Opening Keynote Speaker:
Dr. Sean Ronnekleiv‑Kelly is an Assistant Professor and Ronald E. & Patricia A. Kissinger Endowed Research Professor in the Division of Surgical Oncology at UW–Madison. He holds board certification in general surgical oncology and specializes in treating hepatobiliary and pancreatic cancers. Dr. Ronnekleiv‑Kelly’s research centers on dissecting tumor microenvironment dynamics using single-cell and spatial transcriptomic tools to understand cellular crosstalk in aggressive cancers. His lab explores how PAS family proteins, including the aryl hydrocarbon receptor, influence immune infiltration in hepatobiliary and pancreatic tumors. Key contributions include NIH-funded work analyzing circadian rhythm disruption in pancreatic cancer progression, and studies funded by the Fibrolamellar Cancer Foundation investigating tumor vulnerabilities and potential therapeutic targets.
(Image source: SMPH, UW–Madison)
Session 1 – Computational Focus: To be Announced
Dr. Xiaowu Gai, PhD
Chief, Director, and Professor, Department of Pediatrics, Division of Bioinformatics and Quantitative Child Health
Medical College of Wisconsin
Dr. Xiaowu Gai is a genomicist and bioinformatician currently serving as a Professor of Pediatrics at the Medical College of Wisconsin. He is also the Director of Child Health Bioinformatics and the Division Chief of Bioinformatics and Quantitative Child Health at Children’s Wisconsin.
Dr. Gai’s research focuses on human genetic variations and their role in the development of diseases, particularly congenital disorders and pediatric cancers. He has made significant contributions to the understanding of genetic causes of diseases, including, for example, the discovery of NMNAT1 as a causative gene for Leber congenital amaurosis and FBXL4 for mitochondrial encephalomyopathy. Since 2012, Dr. Gai has co-led the International Mitochondrial Disease Sequence Resource (MSeqDR) Consortium and serves as co-chair of both the ClinGen Mitochondrial Disease Variant Curation Expert Panel and the ClinGen Mitochondrial Disease Gene Curation Expert Panel.
Dr. Gai is a passionate advocate for genomic medicine. Prior to joining MCW in 2024, he served as Director of Bioinformatics at the Center for Personalized Medicine (CPM) at Children’s Hospital Los Angeles (CHLA) for nine years. At CHLA, he led bioinformatics efforts supporting genomics-based diagnostic tests, including OncoKids® for pediatric cancers and Clinical Whole Genome and Exome Sequencing for rare genetic disorders.
(Image source: Medical College of Wisconsin)
Lecture Title: VUS.Life: Harnessing Vector Embeddings for Fast, Precise Pathogenicity Prediction of Genetic Variants
Interpreting pathogenicity of genetic variants, somatic or germline, in genes like BRCA1 and BRCA2 remains a major challenge in genomic medicine. Vector embeddings, key to the success of Large Language Models (LLMs), enable semantic representation of complex multimodal data. We created a framework for semantic vector representations of variants, excluding known pathogenicity assertions to avoid data leakage, that effectively captures nuanced relationships of variant features linked to pathogenicity. Our method enables automated classification with >97% accuracy using top models for genes evaluated. This framework therefore empowers precision medicine in prioritizing Variants of Uncertain Significance (VUS) for clinical review and evidence-based reclassification.
Session 2 – Computational Focus:
Dr. Christina Kendziorski, PhD
Professor, Department of Biostatistics & Medical Informatics
University of Wisconsin–Madison
Dr. Christina Kendziorski is a Professor in the Department of Biostatistics & Medical Informatics at the University of Wisconsin–Madison. She leads the Statistical Genetics and Genomics program at the UW Institute for Clinical and Translational Research and is an affiliate of the UW Genome Center.
Dr. Kendziorski is internationally recognized for her pioneering work in statistical genomics, particularly in developing methods for analyzing high-throughput sequencing data. She co-developed EBSeq, an empirical-Bayes approach that has become a widely adopted tool for RNA-seq differential expression analysis. Her current research focuses on statistical and computational methods for single-cell and spatial transcriptomic data, enabling rigorous interpretation of cellular heterogeneity in complex biological systems.
A Fellow of the American Statistical Association, Dr. Kendziorski is committed to advancing reproducible and scalable statistical methods that support the growing demands of biomedical research and precision medicine. She has received sustained NIH funding and continues to influence both the theoretical and applied dimensions of genomics and transcriptomics.
(Image source: SMPH, UW–Madison)
Session 3 – Technology & Artificial Intelligence Focus:
Dr. Ameen Salahudeen, MD, PhD.
Assistant Professor, Division of Hematology and Oncology
University of Illinois Chicago (UIC)
Dr. Ameen Salahudeen is an Assistant Professor in the Department of Medicine, Division of Hematology and Oncology, at the University of Illinois Chicago. With multidisciplinary training in internal medicine and hematology-oncology—alongside prestigious fellowships at Stanford and NIH-supported career development funding—Dr. Salahudeen brings both clinical depth and technological expertise to his research.
His work harnesses single-cell and spatial transcriptomic platforms to create spatially resolved tumor atlases, with a focus on pancreatic and other solid tumors. He played a central role in establishing UIC’s Spatial and Genome Technologies Core, leading the adoption of advanced 10X Genomics platforms, including Chromium and Visium, to enhance microenvironmental tumor profiling.
Dr. Salahudeen has published impactful work on the spatial deconvolution of tumor microenvironments, particularly in non-small cell lung cancer. His translational research also addresses health disparities; he co-developed AI-powered lung cancer risk models tailored to racially diverse urban populations. Board-certified in both medicine and oncology, he merges clinical insights with innovative methodologies to drive equity-focused precision oncology.
(Image source: University of Illinois College of Medicine)
Session 5 – Technology Focus:
Dr. Nina Steele, PhD
Assistant Scientist & Early‑Stage Investigator, Pancreatic Cancer Center
Henry Ford Health, Detroit, MI
Dr. Nina Steele recently joined the Division of Digestive Diseases in the Department of Internal Medicine at the University of Cincinnati. She was awarded a K99/R00 NCI grant to aid her transition to early-stage faculty and currently holds a Lustgarten Foundation award as co-PI for her translational research. Her lab focuses on cell communication in the pancreatic tumor microenvironment, with a recent focus on utilizing multi-omics data (spatial transcriptomics and proteomics) analysis to longitudinally map pancreatic disease progression over time in the same patient and study racial disparities in pancreatic cancer.
(Image source: Sky Foundation, Inc)
Lecture Title: Spatial transcriptomics on a diverse pancreatic cancer cohort reveals Black African Americans display reduced classical and increased intermediate tumor subtype
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy and is 20% more likely to develop in Black African American (BAA) patients, compared to Non-African American (NAA) patients. A comprehensive analysis of the large-scale gene expression signatures of tumor subtypes and cellular microenvironments of BAA PDAC versus NAA PDAC has not been rigorously evaluated. Here we present, for the first time, a multi-omics interrogation of BAA versus NAA PDAC using laser capture microdissection, spatial transcriptomics (ST), and 100-plex spatial proteomics platforms, with key findings verified by immunohistochemistry. Whole-exome sequencing confirmed African genetic ancestry in the self-reported race of BAA samples. We analyzed 7 BAA and 15 NAA PDAC samples, combining our cohort with Human Tumor Atlas Network (HTAN) ST data. We found that BAA PDAC tumors exhibit a significant decrease in classical subtype cells, accompanied by no change in the aggressive basal-like subtype. Intriguingly, BAA patients show a significant enrichment of the intermediate/hybrid phenotype that co-expresses genes in both subtypes, as well as unique markers, compared to NAA PDAC. BAA PDAC tissues displayed increased B cell interactions and reduced myeloid cell presence, compared to NAA tumors. Our findings suggest BAA tumors show a shift toward intermediate subtypes and a distinct immune cell composition within the tumor microenvironment. This study highlights that health disparities in patients of different ancestry may have a molecular basis that influences tumor aggressiveness and the immune response that may inform therapeutic efficacy and options.
Session 6 – Technology Focus:
Dr. Krishanu Saha, PhD
Professor of Biomedical Engineering
University of Wisconsin–Madison
Dr. Krishanu Saha is a Professor of Biomedical Engineering at the University of Wisconsin–Madison, where he holds the Retina Research Foundation Kathryn and Latimer Murfee Chair through the McPherson Eye Research Institute. He is also a faculty member at the Wisconsin Institute for Discovery.
Dr. Saha’s research centers on human cell engineering, with an emphasis on developing innovative therapeutic approaches through CRISPR gene editing, stem cell-derived disease models, and biomaterial-based delivery systems. His lab is pioneering the use of non-viral nanocarriers for genome editing, particularly targeting inherited retinal diseases and other genetic conditions.
He leads the CRISPR Vision Program, co-directs the NSF-funded Center for Cell Manufacturing Technologies (CMaT), and is an active contributor to the NIH Somatic Cell Genome Editing (SCGE) Consortium. Dr. Saha earned his BS from Cornell University, an MPhil from the University of Cambridge, and a PhD from the University of California, Berkeley. He completed postdoctoral work as a Branco-Weiss Fellow at MIT and through Harvard’s Science, Technology, and Society (STS) Program.
His contributions to the field have earned him numerous accolades, including the NSF CAREER Award, the Gund Harrington Scholar designation, and the Biomedical Engineering Society Rising Star Award.
(Image source: Saha Lab, UW–Madison)
Session 8 – Applications Focus:
Dr. Anna Kuchina, PhD
Assistant Professor, Institute for Systems Biology (ISB)
Affiliate Assistant Professor, Electrical & Computer Engineering, University of Washington
Anna Kuchina is an Assistant Professor at the Institute for Systems Biology (ISB) and an Affiliate Assistant Professor in Electrical and Computer Engineering at the University of Washington. Kuchina received her PhD in Cell Regulation from the University of Texas Southwestern Medical Center and was advised by Dr. Gürol Süel. In her graduate work, she studied single-cell dynamics of cell-fate decision-making in the model soil organism Bacillus subtilis. Kuchina completed her postdoctoral training in Georg Seelig’s lab at the University of Washington. Her postdoctoral work led to the development of single-cell RNA sequencing technology for bacteria.
Kuchina’s research interests lie in the development and application of high-resolution technologies toward understanding the single-cell biology of bacteria within complex communities such as biofilms, and in challenging environments such as the human host. Her research program aims to uncover rare but influential bacterial phenotypes that alter the properties of the whole community, leading to such healthcare challenges as chronic disease and antibiotic resistance.
(Image source: ISB)
Lecture Title: Leveraging single-cell transcriptomics for bacterial functional genomics and deciphering viral interactions
Abstract: Even within the same species, bacteria differentiate into distinct phenotypic states. In a complex consortium such as the microbiota, in the presence of other species and predation by bacteriophages, diverse bacterial phenotypes contribute to community fitness and promote phage resistance. However, population-level gene expression measurements are insufficient to resolve such states. We have employed high-throughput bacterial single-cell RNA sequencing to resolve the progression of a lytic phage infection in a human pathobiont, Bacteroides fragilis. Using both host and viral transcriptomic data, we quantified the asynchronous progression of phage infection in individual bacterial cells and determined that each cell’s vulnerability to phage was influenced by variable expression of multiple genetic loci. Extending our analysis to human fecal microbiota, we quantified the heterogeneous phenotypic states in diverse species and associated them with bacteriophages. Finally, we demonstrate how the coupling of pooled CRISPR screens with a single-cell transcriptomics readout enables large-scale mapping of gene regulatory networks across multiple model species. In conclusion, by overcoming significant technical challenges associated with implementing transcriptome-wide single-cell omics methods in bacteria, we show that these approaches allow scalable interrogation of diverse phenotypic states and responses, such as virus-bacteria interactions and the outcomes of genetic perturbations.
Session 9 – Applications Focus:
Dr. Jessica Vazquez, PhD
Staff Scientist & K01 Investigator, Department of Obstetrics & Gynecology
University of Wisconsin–Madison
Dr. Jessica Vazquez is Scientist in the Department of Obstetrics and Gynecology at the University of Wisconsin–Madison and a K01-funded investigator at the Wisconsin National Primate Research Center. She earned her PhD in Endocrinology and Reproductive Physiology and completed postdoctoral training in Reproductive Immunology. Her work has focused on developing advanced flow cytometry and computational pipelines to map the decidual immunome and the use of scRNA-seq technologies to better understand the maternal-fetal interface immunome.
This work led to the discovery of novel decidual innate lymphoid cell subsets in the human term decidua. Her current research uses non-human primate models and multi-omic approaches—including single-cell RNA sequencing and Spatial Transcriptomics—to dissect how sterile inflammation at the maternal-fetal interface programs the developing fetal immune system.
(Image source: SMPH, UW–Madison)
Title: Mapping Decidual Immunity: Integrating Single-Cell and Spatial Multiomics in Human and Non-Human Primate Pregnancy
Abstract:
The maternal–fetal interface is a specialized immunological niche in which finely tuned interactions between maternal and fetal cells underpin successful pregnancy. Disruption of this balance can precipitate adverse outcomes, highlighting the need to define the cellular and molecular programs that govern local immunity. Here, we integrate multiomic and spatial approaches—including single-cell RNA sequencing (scRNA-seq), CITE-seq, V(D)J profiling, and Parse Biosciences’ Evercode™ platform—to map the transcriptional, functional, and spatial landscapes of decidual immune populations in humans and a non-human primate (NHP) pregnancy model.
In human term decidua, combined scRNA-seq and CITE-seq analyses of T cells uncovered clonal expansions of tissue-resident memory T cells marked by elevated ITGAE (CD103), PDCD1 (PD-1), and metabolic regulators such as SLC16A1. Clonotype mapping demonstrated compartmentalized distributions consistent with localized antigen exposure. Parallel profiling of decidual mucosal-associated invariant T (MAIT) cells revealed a decidua-specific transcriptional program characterized by upregulated tissue-repair genes (ANXA1, HMGB1), type-1 cytokines (IFNG, TNF), and homing receptors (ITGA4, CCR5). CITE-seq confirmed high surface expression of CD69 and CD49a, indicative of a pro-inflammatory yet regulatory, tissue-resident phenotype poised for immune surveillance and tissue remodeling.
Extending these findings to the rhesus macaque, spatial transcriptomic analysis of a sterile placental injury model revealed robust pro-inflammatory niches at sites of tissue damage. High-input single-cell profiling with Parse Evercode™ further demonstrated that sterile inflammation in utero imprints immune programs in fetal tissues, suggesting mechanisms by which the maternal environment shapes fetal immune development.
Together, this comprehensive atlas of decidual immunity—spanning T cell clonotypes, MAIT cell programming, and spatially resolved inflammatory responses—illuminates the cellular circuits that maintain pregnancy homeostasis. By applying single-cell, proteogenomic, and spatial modalities across human and NHP tissues, we uncover conserved pathways of immune regulation at the maternal–fetal interface and identify candidate targets for therapeutic modulation in pregnancy complications.
Closing Keynote Speaker:
Dr. Kathryn Richmond, PhD, MBA
Executive Vice President, The Paul G. Allen Frontiers Group and Office of Science and Innovation, Allen Institute
Dr. Kathryn Richmond is an Executive Vice President at the Allen Institute, leading the Office of Science and Innovation and The Paul G. Allen Frontiers Group. In this role, she leads initiatives across the Institute and oversees scientific strategy, government relations, and business development. With a focus on emerging bioscience and technology areas, she has dramatically grown the Frontiers Group portfolio, overseeing >$275M in award funding to date. Through identification of high-risk, high-reward opportunities, she has also formed >$50M in strategic philanthropic partnerships. Dr. Richmond frequently serves as an invited panel member, speaker, and advisor on topics ranging from open science to technology development. She has convened the inaugural Bioscience and Philanthropy Summit, engaging thought pioneers, technologists, venture capital leaders, and philanthropic funders from around the world. Previously, Dr. Richmond has served as a member of the executive team at the DOE Great Lakes Bioenergy Research Center. Along with a doctorate in Cell and Molecular Biology and an M.B.A. from the University of Wisconsin, Madison, she also attended Stanford University as an American Cancer Society fellow and was funded by DARPA for breakthrough research efforts.
(Image source: Allen Institute)
