We seek to understand the network of cells that cause benign prostatic hyperplasia (BPH), the most common cause of urinary bother in men.
Benign prostatic hyperplasia (BPH) is a near universal finding in men after age 50. Fully 25% of men will require treatment for urinary symptoms due to BPH, costing the health care system over $4 billion. Despite the magnitude of the BPH problem, our understanding of its origins and the factors driving its progression with age are a mystery. BPH is due to a growth of prostate cells in the central region of the prostate, called by the transition zone, defined by Stanford researcher Dr. John McNeal nearly 50 years ago. For many years, scientists who studied BPH have focused on the epithelial cells that line the prostate glands, and the stromal cells that provide structure to the prostate and support the epithelial cells. Recent advances in technology have revealed that these two cell types are not monolithic but are comprised of different populations of epithelial and stromal cells that are in communication with each other, as well as with immune cells, nerves and blood vessels in the prostate. Using single cell sequencing and a new method for multiplex immunohistochemistry developed at Stanford, we seek to define the microenvironment of cells and how they communicate to create an atlas of BPH that can serve as a framework for understanding the disease and developing new therapies.
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Pervasive and understudied: The plight of the prostate
In this Q&A published in Stanford's Scope Magazine, Dr. James Brooks talks about his approach to understanding what causes prostate enlargement -- one of the condition's great mysteries -- and how he plans to harness a new grant from the National Institutes of Health to help decipher its roots and how to better treat it.
Looking at cause of enlarged prostates
Two genes implicated in development of prostate enlargement
Stanford scientists have identified a genetic signature that signals enlarged prostate tissue. The discovery has helped them find possible drivers of the condition.
