Dr. Neal Shore talks about the role of the androgen receptor in prostate cancer.
Dr. Snuffy Myers talks about durable, complete remissions for prostate cancer.
Dr. Hyung Kim is a urologic oncologist at Cedars-Sinai in Los Angeles.
Prostatepedia spoke with him recently about a clinical trial he’s running that looks at the effects of cholesterol-lowering therapy before radical prostatectomy.
What do we know currently about the connection between cholesterol, statins, and prostate cancer?
Dr. Kim: A lot of our data comes from epidemiology studies in which statins were used to lower cholesterol to improve cardiovascular health. In many of these studies, the observation was made that patients with prostate cancer who were on statins were less likely to die of their cancers
The other line of evidence comes from basic science research. People like Dr. Michael Freeman have done preclinical laboratory studies showing that lowering cholesterol levels in mice can slow down the growth of prostate cancer.
We have epidemiology data. We have preclinical data. The missing piece is prospective data in patients to help establish a firm cause/effect relationship between lowering cholesterol and favorable prostate cancer outcomes.
The epidemiology data is interesting because the link between statin use and the incidence of prostate cancer is weak, but there is a stronger link between statin use and the likelihood of dying from prostate cancer.
This suggests the possibility that statin use targets the lethal form of prostate cancer. It also suggests that statin use may not lower the likelihood of developing prostate cancer. However, if you develop prostate cancer, perhaps statin use will improve your likelihood of surviving the disease.
Mouse studies are controlled experiments where you do see a clear cause/effect relationship. You lower the cholesterol level in the mice and the tumors you implant in them grow more slowly. We have some idea of the basic mechanism behind this observation, but does this cause-and-effect relationship carry over to patients? Does that cause/effect relationship explain the epidemiology data that we see?
Those are the unknowns. This is why we’re conducting our trial.