Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
    Clin Exp Metastasis. 2010 May;27(5):279-93. doi: 10.1007/s10585-010-9326-z. Epub 2010 Mar 31.

    Dietary fat-dependent transcriptional architecture and copy number alterations associated with modifiers of mammary cancer metastasis.

    Source

    Department of Nutrition, University of North Carolina Chapel Hill, Chapel Hill, NC 27599, USA. rrgordon@ncsu.edu

    Abstract

    Breast cancer is a complex disease resulting from a combination of genetic and environmental factors. Among environmental factors, body composition and intake of specific dietary components like total fat are associated with increased incidence of breast cancer and metastasis. We previously showed that mice fed a high-fat diet have shorter mammary cancer latency, increased tumor growth and more pulmonary metastases than mice fed a standard diet. Subsequent genetic analysis identified several modifiers of metastatic mammary cancer along with widespread interactions between cancer modifiers and dietary fat. To elucidate diet-dependent genetic modifiers of mammary cancer and metastasis risk, global gene expression profiles and copy number alterations from mammary cancers were measured and expression quantitative trait loci (eQTL) identified. Functional candidate genes that colocalized with previously detected metastasis modifiers were identified. Additional analyses, such as eQTL by dietary fat interaction analysis, causality and database evaluations, helped to further refine the candidate loci to produce an enriched list of genes potentially involved in the pathogenesis of metastatic mammary cancer.

    PMID:
    20354763
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for Springer

      Save items

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk