title: Molecular alterations in AKT1, AKT2 and AKT3 detected in breast and prostatic cancer by FISH.
abstract: OBJECTIVE
  The AKT family is implicated in cancer progression. There are three mammalian AKT isoforms located on chromosomes 14, 19 and 1, respectively. The aim of the study was to investigate genetic alterations of AKT in breast and prostatic cancers using fluorescence in situ hybridization (FISH).
  
  
  RESULTS
  In oestrogen receptor(ER)-positive breast carcinomas, AKT1 was deleted in five (4.8%) and amplified in one (1%) carcinoma. Deletions of AKT2 were seen in 19 (21.1%) cases. No AKT2 amplifications were identified. Ten (9.9%) AKT3 amplifications but no deletions were seen. In prostatic cancer, AKT1 was amplified in one carcinoma (2.6%). No genetic changes were observed for AKT2 and AKT3. High frequencies of aneusomy for all chromosomes were observed in breast and prostatic carcinomas.
  
  
  CONCLUSIONS
  In breast cancer AKT3 amplifications and AKT1 and AKT2 deletions were seen, which, to our knowledge, have not been shown by FISH before. Although these two cohorts cannot be directly compared, only one AKT1 amplification was identified in prostatic carcinomas. This indicates differences in the genetic changes underlying development of breast and prostatic cancers. To evaluate further the role of genetic changes of AKT in breast cancer progression, a cohort of both ER+ and ER- patients should be evaluated.
authors.affiliation: Division of Cancer Sciences and Molecular Pathology, Department of Surgery, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: Tove
authors.initials: T
authors.lastname: Kirkegaard
authors.forename: Caroline J
authors.initials: CJ
authors.lastname: Witton
authors.forename: Joanne
authors.initials: J
authors.lastname: Edwards
authors.forename: Kirsten Vang
authors.initials: KV
authors.lastname: Nielsen
authors.forename: Linda Boye
authors.initials: LB
authors.lastname: Jensen
authors.forename: Fiona M
authors.initials: FM
authors.lastname: Campbell
authors.forename: Timothy G
authors.initials: TG
authors.lastname: Cooke
authors.forename: John M S
authors.initials: JM
authors.lastname: Bartlett
mesh_terms: D000782:Aneuploidy; D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology; D005260:Female; D005784:Gene Amplification; D017353:Gene Deletion; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics*; D011960:Receptors, Estrogen / Q000378:metabolism
chemical_list: D011960:Receptors, Estrogen; C494918:AKT1 protein, human; C494921:AKT2 protein, human; C491754:AKT3 protein, human; D051057:Proto-Oncogene Proteins c-akt