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https://doi.org/10.1101/gr.210502
DC Field | Value | |
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dc.title | A bioinformatics-based strategy identifies c-Myc and Cdc25A as candidates for the Apmt mammary tumor latency modifiers | |
dc.contributor.author | Cozma, D. | |
dc.contributor.author | Lukes, L. | |
dc.contributor.author | Rouse, J. | |
dc.contributor.author | Qiu, T.H. | |
dc.contributor.author | Liu, E.T. | |
dc.contributor.author | Hunter, K.W. | |
dc.date.accessioned | 2016-11-08T08:23:37Z | |
dc.date.available | 2016-11-08T08:23:37Z | |
dc.date.issued | 2002 | |
dc.identifier.citation | Cozma, D., Lukes, L., Rouse, J., Qiu, T.H., Liu, E.T., Hunter, K.W. (2002). A bioinformatics-based strategy identifies c-Myc and Cdc25A as candidates for the Apmt mammary tumor latency modifiers. Genome Research 12 (6) : 969-975. ScholarBank@NUS Repository. https://doi.org/10.1101/gr.210502 | |
dc.identifier.issn | 10889051 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/129527 | |
dc.description.abstract | The epistatically interacting modifier loci (Apmt1 and Apmt2) accelerate the polyoma Middle-T (PyVT)-induced mammary tumor. To identify potential candidate genes loci, a combined bioinformatics and genomics strategy was used. On the basis of the assumption that the loci were functioning in the same or intersecting pathways, a search of the literature databases was performed to identify molecular pathways containing genes from both candidate intervals. Among the genes identified by this method were the cell cycle-associated genes Cdc25A and c-Myc, both of which have been implicated in breast cancer. Genomic sequencing revealed noncoding polymorphism in both genes, in the promoter region of Cdc25A, and in the 3′ UTR of c-Myc. Molecular and in vitro analysis showed that the polymorphisms were functionally significant. In vivo analysis was performed by generating compound PyVT/Myc double-transgenic animals to mimic the hypothetical model, and was found to recapitulate the age-of-onset phenotype. These data suggest that c-Myc and Cdc25A are Apmt1 and Apmt2, and suggest that, at least in certain instances, bioinformatics can be utilized to bypass congenic construction and subsequent mapping in conventional QTL studies. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1101/gr.210502 | |
dc.source | Scopus | |
dc.type | Article | |
dc.contributor.department | MEDICINE | |
dc.description.doi | 10.1101/gr.210502 | |
dc.description.sourcetitle | Genome Research | |
dc.description.volume | 12 | |
dc.description.issue | 6 | |
dc.description.page | 969-975 | |
dc.description.coden | GEREF | |
dc.identifier.isiut | 000176433700014 | |
Appears in Collections: | Staff Publications |
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