title: Energy homeostasis genes and survival after breast cancer  diagnosis: the Breast Cancer Health Disparities Study.
abstract: OBJECTIVE
  The leptin-signaling pathway and other genes involved in energy homeostasis (EH) have been examined in relation to breast cancer risk as well as to obesity. We test the hypothesis that genetic variation in EH genes influences survival after diagnosis with breast cancer and that body mass index (BMI) will modify that risk.
  
  
  METHODS
  We evaluated associations between 10 EH genes and survival among 1,186 non-Hispanic white and 1,155 Hispanic/Native American women diagnosed with breast cancer. Percent Native American (NA) ancestry was determined from 104 ancestry-informative markers. Adaptive rank truncation product (ARTP) was used to determine gene and pathway significance.
  
  
  RESULTS
  The overall EH pathway was marginally significant for all-cause mortality among women with low NA ancestry (P(ARTP) = 0.057). Within the pathway, ghrelin(GHRL) and leptin receptor (LEPR) were significantly associated with all-cause mortality (P(ARTP) = 0.035 and 0.007, respectively). The EH pathway was significantly associated with breast cancer-specific mortality among women with low NA ancestry (P(ARTP) = 0.038). Three genes cholecystokinin (CCK), GHRL, and LEPR were significantly associated with breast cancer-specific mortality among women with low NA ancestry (P(ARTP) = 0.046,0.015, and 0.046, respectively), while neuropeptide Y (NPY) was significantly associated with breast cancer-specific mortality among women with higher NA ancestry(P(ARTP) = 0.038). BMI did not modify these associations.
  
  
  CONCLUSIONS
  Our data support our hypothesis that certain EH genes influence survival after diagnosis with breast cancer; associations appear to be most important among women with low NA ancestry.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Pellatt
authors.forename: Abbie
authors.initials: A
authors.lastname: Lundgreen
authors.forename: Roger K
authors.initials: RK
authors.lastname: Wolff
authors.forename: Lisa
authors.initials: L
authors.lastname: Hines
authors.forename: Esther M
authors.initials: EM
authors.lastname: John
authors.forename: Martha L
authors.initials: ML
authors.lastname: Slattery
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001943:Breast Neoplasms / Q000235:genetics* / Q000401:mortality*; D016022:Case-Control Studies; D002766:Cholecystokinin / Q000235:genetics; D004734:Energy Metabolism / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006630:Hispanic or Latino / Q000235:genetics; D006706:Homeostasis / Q000235:genetics; D006801:Humans; D008875:Middle Aged; D009478:Neuropeptide Y / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D054440:Receptors, Ghrelin / Q000235:genetics; D054411:Receptors, Leptin / Q000235:genetics; D012307:Risk Factors; D015398:Signal Transduction / Q000235:genetics; D044465:White People / Q000235:genetics; D055815:Young Adult
chemical_list: D009478:Neuropeptide Y; D054440:Receptors, Ghrelin; D054411:Receptors, Leptin; D002766:Cholecystokinin