title: Genomic imbalances detected by comparative genomic hybridization are prognostic markers in invasive ductal breast carcinomas.
abstract: OBJECTIVE
  The aim of this work is the study of the prognostic significance of the chromosomal aberrations described in a series of invasive ductal breast carcinomas.
  
  
  RESULTS
  We analysed by comparative genomic hybridization a group of 70 formalin-fixed paraffin-embedded invasive ductal breast carcinomas. Aberrations showed a frequency similar to previous studies using frozen tumours. Interestingly, we identified gains involving 6q16-q24 more frequently than in other series. We analysed the association among the chromosomal imbalances, 11 histopathological factors, relapse rate and overall survival of patients. Associations showed 16q losses as a potential marker of good prognosis, as they were more frequent in node-negative (P=0.025) and in oestrogen-positive tumours (P < 0.001). Furthermore, 100% of bcl-2+ tumours presented this aberration compared with 29.3% in bcl-2- (P=0.014). 1q, 11q, 17q and 20q gains were associated with poor prognosis: 95% of cases with 1q gains were bigger than 20 mm (P=0.041). Tumours with 1q and 11q gains showed a higher relapse rate (P=0.063; P=0.066). Within the good prognosis group of lymph node-negative patients, 17q and 20q gains identify a subgroup with increased relapse rate (P=0.039).
  
  
  CONCLUSIONS
  Chromosomal imbalances, together with histopathological factors, may help to predict outcome in breast cancer patients.
authors.affiliation: Department of Genetics, University of Navarra, Pamplona, Spain. izudaire@unav.es
authors.forename: I
authors.initials: I
authors.lastname: Zudaire
authors.forename: M D
authors.initials: MD
authors.lastname: Odero
authors.forename: C
authors.initials: C
authors.lastname: Caballero
authors.forename: C
authors.initials: C
authors.lastname: Valenti
authors.forename: J M
authors.initials: JM
authors.lastname: Martínez-Penuela
authors.forename: J
authors.initials: J
authors.lastname: Isola
authors.forename: M J
authors.initials: MJ
authors.lastname: Calasanz
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000235:genetics*; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002869:Chromosome Aberrations; D005260:Female; D015894:Genome, Human; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008875:Middle Aged; D009364:Neoplasm Recurrence, Local / Q000235:genetics; D009693:Nucleic Acid Hybridization / Q000379:methods; D011379:Prognosis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D016019:Survival Analysis; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D014408:Biomarkers, Tumor; D019394:Ki-67 Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53