2008
DOI: 10.1038/nature07385
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Abstract: Human cancer cells typically harbor multiple chromosomal aberrations, nucleotide substitutions and epigenetic modifications that drive malignant transformation. The Cancer Genome Atlas (TCGA) pilot project aims to assess the value of large-scale multidimensional analysis of these molecular characteristics in human cancer and to provide the data rapidly to the research community. Here, we report the interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblast… Show more

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Cited by 6,539 publications
(4,272 citation statements)
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References 47 publications
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“…Intriguingly, unlike wild‐type EGFR, our data clearly demonstrate that tyrosine phosphorylation‐impaired CYF10 EGFR mutants are still able to transform NIH‐3T3 and Ba/F3 cells, suggesting that constitutive phosphorylation on mutant EGFR may be dispensable for their transforming potential. These paradoxical results are consistent with our reports that a subset of mutant EGFR is capable of cellular transformation irrespective of asymmetric dimerization16 and that various C‐terminal intragenic deletion mutants identified in glioblastomas and lung adenocarcinoma are oncogenic 29, 30. Furthermore, an Ex19Del mutant was shown to retain its oncogenic activity in the absence of the C‐terminal domain or autophosphorylation,23, 24 putatively through heterodimerization of phosphorylated ErbB3 with C‐terminal domain deleted Ex19Del.…”
Section: Discussionsupporting
confidence: 91%
“…Intriguingly, unlike wild‐type EGFR, our data clearly demonstrate that tyrosine phosphorylation‐impaired CYF10 EGFR mutants are still able to transform NIH‐3T3 and Ba/F3 cells, suggesting that constitutive phosphorylation on mutant EGFR may be dispensable for their transforming potential. These paradoxical results are consistent with our reports that a subset of mutant EGFR is capable of cellular transformation irrespective of asymmetric dimerization16 and that various C‐terminal intragenic deletion mutants identified in glioblastomas and lung adenocarcinoma are oncogenic 29, 30. Furthermore, an Ex19Del mutant was shown to retain its oncogenic activity in the absence of the C‐terminal domain or autophosphorylation,23, 24 putatively through heterodimerization of phosphorylated ErbB3 with C‐terminal domain deleted Ex19Del.…”
Section: Discussionsupporting
confidence: 91%
“…The validation of their prognostic function by Kaplan‐Meier and Cox PH regression analyses revealed that age and the MGMT promoter methylation status were important prognostic markers that provide independent information. Primary GBM comprises 84.21% (265/304) of all adult GBM patients, and this ratio is lower than that reported in previous studies 1, 6. This discrepancy might be due to the classification of primary and secondary GBM based on the clinical history or IDH1/2 status in previous studies.…”
Section: Discussioncontrasting
confidence: 55%
“…Approximately 90% of adult glioblastomas (GBMs) present as de novo GBMs (primary GBMs) without antecedent history of a less‐malignant precursor lesion, and the remaining cases progress from WHO lower grade (WHO II‐III) diffuse gliomas (secondary GBMs) 1, 2. Isocitrate dehydrogenase 1 and 2 (IDH1/2) mutations are recognized as definitive diagnostic molecular biomarkers of secondary GBM and are more prognostically valuable than the history of tumor onset 3.…”
Section: Introductionmentioning
confidence: 99%
“…Since 2002, the number of recognized cancer genes has grown from 115 to 457[94]. Multiple international efforts, including the Cancer Genomes Project[95], the Cancer Genome Atlas[96] and the International Cancer Genome Consortium[97], have set out to uncover new driver mutations and survey the association between mutated genes and drug efficacy.…”
Section: Mps Applications In Mutation Analysismentioning
confidence: 99%