New Days for Rheumatology
Mark Genovese, MD, is one of the world’s leading researchers in rheumatoid arthritis. The James W. Raitt Professor of Medicine in the division of immunology and rheumatology has also been a key player in numerous clinical trials for other diseases including psoriatic arthritis, systemic lupus erythematosus, osteoarthritis and other chronic inflammatory diseases. Over the past two decades, he’s helped establish Stanford’s bench-to-bedside translational medicine program for these conditions. Here is a conversation with Genovese about his progress in chronic inflammatory diseases.
What first drew you to rheumatology?
I became interested in rheumatology in 1989, as a medical student, when I became involved in research on lupus. I was drawn to the field by all the unknowns. The diseases themselves seemed so enigmatic, and there were so few treatment options for patients. It struck me that there was a great opportunity in rheumatology to take care of these patients as well as to try and advance the field through research. While the initial focus of my research was in lupus, I started working on arthritis during my fellowship at Stanford.
How has rheumatology changed since then?
The field has seen substantial changes since the 1990s with the more aggressive use of conventional anti-inflammatories and the development of biologic therapies. For rheumatoid arthritis (RA) in particular, there’s been a quantum leap in what we’re able to do for our patients. It’s gone from a disease with few effective treatments to one in which we can make almost every patient somewhat better. I think that’s really the result of years of hard work in basic immunology research that’s identified new drug targets, coupled with significant efforts on the part of clinicians and clinical researchers. That being said, not all diseases have taken the same course as RA; for many rheumatologic diseases, there remain limited options even today.
What have you been able to accomplish at Stanford during that time?
At Stanford we’ve been able to lead cutting-edge clinical trials in inflammatory diseases that bring our patients treatment options they wouldn’t have anywhere else. In the early 2000s we showed that etanercept worked better than methotrexate to decrease symptoms and slow joint damage in patients with long-standing RA. Then we went on to study how newer agents such as abatacept, rituximab and tocilizumab could help patients with refractory disease; we showed that the combination of leflunomide and methotrexate is effective and safe. More recently, we’ve also looked at novel small molecules like baricitinib that have the potential to change the face of the way we treat RA.
What has allowed Stanford to be a leader in this area?
I think it’s the support from the institution, from the Department of Medicine and from within the division of immunology and rheumatology. The support has given me the opportunity to follow my own interests and focus on what will make the biggest impact. Along with that, the ability to collaborate with really superb clinicians and researchers throughout the university has been a boon to advancing our research.
Where is rheumatology going from here? What’s next?
For RA, we could always live with where things stand now, with this idea that you can make everyone just a little bit better. But ideally, we have to figure out how to make an even bigger difference to patients, how to really eliminate symptoms and long-term joint damage. I think continuing to work on both new small molecules and novel combinations of drugs is going to be key. For other rheumatologic diseases, there’s even more room for improvement, and it’s just going to take a continued commitment to both bench-top basic science and clinical work.