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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004682naa a2200613 4500
001oai:DiVA.org:umu-35334
003SwePub
008100813s2010 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:121077222
009oai:prod.swepub.kib.ki.se:121345743
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-353342 URI
0247 a https://doi.org/10.3109/0284186X.2010.4809802 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1210772222 URI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1213457432 URI
040 a (SwePub)umud (SwePub)kid (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Andersson, Ulrikau Umeå universitet,Onkologi4 aut0 (Swepub:umu)ulan0002
2451 0a A comprehensive study of the association between the EGFR and ERBB2 genes and glioma risk
264 1b Informa Healthcare,c 2010
338 a print2 rdacarrier
520 a Glioma is the most common type of adult brain tumor and glioblastoma, its most aggressive form, has a dismal prognosis. Receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR, ERBB2, ERBB3, ERBB4) family, and the vascular endothelial growth factor receptor (VEGFR), play a central role in tumor progression. We investigated the genetic variants of EGFR, ERBB2, VEGFR and their ligands, EGF and VEGF on glioma and glioblastoma risk. In addition, we evaluated the association of genetic variants of a newly discovered family of genes known to interact with EGFR: LRIG2 and LRIG3 with glioma and glioblastoma risk. Methods. We analyzed 191 tag single nucleotide polymorphisms (SNPs) capturing all common genetic variation of EGF, EGFR, ERBB2, LRIG2, LRIG3, VEGF and VEGFR2 genes. Material from four case-control studies with 725 glioma patients (329 of who were glioblastoma patients) and their 1 610 controls was used. Haplotype analyses were conducted using SAS/Genetics software. Results. Fourteen of the SNPs were significantly associated with glioma risk at p< 0.05, and 17 of the SNPs were significantly associated with glioblastoma risk at p< 0.05. In addition, we found that one EGFR haplotype was related to increased glioblastoma risk at p=0.009, Odds Ratio [OR] = 1.67 (95% confidence interval (CI): 1.14, 2.45). The Bonferroni correction made all p-values non-significant. One SNP, rs4947986 next to the intron/exon boundary of exon 7 in EGFR, was validated in an independent data set of 713 glioblastoma and 2 236 controls, [OR] = 1.42 (95% CI: 1.06,1.91). Discussion. Previous studies show that regulation of the EGFR pathway plays a role in glioma progression but the present study is the first to find that certain genotypes of the EGFR gene may be related to glioblastoma risk. Further studies are required to reinvestigate these findings and evaluate the functional significance.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Cancer och onkologi0 (SwePub)302032 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cancer and Oncology0 (SwePub)302032 hsv//eng
653 a Oncology
653 a Onkologi
653 a onkologi
653 a Oncology
7001 a Schwartzbaum, Judith4 aut
7001 a Wiklund, Fredriku Karolinska Institutet4 aut
7001 a Sjöström, Sarau Karolinska Institutet,Umeå universitet,Onkologi4 aut0 (Swepub:umu)sasj0005
7001 a Liu, Yanhong4 aut
7001 a Tsavachidis, Spyros4 aut
7001 a Ahlbom, Andersu Karolinska Institutet4 aut
7001 a Auvinen, Anssi4 aut
7001 a Collatz-Laier, Helle4 aut
7001 a Feychting, Mariau Karolinska Institutet4 aut
7001 a Johansen, Christoffer4 aut
7001 a Kiuru, Anne4 aut
7001 a Lönn, Stefan4 aut
7001 a Schoemaker, Minouk J4 aut
7001 a Swerdlow, Anthony J4 aut
7001 a Henriksson, Rogeru Umeå universitet,Onkologi4 aut0 (Swepub:umu)rohe0003
7001 a Bondy, Melissa4 aut
7001 a Melin, Beatriceu Umeå universitet,Onkologi4 aut0 (Swepub:umu)bema0010
7102 a Umeå universitetb Onkologi4 org
7730 t Acta Oncologicad : Informa Healthcareg 12, s. 17-17q 49:6<767-775x 0284-186Xx 1651-226X
7730 t NEURO-ONCOLOGYd : Informa Healthcareg 12, s. 17-17q 12<17-17x 1522-8517
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-35334
8564 8u https://doi.org/10.3109/0284186X.2010.480980
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:121077222
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:121345743

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