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Molecular alterations in AKT1, AKT2 and AKT3 detected in breast and prostatic cancer by FISH
Tove Kirkegaard1, Caroline J Witton, Joanne Edwards
1Division of Cancer Sciences and Molecular Pathology, Department of Surgery, Glasgow Royal Infirmary, Glasgow, UK.
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.
Insights
Genetic alterations in the AKT family, including AKT1, AKT2, and AKT3, were investigated in breast and prostate cancers. FISH analysis revealed distinct genetic changes, highlighting differences in cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The AKT signaling pathway is crucial in cancer progression.
- Three mammalian AKT isoforms (AKT1, AKT2, AKT3) are located on different chromosomes.
- Understanding genetic alterations in AKT is vital for cancer research.
Purpose of the Study:
- To investigate genetic alterations of AKT isoforms in breast and prostate cancers.
- To utilize fluorescence in situ hybridization (FISH) for detecting these alterations.
Main Methods:
- Fluorescence in situ hybridization (FISH) was employed.
- Genetic alterations (deletions, amplifications) of AKT1, AKT2, and AKT3 were analyzed.
- Breast and prostate cancer cohorts were examined.
Main Results:
- In ER-positive breast cancer, AKT1 deletions (4.8%) and amplifications (1%) were observed, along with AKT2 deletions (21.1%) and AKT3 amplifications (9.9%).
- Prostate cancer showed one AKT1 amplification (2.6%), with no observed changes in AKT2 or AKT3.
- High frequencies of chromosomal aneusomy were noted in both cancer types.
Conclusions:
- FISH analysis revealed novel AKT3 amplifications and AKT1/AKT2 deletions in breast cancer.
- Differences in AKT genetic alterations suggest distinct mechanisms in breast versus prostate cancer development.
- Further studies with larger, diverse cohorts are needed to fully elucidate AKT's role in breast cancer progression.
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