The same gene found in both prostate and breast cancers has opposite effects on the diseases, new research shows.
Called the androgen receptor, the gene promotes growth of prostate cancer when turned on. However, the gene leads to growth in breast cancer when it is turned off, which often happens during menopause.
The team at Cleveland Clinic's Lerner Research Institute embarked on the study to determine if the androgen receptor shows evidence of the protein PTEN, which is known to suppress tumours. They found that the androgen receptor inhibits PTEN in prostate cancer cells, but encourages it in breast cancer cells. Breast cancer and prostate cancers therefore require entirely different approaches to the gene, with the former focussing on supporting it and the latter looking to suppress it. Common prostate cancer treatments currently look at blocking the androgen receptor, while many cases of breast cancer occur post menopause when production has ceased.
Charis Eng, M.D., Ph.D, chair of the Genomic Medicine Institute, said: "We now see how androgen affects PTEN expression – and ultimately cancer. "Our observations help explain why this prostate cancer risk can be halved by drinking red wine, which increases PTEN expression. Our data also suggest that treatment of the exact same cancer must be personalised for males and for females."
The next step in determining risk of cancer and potential therapies is to assess the regulatory co-factors associated with PTEN. Previous research has linked the androgen receptor with the development of liver cancer in men.Published last year in Science Translational Medicine, the study suggested the gene promotes cases of liver cancer where the hepatitis B virus (HBV) is present by altering its DNA.
The researchers believe the results provide insight as to why men with HBV are much more likely than women to develop liver cancer, adding inhibition of the androgen receptor opens up new possibilities for treatment of the disease.