The Damon Runyon Cancer Research Foundation has named six new Damon Runyon Clinical Investigators, exceptional early-career physician-scientists conducting patient-oriented cancer research at major research centers under the mentorship of the nation's leading scientists and clinicians. The Clinical Investigator Award program was designed to increase the number of physicians capable of translating scientific discoveries into new treatments for cancer patients by addressing the financial deterrents that often prevent MDs from conducting research. Each awardee will receive $600,000 over three years, and Damon Runyon will retire up to $100,000 of medical school debt.
“It’s hard starting out, when you are called to do clinical activities while maintaining a lab and funding on par with senior researchers,” said former Damon Runyon Clinical Investigator Valia Karantza, MD, PhD, in a past interview. “That's where an organization like Damon Runyon plays a huge role.”
The Foundation also awarded Continuation Grants to three Damon Runyon Clinical Investigators for an additional two years of funding, totaling $400,000 each. The Continuation Grants are designed to support Clinical Investigators who are approaching the end of their original award and need more time to work on a promising avenue of research or a clinical trial.
This program is possible through the support of the William K. Bowes, Jr. Foundation. Through partnerships with generous donors, industry sponsors, and its Accelerating Cancer Cures initiative, the Damon Runyon Cancer Research Foundation has committed over $92 million to support the careers of 142 physician-scientists across the United States since 2000.
2026 Clinical Investigators
Francesca Ferraro, MD, PhD, with mentor John F. DiPersio, MD, PhD, at Washington University, St. Louis
Acute myeloid leukemia (AML) is a deadly blood cancer that kills most patients within two years of diagnosis. Chemotherapy can put patients into remission, but the majority relapse because residual leukemia cells survive treatment. The immune system has the potential to eliminate these residual cells, but AML actively suppresses immune responses, preventing the body from finishing what chemotherapy started. Dr. Ferraro aims to understand how AML disables immune defenses and to develop strategies that restore them, so that the immune system and chemotherapy can work together to prevent relapse and improve survival. This work is directly relevant to AML and may ultimately inform treatment approaches for other blood cancers as well.
Gregory Goldgof, MD, PhD, with mentors Omar Abdel-Wahab, MD, and Nikolaus Schultz, PhD, at Memorial Sloan Kettering Cancer Center, New York
Myelodysplastic syndromes (MDS) are blood cancers that begin in the bone marrow, where blood cells are made. Over time, MDS can progress to acute myeloid leukemia, an aggressive and often life-threatening cancer. Diagnosing MDS and predicting how it will behave can be challenging because doctors must look for subtle abnormalities in blood and bone marrow cells under a microscope. Dr. Goldgof is developing artificial intelligence that can analyze these cells automatically and combine what it sees with a patient's genetic and clinical information. The goal is to help doctors detect disease earlier, better predict outcomes, and select the most effective treatment for each patient.
Sydney X. Lu, MD, PhD [Richard Lumsden Foundation Clinical Investigator], with mentors Ravindra Majeti, MD, PhD, and Tait Shanafelt, MD, at Stanford University, Stanford
Dr. Lu studies mutations in a gene called SF3B1 that are commonly found in chronic lymphocytic leukemia (CLL), the most common form of adult leukemia. Patients whose leukemia carries SF3B1 mutations often have worse outcomes, but scientists do not fully understand why. This project aims to determine how mutations in SF3B1 change the behavior of leukemia cells to drive cancer growth and identify treatments that may selectively destroy leukemia cells carrying these mutations while minimizing harm to healthy cells. By improving understanding of how SF3B1 mutations contribute to CLL, this work may help guide the development of more effective and more precise therapies for patients.
Lauren E. Merz, MD [Breast Cancer Research Foundation Clinical Investigator], with mentor Moshe Talpaz, MD, at University of Michigan, Ann Arbor
There are persistent racial disparities in cancer outcomes. One cause may be a common variant predominantly found in people identifying as Black or African American called the Duffy null phenotype, which results in lower absolute neutrophil counts (ANC), a measure of white blood cells known as neutrophils. The Duffy null phenotype does not increase risk for infection but is linked to higher risk of triple-negative breast cancer. Many cancer treatments are stopped or reduced if ANC falls below certain levels, resulting in worse outcomes. Dr. Merz’s work focuses on optimizing cancer screening, risk assessment, treatment selection, and treatment delivery by Duffy status. Dr. Merz uses data from clinical trials and observational cohorts to understand the relationship between ANC, infectious complications, treatment administration, and outcomes by Duffy status. She also plans to complete a clinical trial to assess the safety of lowering ANC thresholds for cancer therapy for people with the Duffy null phenotype. Dr. Merz hopes that this work reduces racial disparities in outcomes and personalizes cancer care.
Juan C. Osorio, MD, with mentors Jonathan Rosenberg, MD and Andy Minn, MD, PhD, at Memorial Sloan Kettering Cancer Center, New York
Dr. Osorio seeks to improve our understanding of how a newer class of cancer therapies, known as antibody-drug conjugates (ADCs), can more effectively eliminate tumors while activating the body's immune system to recognize and attack cancer. Specifically, he is studying enfortumab vedotin (EV), an FDA-approved ADC that targets Nectin-4, a protein commonly expressed in several cancer types. The work aims to uncover how these therapies stimulate anti-tumor immune responses and why some patients respond better than others. By identifying the mechanisms that drive effective anti-tumor immune responses, this research could help guide the design and development of safer, more effective treatments and personalized immunotherapy combinations. While his primary focus is on urothelial carcinoma (bladder cancer), where EV is already used clinically, the findings may also have broader relevance for other Nectin-4–expressing cancers, including breast, lung, ovarian, and head and neck cancers.
Sneha Ramakrishna, MD, with mentor Crystal L. Mackall, MD, at Stanford University, Stanford
Dr. Ramakrishna aims to improve a promising cancer treatment called CAR T cell therapy for children with an aggressive and deadly brain tumor called diffuse midline glioma (DMG). CAR T cell therapy engineers a patient's own immune system, specifically their T cells, to find and kill cancer cells. While early trials show these CAR T cells can initially shrink tumor cells, the cancer can return, often in the setting of suppressive immune cells, called myeloid cells, which could stop CAR T cells from working. This project will identify how suppressive myeloid cells interfere with treatment and develop new strategies to help CAR T cells fight cancer cells longer, with a goal of turning temporary responses into durable cures for children with this fatal disease.
2026 Continuation Grantees
Sylvan C. Baca, MD, PhD, with mentor Toni K. Choueiri, MD, at Dana-Farber Cancer Institute, Boston
Many promising cancer treatments work by homing in on specific proteins on the surface of cancer cells. The effectiveness of these treatments depends on how much of the targeted protein is present, which varies between cancers and can change over time.
Currently, matching the right treatment to the right patient is challenging because doctors lack reliable ways to tell what protein targets are present in a given patient’s cancer. Dr. Baca aims to develop a blood test that can read signals of gene activity from DNA shed by tumor cells into the bloodstream. It will use machine learning to infer which proteins are present on a patient's cancer cells at a given moment. This information will let doctors match each patient to the drug most likely to work for them right now, and to spot when the cancer has changed and a different drug should be tried. If successful, it should allow patients with advanced cancers to live longer by helping doctors find the best treatment for each patient.
Pavan Bachireddy, MD, with mentor Jeffrey J. Molldrem, MD, at University of Texas MD Anderson Cancer Center, Houston
The incomplete elimination of cancer cells leaves a residue of cancer cells called "measurable residual disease" or MRD. MRD is known to lead to cancer regrowth, but the molecular pathways that sustain and enable it to expand remain unknown. Dr. Bachireddy’s lab has developed tools precisely to reveal these MRD pathways and applied them to blood cancers known as myelodysplastic syndromes (MDS). They have found that all MDS cells do not merely expand from MRD but must adapt to signals from immune cells; only these "adapted" MDS cells become selected to drive regrowth. Now, Dr. Bachireddy seeks to understand the mechanism of these adaptations and whether they occur in other blood cancers (such as leukemia). Such knowledge would highlight new targets for designing treatments to prevent cancer regrowth.
Benjamin A. Nacev, MD, PhD, with mentors Jeremy N. Rich, MD (UNC School of Medicine), and Ronald J. Buckanovich, MD, PhD, at University of Pittsburgh, Pittsburgh
Sarcomas are a family of tumors for which there are few targeted treatments and outcomes are poor once the cancer has metastasized. Many sarcomas harbor recurrent mutations in proteins, known as epigenetic regulators, that control which genes are expressed and when. Among the regulators most frequently impacted is ATRX, which condenses regions of DNA into tightly packaged chromatin that cannot be accessed for transcription, effectively “silencing” these genes. The effect of ATRX loss in sarcomas is poorly understood, however, and treatments that leverage ATRX deficiency are lacking. Using patient-derived sarcoma cell lines and tumor samples, Dr. Nacev aims to understand epigenetic dysregulation in ATRX-deficient sarcomas, to determine how this affects antitumor immunity, and to identify new therapies for patients with ATRX-deficient sarcomas.
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To accelerate breakthroughs, the Damon Runyon Cancer Research Foundation provides today's best young scientists with the funding and freedom they need to pursue innovative research in the early stages of their careers, when statistically most major breakthroughs are made. Damon Runyon has gained worldwide prominence for its scientific rigor and outsized impact on cancer research. Thirteen scientists supported by the Foundation have received the Nobel Prize. Since its founding in 1946, in partnership with donors across the nation, the Damon Runyon Cancer Research Foundation has invested over $491 million and funded nearly 4,100 scientists.