Please use this identifier to cite or link to this item: https://doi.org/10.1101/gr.210502
DC FieldValue
dc.titleA bioinformatics-based strategy identifies c-Myc and Cdc25A as candidates for the Apmt mammary tumor latency modifiers
dc.contributor.authorCozma, D.
dc.contributor.authorLukes, L.
dc.contributor.authorRouse, J.
dc.contributor.authorQiu, T.H.
dc.contributor.authorLiu, E.T.
dc.contributor.authorHunter, K.W.
dc.date.accessioned2016-11-08T08:23:37Z
dc.date.available2016-11-08T08:23:37Z
dc.date.issued2002
dc.identifier.citationCozma, 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.issn10889051
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/129527
dc.description.abstractThe 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.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1101/gr.210502
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMEDICINE
dc.description.doi10.1101/gr.210502
dc.description.sourcetitleGenome Research
dc.description.volume12
dc.description.issue6
dc.description.page969-975
dc.description.codenGEREF
dc.identifier.isiut000176433700014
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

28
checked on Aug 21, 2019

WEB OF SCIENCETM
Citations

26
checked on Aug 21, 2019

Page view(s)

13
checked on Aug 16, 2019

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.