Empowering investigators to pursue transformative and innovative ideas.
The Stephenson Global Scholar Grants revolutionize the traditional research model with a dynamic structure designed for agility and rapid progress. These generous awards support investigators with the most innovative and promising ideas, cutting through bureaucracy and red tape to foster a culture of true innovation and courageous risk-taking. This transformative approach drives breakthrough research with the potential to significantly improve pancreatic cancer survival and outcomes.
Congratulations to the following Stephenson Global Scholars, who were collectively awarded a total amount of $6.67 million to advance the most innovative pancreatic cancer research!
Research Title: Empirical Antigen Discovery to Catalyze Effective Pancreatic Cancer Immunotherapies
Lay summary: This Stephenson Global Scholar project aims to develop improved immune-based therapies for pancreatic cancer patients by identifying hidden targets (antigens) on tumor cells. While traditional immunotherapies have not worked for most pancreatic cancer patients, emerging treatments like cancer vaccines and cellular therapies are showing early clinical promise. However, these only work if the immune system can find the right “flags” (antigens) on tumor cells.
The team recently discovered that pancreatic tumors display a unique set of these flags derived from overlooked, “dark” regions of the DNA. However, past research has only looked at a small subset of these antigens. To expand on this, the team will use patient-derived organoids (mini-tumors grown in the lab) to uncover new flags that can activate T cells. By identifying targets that are shared across different patients, this work aims to accelerate “off-the-shelf” vaccines and T-cell therapies, bringing more effective treatment options to the clinic.
Research Title: A Blood-Based Test to Predict Pancreatic Cyst Progression
Lay summary: Pancreatic cysts are increasingly detected through medical imaging, but while most remain harmless, some can progress to pancreatic cancer, one of the deadliest cancers because it is often diagnosed at an advanced stage. Current surveillance relies primarily on periodic imaging, which may not identify the earliest biological changes that signal a cyst is becoming dangerous.
This project seeks to develop a simple blood test that can monitor patients over time by measuring tiny genetic molecules, called microRNAs, that are released into the bloodstream. By combining these molecular markers with routine clinical information, the research aims to identify high-risk cysts before they develop into invasive cancer. The study will also validate the test for future clinical use and develop a risk score to help physicians make more informed decisions about surveillance and treatment.
If successful, this approach could provide a more accurate and noninvasive way to detect pancreatic cancer at its earliest and most treatable stages, reduce unnecessary procedures for patients with low-risk cysts, and ultimately improve survival and quality of life for patients.
Research Title: Targeting Cell Cycle Nodes to Intercept Acquired Resistance to KRAS Inhibitors in Pancreatic Cancer
Lay Summary: Pancreatic cancer is one of the deadliest cancers, and while new KRAS/RAS-targeted therapies are beginning to transform treatment, virtually all tumors eventually develop resistance through a diverse range of genetic, signaling, and epigenetic mechanisms. This project is based on the concept that targeting downstream regulators of cell division—particularly key cyclin-dependent kinases (CDKs)—may provide a broad-acting strategy capable of overcoming many distinct forms of resistance regardless of how they arise. Using advanced laboratory models and analyses of patient samples, the research team will define how resistance emerges, determine how cell-cycle inhibition constrains tumor evolution and therapeutic escape, and assess the impact of these strategies on both cancer cells and the surrounding tumor microenvironment. In parallel, the project will establish a clinical program to investigate the biological basis of resistance in patients receiving RAS inhibitors, identify biomarkers associated with treatment response and failure, and lay the foundation for future clinical trials combining RAS-targeted therapies with next-generation CDK inhibitors. The ultimate goal is to develop broadly effective therapeutic approaches that extend the durability of response to RAS inhibition and improve outcomes for patients with pancreatic cancer.
Research Title: Targeting Lipocalin 2 (LCN2) to Drive Immunotherapy Against Pancreatic Cancer
Lay summary: Pancreatic ductal adenocarcinoma (PDAC) creates a local environment that exclude T cells, immune cells playing a central role in attacking tumors. We discovered that PDAC cells secrete a protein called LCN2 that contributes to the formation of this immunosuppressive state. We developed prototype antibodies blocking LCN2 and found that they enable T cells to reach and attack tumors and thereby inhibit PDAC growth in mice. Targeting LCN2, a soluble factor, represents a new dimension of cancer immunotherapy. This project will advance LCN2-targeting therapy by examining the extent to which it can synergize with other therapeutic approaches that are currently limited by the immunosuppressive environment, and by developing next-generation LCN2-targeting antibodies with enhanced efficacy and safety.
Research Title: Engineering Synthetic T Cell Help to Reverse Immunosuppression in Pancreatic Cancer
Lay summary: Pancreatic cancer is one of the deadliest cancers, with only about 13% of patients surviving five years after diagnosis. Conventional immunotherapies, which have transformed treatment for many other cancers, largely fail against pancreatic tumors. This is because these tumors build a powerful shield: a dense wall of scar-like tissue that keeps immune cells out, an army of suppressive cells that actively shut down any immune attack that gets through, and dysfunctional lymph nodes that compromise the body’s ability to mount a broader immune response. Our team recently made an unexpected discovery that vaccine-boosting adoptively transferred bystander T cells, which don’t even target the pancreatic tumors directly, set off a chain reaction that broke down the tumor’s protective wall and woke up the body’s own cancer-fighting cells. We hypothesized that this approach gives the immune system exactly the signal it needs to overcome the tumor’s defenses. If fully exploited, this finding could offer a safe, off-the-shelf treatment strategy for pancreatic cancer patients who currently have few good options.
Research Title: Targeting Keratin 17 Positive PanIN for Pancreatic Cancer Interception
Lay Summary: Pancreatic cancer is deadly when diagnosed late. To improve patient outcomes, we need to understand how to detect it early or, ideally, prevent its formation. Pancreatic cancer arises from precancerous lesions in the pancreas. These precancers were once considered rare, but parallel work at Johns Hopkins University and the University of Michigan revealed that precancerous lesions in the pancreas are common, with a normal pancreas containing many. That precancerous lesions are common, but pancreatic cancer is rare, raises the question of how to define which precancers are at highest risk of progression. Analysis of these lesions across individuals led to a surprising discovery: not all are the same — while most have “benign” characteristics, a few possess key features of malignant disease. In the latter, we see expression of Keratin 17 (K17), a protein associated with aggressive pancreatic cancer. We hypothesize that these K17-positive precancerous lesions have the potential to give rise to cancer, and thus, should be the target of interception strategies. Here, we propose to characterize K17-positive precancerous lesions to understand how they form and grow. Then, we will use genetically engineered mouse models and human pancreatic cells in culture to follow cells expressing K17 over time and determine whether they give rise to cancer. With this work, we aim to understand the earliest stages of pancreatic cancer formation, with the goal to stop this deadly disease before it forms.
Research Title: Advancing Pancreatic Cancer Treatment Through Next-Generation Splicing Inhibitors
Lay Summary: Pancreatic cancer is one of the deadliest cancers, with fewer than 15% of patients surviving five years after diagnosis. Current treatments provide only limited benefit, highlighting the urgent need for new therapeutic approaches. Most pancreatic tumours are driven by the cancer genes KRAS and MYC, which force tumour cells to produce enormous amounts of protein. This creates a hidden weakness: cancer cells become highly dependent on systems that maintain protein quality, while healthy cells are far less reliant on these mechanisms. Our research aims to exploit this vulnerability through a newly discovered process that we named proteotoxic RNA splicing, a concept I developed together with Prof. Ivan Đikić. We have developed first-in-class proteotoxic RNA splicing drugs that cause cancer cells to accumulate toxic proteins they cannot eliminate, ultimately leading to their death while sparing healthy cells. This project will evaluate this novel strategy in pancreatic cancer models and identify the patients most likely to benefit, laying the foundation for a new generation of precision therapies.
Research Title: Identifying Genetic Vulnerabilities and Paracrine Interactions of the Basal Cell State in Pancreatic Cancer Organoids
Lay summary: Pancreatic cancer remains one of the most difficult cancers to treat, in part because tumor cells can adapt, change their behavior, and become resistant to therapy. Our research focuses on understanding an especially aggressive cancer cell state within pancreatic tumors that appears to help cancers survive treatment and create an environment that prevents the immune system from attacking the tumor effectively. Using advanced pancreatic cancer organoid models—miniature tumor-like systems grown in the laboratory—we aim to identify the key biological programs that allow these aggressive cancer cells to persist. We will also study how these cells communicate with surrounding non-cancer cells to build a protective, immunosuppressive neighborhood around the tumor. By uncovering the signals and vulnerabilities that sustain this dangerous cell state, we hope to reveal new strategies to weaken pancreatic tumors, improve immune responses, and make treatments more effective. Ultimately, this work seeks to uncover therapeutic strategies that target the root causes of treatment resistance and recurrence in pancreatic cancer, with the long-term goal of providing cures for patients and families facing this devastating disease.
The Stephenson Global Pancreatic Cancer Research Institute in July 2025 announced the six inaugural recipients of the prestigious Stephenson Scholar Grants, awarding $5.25 million to support high-impact research aimed at transforming the understanding, early detection and treatment of pancreatic cancer. The grants support a new generation of research that is collaborative, cross-institutional, and deeply innovative.
Yes, you may apply for the grant in collaboration with other researchers. Please denote them in your application.
Yes, as long as this project is substantially different from other currently funded projects. The Stephenson Global Pancreatic Cancer Research Institute (SGPCRI) aims to support new research initiatives to maximize impact.
Due to space limitations in the initial submission, applicants are not required to acknowledge relevant publications at this stage. However, if invited to submit a full 5-page proposal in the second round, they will have the opportunity to include relevant publications at that time. Certainly, if applicants would like to cite their work as a reference or two in the 1 page proposal, they are welcome to do so.
Indirect costs are capped at 10% of the total award amount.
