Stefan is
Blood Cancer United

Not that long ago, leukemia was an invariably fatal disease. These cancers presented with such ferocity and aggression that, in many cases, patient decline was rapid, usually within weeks of initial diagnosis. This all changed in the 1940s when Dr. Sidney Farber pioneered the use of antimetabolite chemicals as a means of killing leukemia cells, the birth of the chemotherapy revolution. While these early agents only led to brief, tantalizing remissions, the seeds of a greater concept were sown; this was the first proof that we could systemically target and eliminate leukemia by exploiting its dependence on certain metabolites, or the fuel cancer uses to grow, by targeting these pathways with drugs. This idea has strongly stuck with me and has formed the basis of much of my professional career thus far.

Unlike many of the other incredible stories The Leukemia & Lymphoma Society (LLS) shared on behalf of patients, caregivers, volunteers, and advocates, my introduction to the LLS family was slightly different. I am a cancer researcher focused on aggressive blood cancers, specifically acute myeloid leukemia (AML). I recently received generous LLS funding for my research under the Research Fellow Career Development Program. I am a post doc fellow at the Dana-Farber Cancer Institute. I am interested in finding new ways of treating pediatric blood cancers, particularly aggressive subtypes of AML and T-ALL, through the lens of metabolism – that is, finding ways in which we can remove certain nutrients from our diet or block how nutrients are processed in the cell to either kill leukemia cells or make them more sensitive to cutting edge therapies. I work in the lab of Dr Stegmaier (also pictured!), who is a recipient of generous competitively awarded research grants from LLS.

I completed my PhD at the Peter MacCallum Cancer Centre and the University of Melbourne in Melbourne, Australia. The focus of my research program was to investigate how certain mutations in blood cells drive leukemia. I discovered that a common leukemia mutation “rewired” cellular metabolism within leukemia cells, making them very dependent on the presence of a particular metabolite (in this case, the amino acid serine) to fuel growth. Most interestingly, I found that blocking the generation of serine using a new class of experimental drugs worked in concert with current standard-of-care chemotherapy. This combination of chemotherapy and an anti-serine drug killed leukemia cells more effectively than either agent alone. This serendipitous discovery had a bit of inherent symbolism for me. While today we have more sophisticated approaches to investigating the cancer cell, my discoveries essentially circled back to Dr. Farber’s seminal observations that we can design therapeutics that specifically target the cancer cell’s ability to fuel its manic growth while sparing healthy cells. It’s not a coincidence that even today many of the agents that form the backbone of leukemia therapy target the cell’s ability to make the raw materials necessary to fuel unrestricted growth.

As such, the journey to my current position as a postdoctoral fellow at the Dana-Farber Cancer Institute was somewhat driven by the romanticism of this institution, Boston, and the U.S. as a whole. I wanted to immerse myself in the place where chemotherapy was born and the place where we have made such enormous strides in leukemia research that we now have certain types of leukemia that are largely curable. Working with my mentor, Professor Kimberly Stegmaier, I’m deploying cutting-edge tools and technologies to identify metabolic pathways that leukemia cells require to maintain their rapid growth. Another more high-risk question is whether we can identify metabolic pathways that, when perturbed, allow a leukemia cell to lose its cancerous properties and mature to become a functional, “normal” white blood cell. Having seen firsthand a close family relative suffer from AML (and witnessing the toll intense chemotherapy took on him, the jubilation of his first remission, and the devastation of his inevitable relapse), I am always conscious that the work I do in the lab has the potential to make real, measurable improvements in patients’ lives and their cancer experience.

My uncle died from AML in 2017. Being a researcher who was studying this exact disease during my PhD at that time, I was hyper-aware of every step he would have to go through, how the cancer would behave when he went through chemotherapy, and the emotional roller coaster that went with it for everyone in our family. AML and T-ALL have good outcomes in kids, but if you don’t respond to chemotherapy upfront, outcomes are still very poor. It is a horrible family of diseases, and I am committed to finding new ways in which we can cure them.

Being a recipient of a competitively awarded LLS fellowship, I jumped at the opportunity to raise funds for LLS via Team in Training (TNT) at the 2024 New York City Marathon. I will be completing the 2025 Chicago Marathon for TNT as well. LLS is a truly incredible organization: the amount of good they do for patients, their families, doctors and researchers is next to none. I am so proud to be part of the LLS family, and this is one small way in which I can give back to the organization that has given me and others so much.

I am incredibly grateful for the support LLS extends to researchers and physicians as we endeavor to discover new therapeutic options for treating blood cancers such as AML.