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 shared by The Leukemia & Lymphoma Society (LLS) 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) and am a recent recipient of generous LLS funding for my research under the Research Fellow Career Development Program. 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.
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.