As I described earlier this week, my colleagues and I had recently discovered a link between resistance to hormone therapy in breast cancer patients and the immune system, and we turned to our colleagues at the Deeley Research Centre to help us advance this important work.
We all have an immune system in our bodies that is designed to detect and eliminate foreign agents (like bacteria) and abnormal cells (like cancer). However, when the immune system does not succeed, infections can take hold and cancer can develop.
We think that cancer develops only when the immune system has been evaded or overwhelmed and that tumours can also manipulate the immune response to support rather than attack the tumour. Just recently we made the discovery that some patterns of inflammation that reflect the immune response within the tumour can actually suppress the estrogen receptor. At the same time—and to our surprise—we realized that this same pattern of inflammation strongly induces psoriasin, the gene we had studied for so long.
This means that the inflammatory response may contribute to resistance to hormone therapy in some patients by suppressing the target of the therapy. It also means that when this occurs it can be recognized by measuring the psoriasin gene. So in some patients it may be possible to target the inflammation with anti-inflammatory therapies, restore the estrogen receptor and make the tumour responsive again to hormone therapy.
If you have read this far in my blog you will have noticed that this research has been very dependent on biobanks. I will return to this topic next week.