title: Molecular signatures mostly associated with NK cells are predictive of relapse free survival in breast cancer patients.
abstract: BACKGROUND
  Recent observations suggest that immune-mediated tissue destruction is dependent upon coordinate activation of immune genes expressed by cells of the innate and adaptive immune systems.
  
  
  METHODS
  Here, we performed a retrospective pilot study to investigate whether the coordinate expression of molecular signature mostly associated with NK cells could be used to segregate breast cancer patients into relapse and relapse-free outcomes.
  
  
  RESULTS
  By analyzing primary breast cancer specimens derived from patients who experienced either 58-116 months (~5-9 years) relapse-free survival or developed tumor relapse within 9-76 months (~1-6 years) we found that the expression of molecules involved in activating signaling of NK cells and in NK cells: target interaction is increased in patients with favorable prognosis.
  
  
  CONCLUSIONS
  The parameters identified in this study, together with the prognostic signature previously reported by our group, highlight the cooperation between the innate and adaptive immune components within the tumor microenvironment.
authors.forename: Maria Libera
authors.initials: ML
authors.lastname: Ascierto
authors.forename: Michael O
authors.initials: MO
authors.lastname: Idowu
authors.forename: Yingdong
authors.initials: Y
authors.lastname: Zhao
authors.forename: Hanif
authors.initials: H
authors.lastname: Khalak
authors.forename: Kyle K
authors.initials: KK
authors.lastname: Payne
authors.forename: Xiang-Yang
authors.initials: XY
authors.lastname: Wang
authors.forename: Catherine I
authors.initials: CI
authors.lastname: Dumur
authors.forename: Davide
authors.initials: D
authors.lastname: Bedognetti
authors.forename: Sara
authors.initials: S
authors.lastname: Tomei
authors.forename: Paolo A
authors.initials: PA
authors.lastname: Ascierto
authors.forename: Anil
authors.initials: A
authors.lastname: Shanker
authors.forename: Harry D
authors.initials: HD
authors.lastname: Bear
authors.forename: Ena
authors.initials: E
authors.lastname: Wang
authors.forename: Francesco M
authors.initials: FM
authors.lastname: Marincola
authors.forename: Andrea
authors.initials: A
authors.lastname: De Maria
authors.forename: Masoud H
authors.initials: MH
authors.lastname: Manjili
mesh_terms: D055610:Antigens, CD1d / Q000378:metabolism; D001943:Breast Neoplasms / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D018572:Disease-Free Survival; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D008213:Lymphocyte Activation / Q000235:genetics; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D009364:Neoplasm Recurrence, Local / Q000235:genetics / Q000276:immunology / Q000473:pathology; D012008:Recurrence; D015398:Signal Transduction / Q000235:genetics; D060388:Support Vector Machine; D016896:Treatment Outcome
chemical_list: D055610:Antigens, CD1d; D015815:Cell Adhesion Molecules; D016169:Lymphocyte Function-Associated Antigen-1