The AACR Trailblazer Cancer Research Grants for Early-stage Investigators aim to empower and support cancer researchers, help launch their careers, and enable them to become thought leaders in the field. These grants are intended to provide talented investigators with the resources and dedicated time to establish innovative, emerging research projects. Projects may be exploratory, developmental, or proof of concept. By funding paradigm-shifting research, these grants are intended to advance the understanding of cancer biology, drive groundbreaking translational discoveries, and/or improve patient outcomes.

2026 Grantees

Scientific Statement of Research 

This project aims to tackle a major challenge in cancer research: how cancer progresses from dormancy to metastasis. Dr. Correia hypothesizes that this switch is controlled by a long-range communication circuit integrating neuronal signals with immune and stromal functions in response to disseminated tumor cells. She plans to characterize the neuro-modulatory functions that shape metastasis formation in the liver, a common and one of the deadliest sites of breast cancer metastasis. Using mouse models, human specimens, and cutting-edge single-cell and spatial technologies, her team will: (1) characterize neuro-modulatory functions in immune cells controlling liver metastasis, (2) determine how liver innervation regulates stromal dynamics, and (3) map neuro-immune circuits in liver metastases. These studies will lay the foundation for a novel class of neuro-modulatory therapies that reinforce dormancy, prevent metastasis and improve outcomes for patients with breast cancer. 

Biography 

Dr. Correia earned her undergraduate degree in Applied Biology at the University of Minho, Portugal. She completed her doctoral degree at Lawrence Berkeley National Laboratory, where she focused on how the microenvironment influences breast cell invasion. She then pursued postdoctoral training at the Friedrich Miescher Institute and the University of Basel, exploring tissue-specific mechanisms controlling breast cancer progression. She currently leads the Cancer Dormancy & Immunity Lab at the Champalimaud Foundation, where her team focuses on how disseminated tumor cells interact with the unique microenvironment at each distant site and leverages this biology to develop more effective therapeutic interventions for patients at risk of metastases.

Acknowledgement of Support 

“This award will catalyze my lab’s efforts to understand how long-range communication between the nervous and immune systems controls the formation of tissue-specific metastases. This is among the most exciting challenges in cancer research in the coming years, and pioneering this work will fulfill my ambition of becoming a leader in the field.”

Scientific Statement of Research 

Dr. Dixon is exploring a previously underappreciated regulator of cancer immunity- the nervous system. She hypothesizes that peripheral nerves form functional circuits with immune cells that actively suppress anti-tumor responses in lung cancer. Using multidisciplinary approaches that integrate in vivo perturbation, spatial genomics, and circuit-level mapping, her lab will define how inflammatory cues activate tumor-innervating neurons and how these signals are transmitted to reshape the tumor microenvironment. The team aims to identify and molecularly resolve neuro-immune hubs in lung cancer and determine how neuronal signaling constrains anti-tumor immunity. This work will establish neuro-immune circuitry as a targetable axis in cancer.  

Biography 

Dr. Dixon trained as a medical scientist in Ireland, specializing in Clinical Immunology and Haematology. She completed her graduate studies in Immunology at Leiden University, Netherlands. She subsequently conducted postdoctoral research at Harvard Medical School. She is currently Assistant Professor at University of Basel, where she leads a research program in cancer neuroimmunology focused on how neural signals shape anti-tumor immunity. More broadly, her lab seeks to understand how tissue-resident signals instruct immune function in health and disease. 

Acknowledgement of Support 

“This award will accelerate my research program and support my team in pursuing high-risk, multidisciplinary studies to define neuro-immune regulation in cancer. It will enable us to establish this emerging field and generate foundational insights to guide new therapeutic strategies.” 

Scientific Statement of Research 

Dr. Milner seeks to overcome fundamental limitations of adoptive T cell therapies in solid tumors by reprogramming T cell fate through activation of underexplored transcriptional programs. Current approaches largely focus on relieving inhibitory pathways, leaving much of the regulatory landscape governing T cell differentiation untested. To address this gap, Dr. Milner has developed an in vivo, single-cell-based screening platform to map how latent transcriptional programs shape T cell differentiation in solid tumor models. In this project, he will: (1) define how these latent programs govern T cell responses and (2) identify combinatorial regulatory circuits that can be leveraged to engineer next-generation CAR-T cells. Together, these studies will establish a generalizable framework for uncovering and deploying gene regulatory programs to enhance T cell fitness and improve immunotherapy outcomes across solid tumors. 

Biography 

Dr. Milner earned his doctoral degree at the University of North Carolina (UNC) and completed postdoctoral training in immunology at University of California, San Diego. He is currently Assistant Professor of Microbiology and Immunology at UNC Chapel Hill and a member of the Lineberger Comprehensive Cancer Center, where his research focuses on transcriptional and epigenetic programs that govern CD8 T cell differentiation in cancer.

Acknowledgement of Support 

“This award provides an incredible opportunity for our team to pursue new approaches to improve how T cells fight cancer. It will accelerate our efforts to develop more effective immunotherapies for solid tumors and advance better treatment options for patients.”

Scientific Statement of Research 

As the number of approved cell therapies continues to grow, the unmet medical need for predictive approaches to match patients with optimal cellular therapies becomes more acute. Although predictive diagnostic testing is widely used to guide antimicrobial therapy, we lack a fundamental understanding of variability in engineered cell therapy function needed to guide cancer treatment decisions. Dr. Roth and his team have developed CRISPR-All, a unified genetic perturbation method capable of generating complex multiplexed genetic perturbations generalized across perturbation types, scales, and numbers, enabling simultaneous head-to-head testing of cellular immunotherapy enhancements. In this project, they will apply CRISPR-All across T cells from multiple donors and functional readouts to build a foundational understanding of variability in engineered T cell function, ultimately enabling next-generation personalized immune cell therapies for cancer patients. 

Biography 

 Dr. Roth earned his medical and doctoral degrees at the University of California, San Francisco and completed residency training in Pathology at Stanford. He is currently an Assistant Professor of Pathology at Stanford, as well as an Arc Institute Innovation Investigator, and Parker Institute Senior Fellow. 

Acknowledgement of Support 

“As scientists dedicated to the exploratory process of uncovering new, more powerful, and ultimately curative medicines for cancer patients, it is the greatest privilege to be able to propose the most ambitious, impactful science we can think of — and through the exceptional support from AACR through the Trailblazer Grant program, we actually get a chance to do it!” 

Scientific Statement of Research 

Transcription factor (TF) dysregulation is a primary driver of malignancies. The majority of therapeutics targeting TFs focus on functional inhibition or protein degradation. However, it has been shown that TF kinetics can be modified by small molecules, leading to stalling or trapping of TFs in the nucleus. Dr. Tsai’s project details a proof-of-concept small molecule that traps the androgen receptor (AR) and uses this tool to better understand trapping as an inhibitory mechanism, to inspire optimization of additional anti-AR compounds, and to develop a platform for broadly screening new “trappers.” This work aims to highlight trapping as a new modality for targeting AR and TFs more broadly and to establish a pipeline for identifying trappers that could be advanced as a novel class of therapeutics. 

Biography 

Dr. Tsai earned his undergraduate degree from the California Institute of Technology and was a Fulbright Scholar at the Weizmann Institute. He received his MD/PhD from Stanford University and completed Clinical Pathology residency and a Molecular Genetic Pathology fellowship at Brigman Women’s Hospital/Massachusetts General Brigham (BWH/MGB). Currently, he is an Assistant Professor of Pathology at BWH/MGB and Harvard Medical School, where his research focuses on ubiquitin-dependent regulation of transcription factors, particularly in hormone-driven malignancies. 

Acknowledgement of Support 

“This award will connect me with a community of accomplished cancer researchers, fostering impactful collaborations and inspiring new directions in my work. The network and resources it provides will be pivotal in shaping my early career and accelerating progress toward my research goals.” 

Scientific Statement of Research 

Chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized treatment for hematologic cancers but poses substantial risks due to immune- and inflammatory-mediated challenges that impact recovery and quality of life. Exercise training (ET) “prehabilitation” is a promising strategy to improve physical and immune functioning and reduce inflammation before cancer treatment, and it may help improve CAR-T outcomes and safety. In this study, Dr. Parker and his team will randomize 104 patients with non-Hodgkin lymphoma or multiple myeloma to ET prehabilitation (home-based aerobic exercise and resistance training) or usual care for two months prior to CAR-T. They will compare changes in functional capacity (1-minute chair stand test; primary outcome), along with physical functioning, body composition, fatigue, quality of life, immune cell proliferation and function, and CAR-T effectiveness and safety. To assess potential for scalability and sustained implementation, they will comprehensively evaluate intervention costs and explore cost-effectiveness for improving patient outcomes.

Biography 

Dr. Parker earned training in public health, kinesiology, and behavioral science. He is currently an Assistant Member in the Department of Health Outcomes and Behavior at Moffitt Cancer Center, where he leads a research program focused on designing and evaluating physical activity and exercise interventions for cancer survivors. His interventional work spans the clinic (e.g., exercise prehabilitation for surgery and cellular therapy) and the community (e.g., YMCA-based pickleball program for survivors), with the overarching goal of improving health and quality of life during and following cancer treatment. 

Acknowledgement of Support 

“I am incredibly grateful for the opportunity AACR has provided to advance my research career. The Trailblazer Grant for Early-Stage Investigators enables me to collaborate with an outstanding team of investigators dedicated to improving patient outcomes while broadening my experience in translational exercise oncology research.”

Scientific Statement of Research 

Although lymph nodes are a major site of melanoma metastasis and immune cell activation, they remain an underexplored setting for understanding how lipid peroxidation influences adaptive immune responses. Dr. Ubellacker discovered that the lymph node protects melanoma cells from ferroptosis, identifying this site as a distinct metabolic niche for metastatic survival. Building on that finding, she aims to determine the extent to which deliberately inducing lipid peroxidation in melanoma cells within lymph nodes can promote anti-cancer immunity. Using syngeneic melanoma models, she will examine whether lipid peroxidation in lymph node tumor cells limits distant metastasis through anti-cancer immune interactions. These studies aim to define a new framework for targeting lymph node metastases to stimulate systemic immune responses against cancer. 

Biography 

 Dr. Ubellacker earned her doctoral degree in Biological and Biomedical Sciences from Harvard Medical School and medical degree from Stanford School of Medicine. She completed postdoctoral training at the University of Texas Southwestern. She is currently an Assistant Professor in the Department of Molecular Metabolism at the Harvard T.H. Chan School of Public Health, where she leads a translational laboratory focused on understanding how metabolic microenvironments influence cancer progression. 

Acknowledgement of Support 

“As an early-stage investigator at a time of tighter research funding, this support from the AACR community is instrumental in helping me grow my lab and launch our work on a new research direction. It provides the resources to pursue higher-risk ideas that would otherwise be out of reach.” 

Scientific Statement of Research

The 9p21 chromosomal locus, containing the tumor suppressor genes CDKN2A and MTAP, is deleted in 15–25% of non–small cell lung cancers (NSCLC). Dr. Vokes’ preliminary data show that CDKN2A/MTAP loss is associated with worse outcomes specifically in patients with chemoimmunotherapy, suggesting distinct biology that may involve impaired antigen presentation and enhanced immunosuppression. At the same time, MTAP loss creates vulnerability to PRMT5 inhibition, with early clinical trials showing promising activity in NSCLC. In this project, Dr. Vokes will investigate how CDKN2A/MTAP loss shapes tumor–immune interactions and treatment response using preclinical models, multi-omic profiling, and patient samples. She and her team will also identify biomarkers of response to combined PRMT5 inhibition and PD-L1/VEGF blockade. These studies aim to guide precision immunotherapy strategies for this genomic subtype of NSCLC.

Biography 

Dr. Vokes earned her undergraduate degree in Chemistry from Williams College and her medical degree from the University of Cambridge. She completed her medical training at Harvard, Brigham and Women’s Hospital, and Dana-Farber Cancer Institute. Her postdoctoral work focused on genomic predictors of response to immunotherapy and targeted therapies. A thoracic oncologist, she is currently an assistant professor at MD Anderson with a joint appointment in Genomic Medicine. Her research integrates multi-omics datasets, clinical trials, and computational modeling to develop predictive models and study resistance.

Acknowledgement of Support 

“This award will accelerate my transition to research independence by supporting high-risk, translational studies at the intersection of genomics and immunotherapy. It will enable the generation of critical multi-omic datasets, strengthen my translational research program integrating correlative studies from clinical trials, and position me to develop precision immunotherapy strategies for genomically defined lung cancer populations.”

Scientific Statement of Research

Lineage plasticity—the ability of tumor cells to alter identity under therapeutic pressure—underpins resistance to androgen receptor pathway inhibitors and drives progression of prostate adenocarcinoma to neuroendocrine prostate cancer (NEPC), an aggressive and lethal disease. Building on the discovery of a highly plastic JAK–high state during prostate cancer progression that can be therapeutically targeted, Dr. Zaidi will identify transcriptional regulators and druggable targets that confer synthetic lethality in JAK–high tumor cells using single-cell multiomic profiling and CRISPR screens, with a focus on the aryl hydrocarbon receptor. He will also investigate tumor–intrinsic and microenvironmental drivers of NEPC transition, including the role of the circadian rhythm regulator ARNTL2 and a subset of cancer–associated fibroblasts. Together, these studies aim to unmask key determinants of lineage plasticity and inform strategies to eliminate therapy–resistant tumor states.

Biography

Dr. Zaidi earned his undergraduate degree in Biology from the Massachusetts Institute of Technology, followed by his medical and doctoral degrees in Genetics from Yale University. He completed his Internal Medicine Residency at Massachusetts General Hospital and a fellowship in Medical Oncology at Memorial Sloan Kettering Cancer Center. He is currently an Assistant Professor of Medical Oncology and Stephen Sherwin MD Investigator at Yale School of Medicine, where his research focuses on lineage plasticity and therapeutic resistance in cancer.

Acknowledgement of Support

“Receiving the 2026 AACR Trailblazer Grant will accelerate my research by enabling high–risk, mechanistic studies on lineage plasticity. It will support the validation of novel therapeutic targets and microenvironmental drivers of plasticity, strengthen the translational impact of my work, and advance strategies to overcome therapy resistance in prostate cancer.”