Race, Ethnicity, and Socioeconomics Tied to Disparities in Myelofibrosis | Anand Patel, MD | #ASH24

Hi, my name is Anand Patel. I'm an assistant professor of medicine at the University of Chicago and a member of the Leukemia Myeloid Malignancy program. Today I'm going to be discussing, our work looking at drivers of disparities in a Chicagoland cohort of patients with myelofibrosis. So we've been, very lucky in the Chicagoland area to have developed a large cohort of academic centers focused on, addressing outcomes in patients with myeloid malignancies, including AML and now myelofibrosis.

Previous work in AML found that patients had inferior outcomes based on their race, ethnicity, or the census tract that they lived in. A term that we, ultimately defined as structural racism. What we wanted to do was see if many of these same factors, were drivers of disparate outcomes in patients with myelofibrosis. So we ultimately identified a cohort of approximately 500 patients with myelofibrosis that included primary myelofibrosis, meaning the NPM that they were originally diagnosed with, or secondary myelofibrosis, which is myelofibrosis that develops subsequently to someone having either Polycythemia vera or essential thrombocytopenia.

What we did find was our, within our cohort, patients who identified as white non-Hispanic had higher rates of secondary myelofibrosis. And then when compared to patients who identified as Hispanic or, black, non-Hispanic, they had higher rates of primary myelofibrosis. Outcomes were still driven by the prognostic scores that we use in these, family of diseases.

So patients with higher risk myelofibrosis, whether it be secondary or primary, had poorer outcomes compared to those, with lower risk disease. So one of the mainstays of therapy in myelofibrosis is the use of Jak inhibitors. We now have four different Jak inhibitors. One thing that we found that was particularly striking within our cohort is despite having similar rates of high risk disease, across race ethnicity, black patients were much less likely to have a Jak inhibitor prescribed to them.

This has meaningful, implications, given the fact that Jak inhibitors are known to reduce spleen size, which is very important for patients who are then being considered for allogeneic transplant. Jak inhibitors are also the only family of therapeutic agents that are FDA approved for myelofibrosis. Now we need to dig further into what could have been driving this disparity, whether it was access to care, whether it was insurance barriers or otherwise.

That's work that is ongoing with the data set that we have. But it certainly highlights the fact that even if you have groups of patients with similar disease, based on the risk criteria we usually usually use, there may still be access or prescription, barriers that happen in terms of patients ultimately receiving the therapies that are most beneficial to them.

So long term drivers of survival for myelofibrosis, the only curative approach that we have is allogeneic transplant. Historically, patients who identify as white have had a much higher likelihood of finding fully matched donors in the registry. Nowadays, we're able to very safely and effectively do allogeneic transplant with half matched donors or even mismatched donors, which is greatly opened up the donor pool for nonwhite patients.

In our cohort, we actually did not find a statistical difference in the rates of allogeneic transplant in white, non-Hispanic patients, black non-Hispanic patients, or Hispanic patients, which was somewhat encouraging to see and maybe reflective of the fact that, we are being able to better utilize Alo transplant outside of the fully matched setting on the other end of things, what are things that could negatively impacts long term survival?

The major things we look at our rates of thrombosis or clotting events, we did not see any difference in the rates of clotting events in our, white, non-Hispanic patients, black non-Hispanic patients or Hispanic patients. The other major complication we watch out for is progression of myelofibrosis to what we call accelerated or blast phase MPN, which is when the disease starts behaving more like an acute leukemia.

And, we did not see any differences in rates of progression to the accelerated or blast phase either. I'll take a step back and talk about the prognostic scores that we use for myelofibrosis. Historically these have been largely derived from patient populations that may be somewhat homogenous and maybe not fully representative of the breadth of diversity we have in the United States.

So the first step is always thinking about are the prognostic tools we have reflective of the patient in front of me. And do these prognostic tools apply to the patient in front of me. So with that being the case, one of this, the potential drivers of kind of, unexpected outcomes in nonwhite patients may be that our risk tools aren't actually capturing their risk in the same way that they would very white, non-Hispanic patient.

The other part becomes as even if disease biology is the same, even if their risk may be the same, is their access to care the same, is their lived environment the same? One very concrete example I could give is, in the Chicagoland area, heavily polluted areas, tend to have higher rates of, black and Hispanic patients living there.

Are these environmental exposure somehow influencing disease in a way that we aren't capturing with a risk score? And then lastly, the type of care that's received not to say that, anyone is delivering care, with bias in mind, but are there structural barriers such as getting access to a Jak inhibitor, such as the likelihood of getting an allergenic transplant that will ultimately serve, as a driver of disparate outcomes in someone who is, otherwise underrepresented or under resourced?