Host genetic influence on papilloma virus-induced tumors in the Horse

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dc.citation.issue4
dc.citation.volume139
dc.contributor.authorStaiger EA
dc.contributor.authorTseng CT
dc.contributor.authorMiller D
dc.contributor.authorCassano J
dc.contributor.authorNasir L
dc.contributor.authorGarrick DJ
dc.contributor.authorBrooks SA
dc.contributor.authorAntczak DF
dc.date.available2016-08-15
dc.date.available2016-02-16
dc.date.issued15/08/2016
dc.description.abstractThe common equine skin tumors known as sarcoids have been causally associated with infection by bovine papillomavirus (BPV). Additionally, there is evidence for host genetic susceptibility to sarcoids. We investigated the genetic basis of susceptibility to sarcoid tumors on a cohort of 82 affected horses and 270 controls genotyped on a genome-wide platform and two custom panels. A Genome Wide Association Study (GWAS) identified candidate regions on six chromosomes. Bayesian probability analysis of the same dataset verified only the regions on equine chromosomes (ECA) 20 and 22. Fine mapping using custom-produced SNP arrays for ECA20 and ECA22 regions identified two marker loci with high levels of significance: SNP BIEC2-530826 (map position 32,787,619) on ECA20 in an intron of the DQA1 gene in the Major Histocompatibility Complex (MHC) class II region (p = 4.6e-06), and SNP BIEC2-589604 (map position 25,951,536) on ECA22 in a 200 kb region containing four candidate genes: PROCR, EDEM2, EIF6 and MMP24 (p = 2.14e-06). The marker loci yielded odds ratios of 5.05 and 4.02 for ECA20 and ECA22, respectively. Associations between genetic MHC class II variants and papillomavirus-induced tumors have been reported for human papillomavirus and cottontail rabbit papillomavirus infections. This suggests a common mechanism for susceptibility to tumor progression that may involve subversion of the host immune response. This study also identified a genomic region other than MHC that influenced papillomavirus-induced tumor development in the studied population.
dc.description.publication-statusPublished
dc.format.extent784 - 792
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000378418300014&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=c5bb3b2499afac691c2e3c1a83ef6fef
dc.identifier.citationINTERNATIONAL JOURNAL OF CANCER, 2016, 139 (4), pp. 784 - 792
dc.identifier.doi10.1002/ijc.30120
dc.identifier.eissn1097-0215
dc.identifier.elements-id262939
dc.identifier.harvestedMassey_Dark
dc.identifier.issn0020-7136
dc.identifier.urihttps://hdl.handle.net/10179/13213
dc.publisherJohn Wiley & Sons
dc.relation.isPartOfINTERNATIONAL JOURNAL OF CANCER
dc.relation.urihttps://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.30120
dc.subjectpapillomavirus
dc.subjectsarcoid tumor
dc.subjecthorse
dc.subjectMHC
dc.subjectGWAS
dc.subject.anzsrc1112 Oncology and Carcinogenesis
dc.titleHost genetic influence on papilloma virus-induced tumors in the Horse
dc.typeJournal article
pubs.notesNot known
pubs.organisational-group/Massey University
pubs.organisational-group/Massey University/College of Sciences
pubs.organisational-group/Massey University/College of Sciences/School of Agriculture & Environment
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