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Molecular alterations in AKT1 , AKT2 and AKT3 detected in breast and prostatic cancer by FISH
Author(s) -
Kirkegaard Tove,
Witton Caroline J,
Edwards Joanne,
Nielsen Kirsten Vang,
Jensen Linda Boye,
Campbell Fiona M,
Cooke Timothy G,
Bartlett John M S
Publication year - 2010
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2009.03467.x
Subject(s) - akt1 , akt2 , akt3 , breast cancer , fluorescence in situ hybridization , cancer , cancer research , biology , protein kinase b , pathology , medicine , oncology , gene , genetics , chromosome , apoptosis
Kirkegaard T, Witton C J, Edwards J, Nielsen K V, Jensen L B, Campbell F M, Cooke T G & Bartlett J M S
(2010) Histopathology 56, 203–211 Molecular alterations in AKT1 , AKT2 and AKT3 detected in breast and prostatic cancer by FISHAims: 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.