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  • 1
    Language: English
    In: Clinical cancer research, 2008-01-01, Vol.14 (1), p.123-129
    Description: Purpose: The CD133 antigen has been identified as a putative stem cell marker in normal and malignant brain tissues. In gliomas, it is used to enrich a subpopulation of highly tumorigenic cancer cells. According to the cancer stem cell hypothesis, CD133-positive cells determine long-term tumor growth and, therefore, are suspected to influence clinical outcome. To date, a correlation between CD133 expression in primary tumor tissues and patients' prognosis has not been reported. Experimental Design: To address this question, we analyzed the expression of the CD133 stem cell antigen in a series of 95 gliomas of various grade and histology by immunohistochemistry on cryostat sections. Staining data were correlated with patient outcome. Results: By multivariate survival analysis, we found that both the proportion of CD133-positive cells and their topological organization in clusters were significant ( P 〈 0.001) prognostic factors for adverse progression-free survival and overall survival independent of tumor grade, extent of resection, or patient age. Furthermore, proportion of CD133-positive cells was an independent risk factor for tumor regrowth and time to malignant progression in WHO grade 2 and 3 tumors. Conclusions: These findings constitute the first conclusive evidence that CD133 stem cell antigen expression correlates with patient survival in gliomas, lending support to the current cancer stem cell hypothesis.
    Subject(s): stem cells ; glioma ; prognosis ; CD133 ; Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Antineoplastic agents ; Pharmacology. Drug treatments ; Immunohistochemistry ; Glioma - mortality ; Prognosis ; Peptides ; Antigens, CD - biosynthesis ; Humans ; Middle Aged ; Brain Neoplasms - pathology ; Kaplan-Meier Estimate ; Male ; Stem Cells - metabolism ; AC133 Antigen ; Brain Neoplasms - metabolism ; Glioma - metabolism ; Glycoproteins - biosynthesis ; Disease-Free Survival ; Glioma - pathology ; Survival Analysis ; Adult ; Female ; Brain Neoplasms - mortality ; Index Medicus
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Nature medicine, 2013-07, Vol.19 (7), p.901-908
    Description: Here we show that glioblastoma express high levels of branched-chain amino acid transaminase 1 (BCAT1), the enzyme that initiates the catabolism of branched-chain amino acids (BCAAs). Expression of BCAT1 was exclusive to tumors carrying wild-type isocitrate dehydrogenase 1 (IDH1) and IDH2 genes and was highly correlated with methylation patterns in the BCAT1 promoter region. BCAT1 expression was dependent on the concentration of α-ketoglutarate substrate in glioma cell lines and could be suppressed by ectopic overexpression of mutant IDH1 in immortalized human astrocytes, providing a link between IDH1 function and BCAT1 expression. Suppression of BCAT1 in glioma cell lines blocked the excretion of glutamate and led to reduced proliferation and invasiveness in vitro, as well as significant decreases in tumor growth in a glioblastoma xenograft model. These findings suggest a central role for BCAT1 in glioma pathogenesis, making BCAT1 and BCAA metabolism attractive targets for the development of targeted therapeutic approaches to treat patients with glioblastoma.
    Subject(s): Transaminases - physiology ; Cell Proliferation ; Transaminases - genetics ; Amino Acids, Branched-Chain - metabolism ; Humans ; Brain Neoplasms - pathology ; Brain Neoplasms - genetics ; Isocitrate Dehydrogenase - genetics ; Brain Neoplasms - metabolism ; Glioma - metabolism ; Isocitrate Dehydrogenase - physiology ; Glioma - genetics ; Animals ; Mice, Nude ; Models, Biological ; Glioma - pathology ; HEK293 Cells ; Transaminases - metabolism ; Cell Line, Tumor ; Female ; Mice ; Metabolism - genetics ; Cell proliferation ; Care and treatment ; Gliomas ; Physiological aspects ; Genetic aspects ; Research ; Methylation ; Amino acid metabolism ; Index Medicus
    ISSN: 1078-8956
    E-ISSN: 1546-170X
    Source: Single Journals
    Source: Academic Search Ultimate
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Hepatology (Baltimore, Md.), 2012-11, Vol.56 (5), p.1817-1827
    Description: To identify new tumor‐suppressor gene candidates relevant for human hepatocarcinogenesis, we performed genome‐wide methylation profiling and vertical integration with array‐based comparative genomic hybridization (aCGH), as well as expression data from a cohort of well‐characterized human hepatocellular carcinomas (HCCs). Bisulfite‐converted DNAs from 63 HCCs and 10 healthy control livers were analyzed for the methylation status of more than 14,000 genes. After defining the differentially methylated genes in HCCs, we integrated their DNA copy‐number alterations as determined by aCGH data and correlated them with gene expression to identify genes potentially silenced by promoter hypermethylation. Aberrant methylation of candidates was further confirmed by pyrosequencing, and methylation dependency of silencing was determined by 5‐aza‐2′‐deoxycytidine (5‐aza‐dC) treatment. Methylation profiling revealed 2,226 CpG sites that showed methylation differences between healthy control livers and HCCs. Of these, 537 CpG sites were hypermethylated in the tumor DNA, whereas 1,689 sites showed promoter hypomethylation. The hypermethylated set was enriched for genes known to be inactivated by the polycomb repressive complex 2, whereas the group of hypomethylated genes was enriched for imprinted genes. We identified three genes matching all of our selection criteria for a tumor‐suppressor gene (period homolog 3 [PER3], insulin‐like growth‐factor–binding protein, acid labile subunit [IGFALS], and protein Z). PER3 was down‐regulated in human HCCs, compared to peritumorous and healthy liver tissues. 5‐aza‐dC treatment restored PER3 expression in HCC cell lines, indicating that promoter hypermethylation was indeed responsible for gene silencing. Additionally, functional analysis supported a tumor‐suppressive function for PER3 and IGFALS in vitro. Conclusion: The present study illustrates that vertical integration of methylation data with high‐resolution genomic and transcriptomic data facilitates the identification of new tumor‐suppressor gene candidates in human HCC. (HEPATOLOGY 2012;56:1817–1827)
    Subject(s): Gastroenterology. Liver. Pancreas. Abdomen ; Biological and medical sciences ; Medical sciences ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Tumors ; Humans ; Middle Aged ; Blood Proteins - drug effects ; Male ; Gene Expression Profiling ; Glycoproteins - drug effects ; Carrier Proteins - drug effects ; Promoter Regions, Genetic - genetics ; Case-Control Studies ; Genes, Tumor Suppressor - drug effects ; Young Adult ; Period Circadian Proteins - genetics ; Blood Proteins - genetics ; Carcinoma, Hepatocellular - genetics ; Adult ; Antimetabolites, Antineoplastic - pharmacology ; Female ; Glycoproteins - genetics ; Liver Neoplasms - genetics ; Down-Regulation ; Liver - metabolism ; Gene Silencing ; Azacitidine - analogs & derivatives ; Period Circadian Proteins - drug effects ; Azacitidine - pharmacology ; Carrier Proteins - genetics ; Comparative Genomic Hybridization ; Adolescent ; Cell Line, Tumor ; CpG Islands - genetics ; Aged ; DNA Methylation - drug effects ; Index Medicus
    ISSN: 0270-9139
    E-ISSN: 1527-3350
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: Nature communications, 2020-12-18, Vol.11 (1), p.6434-6434
    Description: Glioblastoma frequently exhibits therapy-associated subtype transitions to mesenchymal phenotypes with adverse prognosis. Here, we perform multi-omic profiling of 60 glioblastoma primary tumours and use orthogonal analysis of chromatin and RNA-derived gene regulatory networks to identify 38 subtype master regulators, whose cell population-specific activities we further map in published single-cell RNA sequencing data. These analyses identify the oligodendrocyte precursor marker and chromatin modifier SOX10 as a master regulator in RTK I-subtype tumours. In vitro functional studies demonstrate that SOX10 loss causes a subtype switch analogous to the proneural-mesenchymal transition observed in patients at the transcriptomic, epigenetic and phenotypic levels. SOX10 repression in an in vivo syngeneic graft glioblastoma mouse model results in increased tumour invasion, immune cell infiltration and significantly reduced survival, reminiscent of progressive human glioblastoma. These results identify SOX10 as a bona fide master regulator of the RTK I subtype, with both tumour cell-intrinsic and microenvironmental effects.
    Subject(s): Index Medicus ; CNS cancer ; Cancer genomics
    E-ISSN: 2041-1723
    Source: Nature Open Access
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: Journal of clinical oncology, 2009-04-01, Vol.27 (10), p.1627-1636
    Description: Medulloblastoma is the most common malignant brain tumor in children. Current treatment decisions are based on clinical variables. Novel tumor-derived biomarkers may improve the risk stratification of medulloblastoma patients. A model for the molecular risk stratification was proposed from an array-based comparative genomic hybridization (array-CGH) screen (n = 80). Fluorescence in situ hybridization (FISH) analyses for chromosome arms 6q, 17p, and 17q and the MYC and MYCN loci were performed in an independent validation set (n = 260). Copy number aberrations were correlated with clinical, histologic, and survival data. Gain of 6q and 17q and genomic amplification of MYC or MYCN were each associated with poor outcome in the array-CGH study (n = 80). In contrast, all patients with 6q-deleted tumors survived. Given these findings, the following hierarchical molecular staging system was defined: (1) MYC/MYCN amplification, (2) 6q gain, (3) 17q gain, (4) 6q and 17q balanced, and (5) 6q deletion. The prognostic value of this staging system was investigated by FISH analysis (n = 260). The addition of molecular markers to clinical risk factors resulted in the identification of a large proportion of patients (72 of 260 patients; 30%) at high risk for relapse and death who would be considered standard risk by application of clinical variables alone. Genomic aberrations in medulloblastoma are powerful independent markers of disease progression and survival. By adding genomic markers to established clinical and histologic variables, outcome prediction can be substantially improved. Because the analyses can be conducted on routine paraffin-embedded material, it will be especially feasible to use this novel molecular staging system in large multicenter clinical trials.
    Subject(s): Oncogene Proteins - genetics ; Prognosis ; Area Under Curve ; Tissue Array Analysis ; Humans ; Cerebellar Neoplasms - mortality ; Kaplan-Meier Estimate ; Child, Preschool ; In Situ Hybridization, Fluorescence ; Male ; Gene Dosage ; Cerebellar Neoplasms - genetics ; Medulloblastoma - mortality ; Chromosomes, Human, Pair 17 - genetics ; Chromosomes, Human, Pair 6 - genetics ; Comparative Genomic Hybridization ; Genes, myc - genetics ; Chromosome Aberrations ; Female ; ROC Curve ; N-Myc Proto-Oncogene Protein ; Medulloblastoma - genetics ; Nuclear Proteins - genetics ; Child ; Index Medicus
    ISSN: 0732-183X
    E-ISSN: 1527-7755
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Genetics (Austin), 2001-08-01, Vol.158 (4), p.1697-1710
    Description: To better understand the evolution of red-green color vision in vertebrates, we inferred the amino acid sequences of the ancestral pigments of 11 selected visual pigments: the LWS pigments of cave fish (Astyanax fasciatus), frog (Xenopus laevis), chicken (Gallus gallus), chameleon (Anolis carolinensis), goat (Capra hircus), and human (Homo sapiens);and the MWS pigments of cave fish, gecko (Gekko gekko), mouse (Mus musculus), squirrel (Sciurus carolinensis), and human. We constructed these ancestral pigments by introducing the necessary mutations into contemporary pigments and evaluated their absorption spectra using an in vitro assay. The results show that the common ancestor of vertebrates and most other ancestors had LWS pigments. Multiple regression analyses of ancestral and contemporary MWS and LWS pigments show that single mutations S180A, H197Y, Y277F, T285A, A308S, and double mutations S180A/H197Y shift the lambda(max) of the pigments by -7, -28, -8, -15, -27, and 11 nm, respectively. It is most likely that this "five-sites" rule is the molecular basis of spectral tuning in the MWS and LWS pigments during vertebrate evolution.
    Subject(s): Models, Theoretical ; Amino Acid Sequence ; Goats ; Sciuridae ; Humans ; Xenopus laevis ; Color ; Amino Acids - chemistry ; Molecular Sequence Data ; Phylogeny ; Sequence Analysis, DNA ; Sequence Homology, Amino Acid ; Animals ; Base Sequence ; Chickens ; Fishes ; Lizards ; Cloning, Molecular ; Color Perception - genetics ; Mice ; Spectrophotometry ; DNA, Complementary - metabolism ; Evolution, Molecular ; Genetic aspects ; Color vision ; Research ; Molecular genetics ; Color blindness ; Index Medicus
    ISSN: 0016-6731
    E-ISSN: 1943-2631
    Source: PubMed Central
    Source: Genetics Society of America
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: The Journal of clinical investigation, 2008-05, Vol.118 (5), p.1739-1749
    Description: The molecular pathogenesis of pediatric astrocytomas is still poorly understood. To further understand the genetic abnormalities associated with these tumors, we performed a genome-wide analysis of DNA copy number aberrations in pediatric low-grade astrocytomas by using array-based comparative genomic hybridization. Duplication of the BRAF protooncogene was the most frequent genomic aberration, and tumors with BRAF duplication showed significantly increased mRNA levels of BRAF and a downstream target, CCND1, as compared with tumors without duplication. Furthermore, denaturing HPLC showed that activating BRAF mutations were detected in some of the tumors without BRAF duplication. Similarly, a marked proportion of low-grade astrocytomas from adult patients also had BRAF duplication. Both the stable silencing of BRAF through shRNA lentiviral transduction and pharmacological inhibition of MEK1/2, the immediate downstream phosphorylation target of BRAF, blocked the proliferation and arrested the growth of cultured tumor cells derived from low-grade gliomas. Our findings implicate aberrant activation of the MAPK pathway due to gene duplication or mutation of BRAF as a molecular mechanism of pathogenesis in low-grade astrocytomas and suggest inhibition of the MAPK pathway as a potential treatment.
    Subject(s): Gene Duplication ; MAP Kinase Signaling System - physiology ; Humans ; Brain Neoplasms - pathology ; Cyclins - genetics ; Male ; Astrocytoma - pathology ; Cyclins - metabolism ; Microarray Analysis ; Astrocytoma - enzymology ; Female ; Cyclin D ; Child ; Proto-Oncogene Proteins B-raf - metabolism ; Astrocytoma - genetics ; Nucleic Acid Hybridization - methods ; Brain Neoplasms - enzymology ; Enzyme Inhibitors - metabolism ; Brain Neoplasms - genetics ; Proto-Oncogene Proteins B-raf - genetics ; Chromosome Aberrations ; Cell Cycle - physiology ; Mitogen-Activated Protein Kinases - genetics ; Enzyme Activation ; Mutation ; Mitogen-Activated Protein Kinases - metabolism ; Care and treatment ; Prognosis ; Gene mutations ; Genetic aspects ; Diagnosis ; Research ; Identification and classification ; Health aspects ; Astrocytoma ; Risk factors ; Methods ; Cancer ; Index Medicus ; Abridged Index Medicus
    ISSN: 0021-9738
    E-ISSN: 1558-8238
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: International journal of cancer, 2014-10-15, Vol.135 (8), p.1822-1831
    Description: The prognosis of glioblastoma, the most malignant type of glioma, is still poor, with only a minority of patients showing long‐term survival of more than three years after diagnosis. To elucidate the molecular aberrations in glioblastomas of long‐term survivors, we performed genome‐ and/or transcriptome‐wide molecular profiling of glioblastoma samples from 94 patients, including 28 long‐term survivors with 〉36 months overall survival (OS), 20 short‐term survivors with 〈12 months OS and 46 patients with intermediate OS. Integrative bioinformatic analyses were used to characterize molecular aberrations in the distinct survival groups considering established molecular markers such as isocitrate dehydrogenase 1 or 2 (IDH1/2) mutations, and O6‐methylguanine DNA methyltransferase (MGMT) promoter methylation. Patients with long‐term survival were younger and more often had IDH1/2‐mutant and MGMT‐methylated tumors. Gene expression profiling revealed over‐representation of a distinct (proneural‐like) expression signature in long‐term survivors that was linked to IDH1/2 mutation. However, IDH1/2‐wildtype glioblastomas from long‐term survivors did not show distinct gene expression profiles and included proneural, classical and mesenchymal glioblastoma subtypes. Genomic imbalances also differed between IDH1/2‐mutant and IDH1/2‐wildtype tumors, but not between survival groups of IDH1/2‐wildtype patients. Thus, our data support an important role for MGMT promoter methylation and IDH1/2 mutation in glioblastoma long‐term survival and corroborate the association of IDH1/2 mutation with distinct genomic and transcriptional profiles. Importantly, however, IDH1/2‐wildtype glioblastomas in our cohort of long‐term survivors lacked distinctive DNA copy number changes and gene expression signatures, indicating that other factors might have been responsible for long survival in this particular subgroup of patients.© 2014 UICC What's new? Long‐term survival of more than 3 years after the diagnosis of glioblastoma is a rare and poorly understood phenomenon. Here, the authors sought to elucidate the molecular aberrations in glioblastomas of long‐term survivors. They demonstrate that gene expression changes and genomic imbalances in glioblastomas from long‐term survivors are closely associated with IDH1/2 mutation, but not with IDH1/2‐independent long‐term survival. Moreover, they disclose that most gene signatures previously linked to long‐term survival are indeed associated with IDH1/2 mutation and are not prognostic in patients with IDH1/2‐wildtype tumors. The molecular basis of long‐term survival with IDH1/2‐wildtype glioblastoma remains to be resolved.
    Subject(s): glioblastoma ; MGMT ; IDH1 ; gene expression profiles ; array‐based comparative genomic hybridization ; integrative bioinformatics ; long‐term survival ; Neurology ; Biological and medical sciences ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Tumors ; Promoter Regions, Genetic ; Prospective Studies ; Oligonucleotide Array Sequence Analysis ; Humans ; DNA Repair Enzymes - genetics ; Survivors ; Transcriptome ; Brain Neoplasms - genetics ; Isocitrate Dehydrogenase - genetics ; Gene Dosage ; Gene Expression Profiling ; Brain Neoplasms - metabolism ; DNA Modification Methylases - genetics ; Glioblastoma - genetics ; Tumor Suppressor Proteins - genetics ; Glioblastoma - metabolism ; Brain Neoplasms - mortality ; Mutation ; Genome, Human ; Glioblastoma - mortality ; Analysis ; Genomics ; Stem cells ; Cytogenetics ; Genomes ; Methylation ; Gene expression ; Glioblastoma multiforme ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Nature protocols, 2013-10, Vol.8 (10), p.2022-2032
    Description: Epigenetic modifications such as carbon 5 methylation of the cytosine base in a CpG dinucleotide context are involved in the onset and progression of human diseases. A comprehensive understanding of the role of genome-wide DNA methylation patterns, the methylome, requires quantitative determination of the methylation states of all CpG sites in a genome. So far, analyses of the complete methylome by whole-genome bisulfite sequencing (WGBS) are rare because of the required large DNA quantities, substantial bioinformatic resources and high sequencing costs. Here we describe a detailed protocol for tagmentation-based WGBS (T-WGBS) and demonstrate its reliability in comparison with conventional WGBS. In T-WGBS, a hyperactive Tn5 transposase fragments the DNA and appends sequencing adapters in a single step. T-WGBS requires not more than 20 ng of input DNA; hence, the protocol allows the comprehensive methylome analysis of limited amounts of DNA isolated from precious biological specimens. The T-WGBS library preparation takes 2 d.
    Subject(s): DNA Methylation ; Animals ; Epigenesis, Genetic ; Humans ; Mice ; Genomics - methods ; Sequence Analysis, DNA - methods ; Sulfites - chemistry ; Sulfites ; Nucleotide sequence ; Methylation ; Analysis ; Index Medicus
    ISSN: 1754-2189
    E-ISSN: 1750-2799
    Source: Nature Journals Online
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Clinical cancer research, 2006-04-01, Vol.12 (7), p.2070-2079
    Description: Purpose: Pathogenesis of ependymomas is still poorly understood and molecular markers for risk-adapted patient stratification are not available. Our aim was to screen for novel genomic imbalances and prognostic markers in ependymal tumors. Experimental Design: We analyzed 68 sporadic tumors by matrix-based comparative genomic hybridization using DNA microarrays containing 〉6,400 genomic DNA fragments. Novel recurrent genomic gains were validated by fluorescence in situ hybridization using a tissue microarray consisting of 170 intracranial ependymomas. Candidate genes were also tested for mRNA expression by quantitative real-time PCR, and protein expression was determined by immunohistochemistry on the tissue microarray. Results: Chromosomal gain of 1q correlated with pediatric patients ( P = 0.004), intracranial ependymomas ( P = 0.05), and tumors of grade III ( P = 0.002). Gain of 1q21.1-32.1 was associated with tumor recurrence in intracranial ependymomas ( P 〈 0.001). Furthermore, gain of 1q25 as determined by fluorescence in situ hybridization represented an independent prognostic marker for either recurrence-free survival ( P 〈 0.001) or overall survival ( P = 0.003). Recurrent gains at 5p15.33 covering hTERT were validated by immunohistochemistry, and elevated protein levels correlated with adverse prognosis ( P = 0.01). In addition to frequent gains and high-level amplification of epidermal growth factor receptor ( EGFR ) at 7p11.2, immunohistochemistry revealed protein overexpression to be correlated with poor prognosis ( P = 0.002). EGFR protein status subdivides intracranial grade II ependymomas into two different risk groups ( P = 0.03) as shown by multivariate analysis. Conclusions: Thus, the states of 1q25 and EGFR represent independent prognostic markers for intracranial ependymomas to identify patient subgroups with different risk profiles in further clinical investigations. Moreover, EGFR might serve as therapeutic target for more specific chemotherapy applications.
    Subject(s): matrix-based CGH ; cancer genetics ; prognostic markers ; BAC microarray ; array-CGH ; Multivariate Analysis ; Receptor, Epidermal Growth Factor - genetics ; Prognosis ; Humans ; Gene Expression Regulation, Neoplastic ; Male ; Gene Expression Profiling ; Ependymoma - diagnosis ; Female ; Retrospective Studies ; Chromosomes, Human, Pair 1 - genetics ; Receptor, Epidermal Growth Factor - biosynthesis ; Oligonucleotide Array Sequence Analysis - methods ; RNA, Messenger - genetics ; Risk Factors ; Gene Dosage ; Ependymoma - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; DNA - genetics ; Ependymoma - surgery ; Adolescent ; Chromosome Aberrations ; Survival Analysis ; Biomarkers, Tumor - genetics ; In Situ Hybridization, Fluorescence - methods ; Index Medicus
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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