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n2:pmcid: PMC0
bibo:doi: 10.1371%2Fjournal.pone.0007887
n4:contains: _:vb6442638 _:vb6442644 _:vb6442668 _:vb6442670

Subject Item: _:vb6442638
rdf:type: n4:Section
dc:title: introduction
n4:contains: _:vb6442640 _:vb6442641 _:vb6442642 _:vb6442643 _:vb6442639

Subject Item: _:vb6442639
rdf:type: n2:Context
rdf:value: Well-established examples include KIT mutations in gastrointestinal stromal tumors (GISTs) that predict response to imatinib or nilotinib, and non-small cell lung cancers with EGFR mutations that are sensitive to erlotinib[>>1<<], [2], [3].
n2:mentions: n3:15118073

Subject Item: _:vb6442640
rdf:type: n2:Context
rdf:value: Well-established examples include KIT mutations in gastrointestinal stromal tumors (GISTs) that predict response to imatinib or nilotinib, and non-small cell lung cancers with EGFR mutations that are sensitive to erlotinib[1], [>>2<<], [3]. The presence of other mutations predicts a lack of response to targeted therapy.
n2:mentions: n3:15118125

Subject Item: _:vb6442641
rdf:type: n2:Context
rdf:value: Well-established examples include KIT mutations in gastrointestinal stromal tumors (GISTs) that predict response to imatinib or nilotinib, and non-small cell lung cancers with EGFR mutations that are sensitive to erlotinib[1], [2], [>>3<<]. The presence of other mutations predicts a lack of response to targeted therapy.
n2:mentions: n3:15329413

Subject Item: _:vb6442642
rdf:type: n2:Context
rdf:value: For example, lung and colorectal cancers that harbor mutations in the KRAS oncogene are unresponsive to treatment with anti-EGFR agents[>>4<<], and inactivating PTEN mutations (or protein loss) in glioblastomas predict resistance to erlotinib[5].
n2:mentions: n3:17664471

Subject Item: _:vb6442643
rdf:type: n2:Context
rdf:value: example, lung and colorectal cancers that harbor mutations in the KRAS oncogene are unresponsive to treatment with anti-EGFR agents[4], and inactivating PTEN mutations (or protein loss) in glioblastomas predict resistance to erlotinib[>>5<<]. Thus, clinical decision-making based on tumor genetic information will increasingly be informed by the mutational status of multiple cancer genes.
n2:mentions: n3:19398573

Subject Item: _:vb6442644
rdf:type: n4:Section
dc:title: results
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Subject Item: _:vb6442645
rdf:type: n2:Context
rdf:value: In contrast, the sensitivity of conventional Sanger sequencing was 83.3% for fresh frozen tissue and 76.0% for FFPE-derived DNA, confirming the heightened performance of genotyping-based mutation profiling [>>7<<].
n2:mentions: n3:17293865

Subject Item: _:vb6442646
rdf:type: n2:Context
rdf:value: Tumors harboring these mutations may respond to a selective BRAF inhibitor[>>6<<], [9]. We also identified 96 samples across seven different cancer types (breast n = 14, colorectal n = 24, endometrial n = 15, esophageal n = 4, gastric n = 34, prostate n = 3, and pediatric astrocytoma n = 2) harboring mutations in
n2:mentions: n3:11181995

Subject Item: _:vb6442647
rdf:type: n2:Context
rdf:value: Established examples include KRAS mutations in non-small cell lung cancer (23%) and colorectal cancer (38%) that confer resistance to erlotinib, gefitinib (lung) or cetuximab (colorectal)[>>4<<], [10], [11].
n2:mentions: n3:17664471

Subject Item: _:vb6442648
rdf:type: n2:Context
rdf:value: Established examples include KRAS mutations in non-small cell lung cancer (23%) and colorectal cancer (38%) that confer resistance to erlotinib, gefitinib (lung) or cetuximab (colorectal)[4], [>>10<<], [11]. While 94% of KRAS mutations identified localized to codons 12 or 13, 6% occurred elsewhere in the gene (most commonly at codon 61). Since most studies of KRAS-associated resistance have focused exclusively on codons 12 and 13[3],
n2:mentions: n3:16618717

Subject Item: _:vb6442649
rdf:type: n2:Context
rdf:value: Established examples include KRAS mutations in non-small cell lung cancer (23%) and colorectal cancer (38%) that confer resistance to erlotinib, gefitinib (lung) or cetuximab (colorectal)[4], [10], [>>11<<]. While 94% of KRAS mutations identified localized to codons 12 or 13, 6% occurred elsewhere in the gene (most commonly at codon 61). Since most studies of KRAS-associated resistance have focused exclusively on codons 12 and 13[3], [12],
n2:mentions: n3:16166444

Subject Item: _:vb6442650
rdf:type: n2:Context
rdf:value: Since most studies of KRAS-associated resistance have focused exclusively on codons 12 and 13[>>3<<], [12], [13], OncoMap identified additional KRAS mutations that may influence sensitivity to anti-EGFR treatment.
n2:mentions: n3:15329413

Subject Item: _:vb6442651
rdf:type: n2:Context
rdf:value: Since most studies of KRAS-associated resistance have focused exclusively on codons 12 and 13[3], [>>12<<], [13], OncoMap identified additional KRAS mutations that may influence sensitivity to anti-EGFR treatment.
n2:mentions: n3:16043828

Subject Item: _:vb6442652
rdf:type: n2:Context
rdf:value: Since most studies of KRAS-associated resistance have focused exclusively on codons 12 and 13[3], [12], [>>13<<], OncoMap identified additional KRAS mutations that may influence sensitivity to anti-EGFR treatment.
n2:mentions: n3:18946061

Subject Item: _:vb6442653
rdf:type: n2:Context
rdf:value: In GIST tumors, where 31 KIT mutations were identified in 25 samples; both primary (imatinib-responsive) and secondary (imatinib-resistant) KIT mutations were observed, in keeping with prior mutation profiling studies [>>7<<]. In particular, several KIT mutations involving exon 9 (KIT Y503_or F504insAY; 5 cases) were detected in untreated GIST tumors. These mutations are associated with an increased drug requirement to elicit a clinical response [14], [15]. A
n2:mentions: n3:17293865

Subject Item: _:vb6442654
rdf:type: n2:Context
rdf:value: These mutations are associated with an increased drug requirement to elicit a clinical response [>>14<<], [15]. A PDGFRA mutation (D842V) predictive of resistance to imatinib [15] was also identified in one GIST sample.
n2:mentions: n3:16534250

Subject Item: _:vb6442655
rdf:type: n2:Context
rdf:value: These mutations are associated with an increased drug requirement to elicit a clinical response [14], [>>15<<]. A PDGFRA mutation (D842V) predictive of resistance to imatinib [15] was also identified in one GIST sample.
n2:mentions: n3:12181401

Subject Item: _:vb6442656
rdf:type: n2:Context
rdf:value: A PDGFRA mutation (D842V) predictive of resistance to imatinib [>>15<<] was also identified in one GIST sample.
n2:mentions: n3:12181401

Subject Item: _:vb6442657
rdf:type: n2:Context
rdf:value: This mutation may predict resistance to PI3 kinase inhibition (and conceivably receptor tyrosine kinase inhibition) in some contexts [>>16<<].
n2:mentions: n3:17611497

Subject Item: _:vb6442658
rdf:type: n2:Context
rdf:value: While coincident mutations in these genes have previously been reported in cancers of the large intestine [>>17<<], PIK3CA and KRAS mutations have typically exhibited a mutually exclusive pattern of occurrence in endometrial cancer [18], [19].
n2:mentions: n3:18434431

Subject Item: _:vb6442659
rdf:type: n2:Context
rdf:value: While coincident mutations in these genes have previously been reported in cancers of the large intestine [17], PIK3CA and KRAS mutations have typically exhibited a mutually exclusive pattern of occurrence in endometrial cancer [>>18<<], [19]. An endometrial adenocarcinoma with co-occurring FGFR2 and PTEN mutations was also identified.
n2:mentions: n3:18987734

Subject Item: _:vb6442660
rdf:type: n2:Context
rdf:value: While coincident mutations in these genes have previously been reported in cancers of the large intestine [17], PIK3CA and KRAS mutations have typically exhibited a mutually exclusive pattern of occurrence in endometrial cancer [18], [>>19<<]. An endometrial adenocarcinoma with co-occurring FGFR2 and PTEN mutations was also identified.
n2:mentions: n3:16949921

Subject Item: _:vb6442661
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rdf:value: Two pediatric LGAs harbored mutations in MYC, a well established oncogene homologue of NMYC, which is amplified and indicative of poor prognosis in pediatric neuroblastoma [>>20<<], [21]. Thus, tumor mutation profiling may refine patient stratification and/or disease prognosis in some pediatric brain cancers.
n2:mentions: n3:6888561

Subject Item: _:vb6442662
rdf:type: n2:Context
rdf:value: Two pediatric LGAs harbored mutations in MYC, a well established oncogene homologue of NMYC, which is amplified and indicative of poor prognosis in pediatric neuroblastoma [20], [>>21<<]. Thus, tumor mutation profiling may refine patient stratification and/or disease prognosis in some pediatric brain cancers.
n2:mentions: n3:6719137

Subject Item: _:vb6442663
rdf:type: n2:Context
rdf:value: Duplication of the BRAF locus has been reported as the most frequent aberration in pediatric LGAs (66% [>>18<<]), whereas activating point mutations in BRAF occur less commonly (4–6%) [22], [23].
n2:mentions: n3:18987734

Subject Item: _:vb6442664
rdf:type: n2:Context
rdf:value: Duplication of the BRAF locus has been reported as the most frequent aberration in pediatric LGAs (66% [18]), whereas activating point mutations in BRAF occur less commonly (4–6%) [>>22<<], [23]. We identified activating BRAFV600E mutations in 11% (10/88) of pediatric LGAs—a higher percentage than previously reported [22], [23].
n2:mentions: n3:18398503

Subject Item: _:vb6442665
rdf:type: n2:Context
rdf:value: Duplication of the BRAF locus has been reported as the most frequent aberration in pediatric LGAs (66% [18]), whereas activating point mutations in BRAF occur less commonly (4–6%) [22], [>>23<<]. We identified activating BRAFV600E mutations in 11% (10/88) of pediatric LGAs—a higher percentage than previously reported [22], [23].
n2:mentions: n3:19373855

Subject Item: _:vb6442666
rdf:type: n2:Context
rdf:value: We identified activating BRAFV600E mutations in 11% (10/88) of pediatric LGAs—a higher percentage than previously reported [>>22<<], [23]. Interestingly, the BRAFV600E mutation was most prevalent within the ganglioglioma subtype of pediatric LGAs (classical and non-classical; 8/14 tumors, p = 0.00005), as shown in Fig. 2 . BRAFV600E mutations were not identified in
n2:mentions: n3:18398503

Subject Item: _:vb6442667
rdf:type: n2:Context
rdf:value: We identified activating BRAFV600E mutations in 11% (10/88) of pediatric LGAs—a higher percentage than previously reported [22], [>>23<<]. Interestingly, the BRAFV600E mutation was most prevalent within the ganglioglioma subtype of pediatric LGAs (classical and non-classical; 8/14 tumors, p = 0.00005), as shown in Fig. 2 . BRAFV600E mutations were not identified in any of
n2:mentions: n3:19373855

Subject Item: _:vb6442668
rdf:type: n4:Section
dc:title: methods
n4:contains: _:vb6442669

Subject Item: _:vb6442669
rdf:type: n2:Context
rdf:value: Selection of cancer gene mutations for assay design and mass spectrometric genotyping were performed as previously described[>>6<<] with modifications indicated in Methods S1. Assay, primer and probe sequences are indicated in Table S1.
n2:mentions: n3:11181995

Subject Item: _:vb6442670
rdf:type: n4:Section
dc:title: discussion
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Subject Item: _:vb6442671
rdf:type: n2:Context
rdf:value: Knowledge of the genetic abnormalities present in pediatric LGAs is limited, though recent studies have identified BRAF translocations, chromosomal duplications, and occasional base mutations in low-grade astrocytomas[>>18<<], [25], as well as diverse mechanisms for activating the ERK/MAPK pathway in pilocytic astrocytomas [23].
n2:mentions: n3:18987734

Subject Item: _:vb6442672
rdf:type: n2:Context
rdf:value: Knowledge of the genetic abnormalities present in pediatric LGAs is limited, though recent studies have identified BRAF translocations, chromosomal duplications, and occasional base mutations in low-grade astrocytomas[18], [>>25<<], as well as diverse mechanisms for activating the ERK/MAPK pathway in pilocytic astrocytomas [23].
n2:mentions: n3:19016743

Subject Item: _:vb6442673
rdf:type: n2:Context
rdf:value: studies have identified BRAF translocations, chromosomal duplications, and occasional base mutations in low-grade astrocytomas[18], [25], as well as diverse mechanisms for activating the ERK/MAPK pathway in pilocytic astrocytomas [>>23<<]. These findings suggest that the small molecule inhibitors of BRAF already in adult trials may also represent promising therapeutics for subsets of these tumors.
n2:mentions: n3:19373855

Subject Item: _:vb6442674
rdf:type: n2:Context
rdf:value: In concordance with previous reports [>>22<<], [26], [27] we observe that mutations in genes frequently observed in adult anaplastic astrocytomas and/or glioblastomas, such as TP53 or PTEN, are only rarely encountered in pediatric pilocytic and low-grade diffuse astrocytomas.
n2:mentions: n3:18398503

Subject Item: _:vb6442675
rdf:type: n2:Context
rdf:value: In concordance with previous reports [22], [>>26<<], [27] we observe that mutations in genes frequently observed in adult anaplastic astrocytomas and/or glioblastomas, such as TP53 or PTEN, are only rarely encountered in pediatric pilocytic and low-grade diffuse astrocytomas.
n2:mentions: n3:11119125

Subject Item: _:vb6442676
rdf:type: n2:Context
rdf:value: In concordance with previous reports [22], [26], [>>27<<] we observe that mutations in genes frequently observed in adult anaplastic astrocytomas and/or glioblastomas, such as TP53 or PTEN, are only rarely encountered in pediatric pilocytic and low-grade diffuse astrocytomas.
n2:mentions: n3:18772890

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