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

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

  • Ryan A Gordon, Department of Nutrition, University of North Carolina, USA
  • Michele La Merrill, Department of Preventive Medicine, Mount Sinai School of Medicine, New York, USA
  • Kent W Hunter, Laboratory of Cancer Biology & Genetics, NIH/NCI, USA
  • Peter Sørensen
  • David W Threadgill, Department of Genetics, University of North Carolina, USA
  • Daniel Pomp, Department of Nutrition, University of North Carolina, USA
  • Biostatistik
  • Institut for Genetik og Bioteknologi
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
Udgivelsesdato: May 2010
TidsskriftClinical and Experimental Metastasis
Sider (fra-til)279-293
StatusUdgivet - 2010

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