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1. Bello MJ, Alonso ME, Amiñoso C, Anselmo NP, Arjona D, Gonzalez-Gomez P, Lopez-Marin I, de Campos JM, Gutierrez M, Isla A, Kusak ME, Lassaletta L, Sarasa JL, Vaquero J, Casartelli C, Rey JA: Hypermethylation of the DNA repair gene MGMT: association with TP53 G:C to A:T transitions in a series of 469 nervous system tumors. Mutat Res; 2004 Oct 4;554(1-2):23-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypermethylation of the DNA repair gene MGMT: association with TP53 G:C to A:T transitions in a series of 469 nervous system tumors.
  • O6-methylguanine-DNA methyltransferase (MGMT) plays a major role in repairing DNA damage from alkylating agents.
  • By removing alkyl groups from the O6-position in guanine, MGMT can prevent G:C to A:T transition mutations, a type of variation frequently involving TP53 mutations in brain tumors.
  • Promoter hypermethylation of CpG islands in tumor-related genes can lead to their transcriptional inactivation, and this epigenetic mechanism has been shown to participate in MGMT silencing in some cancers, including those affecting the nervous system.
  • To determine the relevance of defective MGMT function due to aberrant methylation in relation to the presence of TP53 mutations, we studied 469 nervous system tumors (including all major histological subtypes) for MGMT promoter methylation and TP53 mutations at exons 5-8.
  • Overall, aberrant methylation occurred in 38% of the samples (180/469), with values higher than 50% in the more malignant forms such as glioblastomas and anaplastic gliomas including those with astrocytic, oligodendroglial and ependymal differentiation.
  • In contrast, the non-glial tumors displayed an overall aberrant MGMT promoter methylation of 26%, even though this group includes highly malignant tumors such as neuroblastomas, medulloblastomas and brain metastases.
  • Overall, TP53 mutations were found in 25% of the methylated MGMT tumors (45/180), whereas only 10% of the unmethylated MGMT tumors (30/289) showed TP53 changes (P < 0.001).
  • G:C to A:T changes occurred at CpG sites in 9% of methylated tumors, and in 0.7% of the unmethylated samples.
  • This type of transition at non-CpG dinucleotides was also more frequent in the tumors with aberrant MGMT methylation (5%) than the unmethylated tumors (0.7%).
  • These data suggest that MGMT silencing as a result of promoter hypermethylation may lead to G:C to A:T transition mutations in the TP53 gene of some histological nervous system tumor subtypes.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Child, Preschool. DNA Primers. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational

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  • (PMID = 15450401.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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2. Phan TG, O'Neill BP, Kurtin PJ: Posttransplant primary CNS lymphoma. Neuro Oncol; 2000 10;2(4):229-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Compared with the initial computed tomographic study, MRI showed 25 additional brain lesions.
  • Only 43.7% of lesions enhanced with contrast agent; of those that did, all but one were heterogeneous.
  • Ependymal contact occurred in 5 patients.
  • Diagnostic tissue was obtained by stereotactic biopsy from 6 patients and by open biopsy from 2.
  • Slides available for review (7 patients) showed that the tumors were of CD20-positive lineage and were positive for Epstein-Barr virus, using in situ hybridization.
  • In our series, (1) PT-PCNSL presented nonspecifically and progressed rapidly, (2) stereotactic brain biopsy had significant morbidity, and (3) despite multimodal therapy, survival was poor.
  • [MeSH-major] Brain Neoplasms / etiology. Brain Neoplasms / pathology. Immunosuppressive Agents / adverse effects. Lymphoma, Non-Hodgkin / etiology. Lymphoma, Non-Hodgkin / pathology. Organ Transplantation / adverse effects
  • [MeSH-minor] Adult. Brain / drug effects. Brain / pathology. Brain / physiopathology. Cerebrospinal Fluid / chemistry. Cerebrospinal Fluid / cytology. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed

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  • (PMID = 11265232.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA15083
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
  • [Other-IDs] NLM/ PMC1920594
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3. Ginguené C, Champier J, Maallem S, Strazielle N, Jouvet A, Fèvre-Montange M, Ghersi-Egea JF: P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) localize in the microvessels forming the blood-tumor barrier in ependymomas. Brain Pathol; 2010 Sep;20(5):926-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) localize in the microvessels forming the blood-tumor barrier in ependymomas.
  • Ependymomas are neuroepithelial tumors that arise from the ependymal layer bordering the cerebral ventricles and spinal canal.
  • Intracranial ependymoma represents a major encephalic tumor in children, while spinal ependymoma develops more frequently in adults.
  • To understand the pharmacoresistance that characterizes this tumoral entity, we analyzed the level of expression and localization of three major efflux transport proteins with a multidrug resistance function, P-glycoprotein, multidrug resistance-related protein 1 (MRP1) and breast cancer resistance protein (BCRP), in a series of 25 ependymomas from both children and adults.
  • Real-time-PCR analysis showed that all three genes were expressed in all tumors, with no apparent correlation between the level of expression and either age or tumor grade.
  • The MRP1 transcript was expressed at a significantly higher level in spinal tumors than in intracranial tumors.
  • The expression of the proteins corresponding to these genes was confirmed by Western blot analysis.
  • In an immunohistochemical study, P-glycoprotein and BCRP were shown to be associated with the tumoral vessels, where they presented a luminal localization, a prerequisite for their efflux drug activity into the blood.
  • These data indicate that a biochemical, transporter-dependent blood-tumor barrier may exist in ependymomas, which may reduce the tumoral bioavailability of lipophilic and amphiphilic anticancer drugs.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Blood-Testis Barrier / metabolism. Cerebral Ventricle Neoplasms / pathology. Ependymoma / pathology. Microvessels / metabolism. Neoplasm Proteins / metabolism. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family B. ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adolescent. Adult. Aged. Child. Child, Preschool. Humans. Infant. Laminin / metabolism. Middle Aged. Models, Biological. Young Adult. von Willebrand Factor / metabolism

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  • (PMID = 20406235.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Laminin; 0 / Neoplasm Proteins; 0 / von Willebrand Factor
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4. Preusser M, Hoischen A, Novak K, Czech T, Prayer D, Hainfellner JA, Baumgartner C, Woermann FG, Tuxhorn IE, Pannek HW, Bergmann M, Radlwimmer B, Villagrán R, Weber RG, Hans VH: Angiocentric glioma: report of clinico-pathologic and genetic findings in 8 cases. Am J Surg Pathol; 2007 Nov;31(11):1709-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiocentric glioma has recently been described as a novel epilepsy associated tumor with distinct clinico-pathologic features.
  • We report the clinical and pathologic findings in 8 additional cases of this rare tumor type and extend its characterization by genomic profiling.
  • Almost all patients had a history of long-standing drug-resistant epilepsy.
  • Cortico-subcortical tumors were located in the temporal and parietal lobes.
  • Histologically, the tumors were characterized by diffuse growth and prominent perivascular tumor cell arrangements with features of astrocytic/ependymal differentiation, but lacking neoplastic neuronal features.
  • Electron microscopy showed ependymal characteristics in 2 of 3 cases investigated.
  • In 1 of 3 cases, a high-resolution screen by array-comparative genomic hybridization identified a copy number gain of 2 adjacent clones from chromosomal band 11p11.2 containing the protein-tyrosine phosphatase receptor type J (PTPRJ) gene.
  • All patients are seizure free and without evidence of tumor recurrence at follow-up times ranging from 1/2 to 6.9 years.
  • Our findings support 2 previous reports proposing that angiocentric glioma is a novel glial tumor entity of low-grade malignancy.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / ultrastructure. Epilepsy / genetics. Gene Expression Regulation, Neoplastic. Glioma / genetics. Glioma / ultrastructure
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytes / pathology. Cell Differentiation. Cell Proliferation. Child. Child, Preschool. Chromosome Deletion. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 6. Ependyma / pathology. Europe. Female. Follow-Up Studies. Gene Dosage. Gene Expression Profiling / methods. Glial Fibrillary Acidic Protein / analysis. Humans. Magnetic Resonance Imaging. Male. Membrane Glycoproteins / analysis. Middle Aged. Mucin-1 / analysis. Nerve Growth Factors / analysis. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Receptor-Like Protein Tyrosine Phosphatases, Class 3 / genetics. S100 Calcium Binding Protein beta Subunit. S100 Proteins / analysis. Time Factors. Treatment Outcome. Vimentin / analysis

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  • (PMID = 18059228.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Membrane Glycoproteins; 0 / Mucin-1; 0 / Nerve Growth Factors; 0 / PDPN protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / Vimentin; EC 3.1.3.48 / PTPRJ protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 3
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