Bailey-Lundberg Lab
Pancreatic Cancer Immunology
Jennifer M. Bailey-Lundberg, PhD
Associate Professor, UNMC Department of Pathology, Microbiology and Immunology
Director, Solid Tumor Cancer Immunology Section
Dr. Jennifer M. Bailey-Lundberg’s research aims to uncover the complex biological mechanisms behind pancreatic diseases, with particular emphasis on pancreatic cancer and chronic pancreatitis. Her lab explores therapeutic strategies involving immune modulation, tumor microenvironment remodeling, and cellular signaling pathways to improve patient outcomes. Utilizing advanced techniques such as scRNA-seq, spatial transcriptomics, and TCR sequencing, the lab investigates various facets of pancreatic diseases, with a special focus on oncogenic K-Ras signaling, adenosine signaling, and interventional therapies like pulse field ablation and radiofrequency ablation.
Her early work identified the acinar cell as a key origin for pancreatic cancer, demonstrating that in response to oncogenic mutations in Kras, Trp53, or loss of CTNND1 (p120 catenin), acinar cells undergo epithelial-to-mesenchymal transition, basal cell extrusion, can form morphologically distinct tuft cells and progress toward adenocarcinoma. Her lab has also published cellular plasticity within the pancreatic ductal tree and acinar-to-ductal metaplasia, revealing crucial insights into pancreatic regeneration and exocrine pathogenesis. More recently, her lab has focused on the roles of adenosine receptors and CD73+ metaplastic ducts in chronic pancreatitis, investigating mechanisms of tissue injury and metaplasia to identify therapeutic targets.
What We Do
Current research efforts in the Bailey-Lundberg Lab evaluate therapeutic strategies targeting immune modulation and tumor microenvironment remodeling to improve pancreatic cancer outcomes. Central to this work is CD73, a key enzyme in adenosine signaling. Her lab has published inhibiting CD73 enhances immune surveillance, potentially improving treatments for K-Ras mutant pancreatic intraepithelial neoplasia and ductal pancreatic cancer by promoting B cell, CD4+ and CD8+ T cell anti-tumor immunity.
Another key current recent focus involves using local ablation techniques including radiofrequency ablation and pulse field ablation to reshape the pancreatic cancer microenvironment and induce local and systemic immune modulation. These approaches aim to not only induce necrosis in local ablated tumors, but also to enhance the efficacy of immunotherapies, such as CD73 inhibitors or αPD-L1, by increasing the tumor’s susceptibility to immune-mediated destruction. The lab is studying how combination therapies can modulate immune responses via neutrophil- and T cell-dependent processes, potentially improving the activation of B cells, CD4+ and CD8+ T cells, NK cells, and macrophages to promote immune responses against distant tumors, demonstrating an abscopal effect. She collaborates with clinical colleagues in interventional gastroenterology and medical and surgical oncology in the Texas Medical Center and now at UNMC.
By studying the mechanisms that are altered by combining strategies to induce tumor cell death, immune modulation and tumor microenvironment remodeling, the lab aims to develop therapies that improve both local and systemic immune responses, ultimately enhancing treatment efficacy in pancreatic cancer patients.
About Us
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