Caner Saygin, M.D. (Fellow)



Project Title

Dissecting the Evolution of Clonal Hematopoiesis to Prevent Acute Leukemias

Named Award

Awesome Games Done Quick




University of Chicago, Chicago, Ill.

My “Why”

As a physician scientist, I conduct research to understand how leukemias develop from pre-leukemic precursor conditions to develop better preventive interventions. My interest in cancer research stems from my experience in medical school, closely working with blood cancer patients and my mother’s breast cancer diagnosis. I moved to the U.S. to receive training in a cancer research lab and developed myself as a physician scientist. I feel fulfilled when I develop new therapies in the lab and work hard to translate them into clinical studies in the hopes of improving the care of our future patients.

My Mission

Acute leukemia is an aggressive cancer with significant morbidity and mortality rates. Most patients are transfusion dependent, requiring visits to hospital at least once a week. While our current therapies can cure a fraction of these patients, most patients have high-risk leukemias that can be fatal. In the past 10 years, we have learned a great deal about the pre-leukemic precursor conditions in the blood system which can be detected years before leukemia arises.

The goal of my laboratory is to understand the mechanisms driving the progression of precursor lesions into leukemia and develop new approaches to halt this progression.

Research Overview

Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) are aggressive blood cancers that are among the top ten causes of cancer deaths in the U.S. Clonal hematopoiesis (CH) is a well-known precursor lesion to AML and is defined by the presence of genetic abnormalities (i.e., mutations) in the blood cells of an individual, years before they get a clinical diagnosis of blood cancer. Individuals with CH are at 11-times higher risk to develop AML.

Our research has shown that a third of adult patients with ALL also harbor CH-type mutations in their leukemias. We were also able to demonstrate that mutations can exist in blood cells of ALL patients many years before they are diagnosed with leukemia. Since CH can predict the risk of leukemia for both AML and ALL patients, we may have a window of opportunity to implement risk-reduction strategies in high-risk individuals to halt the progression of CH to fatal acute leukemias.

The aim of this project is to have a detailed genetic characterization of CH evolution to help understand the critical pathways driving leukemias, which can then be targeted to prevent leukemia before it happens.

We will explore:

  • Mechanisms by which CH causes ALL by using a sophisticated single cell sequencing technology.
  • Patterns of evolution of CH in solid tumor patients who are receiving chemotherapy or immunotherapy for their cancer, which can help us predict the risk for therapy-related leukemias.
  • Expansion of our CH clinic`s efforts to enroll more high-risk patients in prevention clinical trials.

These studies will help us discover the pathways driving leukemias in adults. This will allow us to use risk reduction strategies to prevent leukemia in high-risk patients.   

Why Funding Matters

Mechanisms responsible for development of leukemias from precursor lesions, characterized by blood count abnormalities, are currently unknown. Funding from the Prevent Cancer Foundation will allow us to discover the unknown as we perform a large-scale genomic analysis of samples to identify drivers of leukemia progression.

My Hope

Our goal is to identify new biomarkers and mechanisms responsible for leukemic transformation so that we can develop better models of risk assessment and discover new therapies that focus on prevention through precision medicine. We hope to bring new insights into leukemia prevention and inform physicians taking care of patients who are at high risk for leukemias.