozolomide, and include correlative investigations of aberrant molecular events in these neoplasms, which may lead to future therapeutic strategies that are based on specific molecular signatures.

[MeSH-major] Central Nervous System Neoplasms / therapy. Oligodendroglioma / therapy

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(PMID = 16525179.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 68