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dc.contributor.authorMargres, Mark J
dc.contributor.authorRuiz-Aravena, Manuel
dc.contributor.authorHamede, Rodrigo
dc.contributor.authorChawla, Kusum
dc.contributor.authorPatton, Austin H
dc.contributor.authorLawrance, Matthew F
dc.contributor.authorFraik, Alexandra K
dc.contributor.authorStahlke, Amanda R
dc.contributor.authorDavis, Brian W
dc.contributor.authorOstrander, Elaine A
dc.contributor.authorJones, Menna E
dc.contributor.authorMcCallum, Hamish
dc.contributor.authorPaddison, Patrick J
dc.contributor.authorHohenlohe, Paul A
dc.contributor.authorHockenbery, David
dc.contributor.authorStorfer, Andrew
dc.date.accessioned2020-10-07T21:46:44Z
dc.date.available2020-10-07T21:46:44Z
dc.date.issued2020
dc.identifier.issn0016-6731
dc.identifier.doi10.1534/genetics.120.303428
dc.identifier.urihttp://hdl.handle.net/10072/398174
dc.description.abstractSpontaneous tumor regression has been documented in a small proportion of human cancer patients, but the specific mechanisms underlying tumor regression without treatment are not well understood. Tasmanian devils are threatened with extinction from a transmissible cancer due to universal susceptibility and a near 100% case fatality rate. In over 10,000 cases,,20 instances of natural tumor regression have been detected. Previous work in this system has focused on Tasmanian devil genetic variation associated with the regression phenotype. Here, we used comparative and functional genomics to identify tumor genetic variation associated with tumor regression. We show that a single point mutation in the 59 untranslated region of the putative tumor suppressor RASL11A significantly contributes to tumor regression. RASL11A was expressed in regressed tumors but silenced in wild-type, nonregressed tumors, consistent with RASL11A downregulation in human cancers. Induced RASL11A expression significantly reduced tumor cell proliferation in vitro. The RAS pathway is frequently altered in human cancers, and RASL11A activation may provide a therapeutic treatment option for Tasmanian devils as well as a general mechanism for tumor inhibition.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherGenetics Society of America
dc.relation.ispartofpagefrom1143
dc.relation.ispartofpageto1152
dc.relation.ispartofissue4
dc.relation.ispartofjournalGenetics
dc.relation.ispartofvolume215
dc.subject.fieldofresearchGenetics
dc.subject.fieldofresearchcode3105
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsGenetics & Heredity
dc.subject.keywordscancer
dc.subject.keywordstumor regression
dc.titleSpontaneous Tumor Regression in Tasmanian Devils Associated withRASL11AActivation
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationMargres, MJ; Ruiz-Aravena, M; Hamede, R; Chawla, K; Patton, AH; Lawrance, MF; Fraik, AK; Stahlke, AR; Davis, BW; Ostrander, EA; Jones, ME; McCallum, H; Paddison, PJ; Hohenlohe, PA; Hockenbery, D; Storfer, A, Spontaneous Tumor Regression in Tasmanian Devils Associated withRASL11AActivation, Genetics, 2020, 215 (4), pp. 1143-1152
dcterms.dateAccepted2020-06-12
dc.date.updated2020-10-07T21:43:39Z
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
gro.hasfulltextNo Full Text
gro.griffith.authorMcCallum, Hamish


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