PMID- 20102399
OWN - NLM
STAT- MEDLINE
DCOM- 20100721
LR  - 20161125
IS  - 1365-2559 (Electronic)
IS  - 0309-0167 (Linking)
VI  - 56
IP  - 2
DP  - 2010 Jan
TI  - Molecular alterations in AKT1, AKT2 and AKT3 detected in breast and prostatic 
      cancer by FISH.
PG  - 203-11
LID - 10.1111/j.1365-2559.2009.03467.x [doi]
AB  - AIMS: 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). METHODS AND 
      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.
FAU - Kirkegaard, Tove
AU  - Kirkegaard T
AD  - Division of Cancer Sciences and Molecular Pathology, Department of Surgery, 
      Glasgow Royal Infirmary, Glasgow, UK.
FAU - Witton, Caroline J
AU  - Witton CJ
FAU - Edwards, Joanne
AU  - Edwards J
FAU - Nielsen, Kirsten Vang
AU  - Nielsen KV
FAU - Jensen, Linda Boye
AU  - Jensen LB
FAU - Campbell, Fiona M
AU  - Campbell FM
FAU - Cooke, Timothy G
AU  - Cooke TG
FAU - Bartlett, John M S
AU  - Bartlett JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Histopathology
JT  - Histopathology
JID - 7704136
RN  - 0 (Receptors, Estrogen)
RN  - EC 2.7.11.1 (AKT1 protein, human)
RN  - EC 2.7.11.1 (AKT2 protein, human)
RN  - EC 2.7.11.1 (AKT3 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Aneuploidy
MH  - Animals
MH  - Breast Neoplasms/*genetics/pathology
MH  - Female
MH  - Gene Amplification
MH  - Gene Deletion
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Prostatic Neoplasms/*genetics/pathology
MH  - Proto-Oncogene Proteins c-akt/*genetics
MH  - Receptors, Estrogen/metabolism
EDAT- 2010/01/28 06:00
MHDA- 2010/07/22 06:00
CRDT- 2010/01/28 06:00
PHST- 2010/01/28 06:00 [entrez]
PHST- 2010/01/28 06:00 [pubmed]
PHST- 2010/07/22 06:00 [medline]
AID - HIS3467 [pii]
AID - 10.1111/j.1365-2559.2009.03467.x [doi]
PST - ppublish
SO  - Histopathology. 2010 Jan;56(2):203-11. doi: 10.1111/j.1365-2559.2009.03467.x.