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Speaker

Daniel K. Nomura, PhD
Professor of Chemical Biology and Molecular Therapeutics
Departments of Chemistry and Molecular and Cell Biology
University of California, Berkeley

“Reimagining Druggability using Chemoproteomic Platforms”

Dan Nomura is a Professor of Chemical Biology and Molecular Therapeutics in the Department of Chemistry and the Department of Molecular and Cell Biology in the Division of Molecular Therapeutics at the University of California, Berkeley. He is the Co-Director of the Molecular Therapeutics Initiative and an Investigator at the Innovative Genomics Institute at UC Berkeley. He is also an Adjunct Professor in the Department of Pharmaceutical Chemistry at UCSF. Since 2017, he has been the Director of the Novartis-Berkeley Translational Chemical Biology Institute focused on using chemoproteomic platforms to tackle the undruggable proteome. He is Co-Founder of Frontier Medicines, a start-up company focused on using chemoproteomics and machine learning approaches to tackle the undruggable proteome. He is also a co-founder of Zenith Therapeutics focused on targeted protein degradation of undruggable targets. He is on the Scientific Advisory Boards for Frontier Medicines, Zenith, Photys Therapeutics, Apertor Pharma, Axiom Therapeutics, Deciphera, and Ten30 Biosciences. Nomura is also on the scientific advisory committees of The Mark Foundation for Cancer Research and American Association for Cancer Research (AACR). He is also an Investment Advisory Partner at a16z Bio+Health, an Investment Advisory Board member at Droia Ventures, and an iPartner with The Column Group. In 2025, Nomura also became the Editor-in-Chief for Molecular Cancer Therapeutics. He earned his B.A. in Molecular and Cell Biology in 2003 and Ph.D. in Molecular Toxicology in 2008 at UC Berkeley with Professor John Casida and was a postdoctoral fellow at Scripps Research with Professor Benjamin F. Cravatt before returning to Berkeley as a faculty member in 2011. Among his honors are the National Cancer Institute Outstanding Investigator Award, Searle Scholar, and the Mark Foundation for Cancer Research ASPIRE award.

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Speaker

Anne Carpenter, PhD
Institute Scientist
Broad Institute

“Insights from cell images: drug discovery in the age of AI”

Fewer than 13% of the 22,000 recognized diseases in the world have FDA-approved treatments – and more diseases are discovered every day. Studying them one by one costs far too much time and money. Could we find ways to tackle many diseases systematically, in parallel? Broad Institute Scientist Anne Carpenter, PhD, will overview several strategies for early drug discovery that are powered by clever advancements in biotechnology and AI. These are accelerating biological discovery and may ultimately break the bottleneck, bringing more treatments to more patients. Robotic instrumentation can screen millions of drugs, and computer vision can identify those that impact cellular disease phenotypes. Pooled optical barcode-based profiling allows testing thousands of genetic samples, which can identify their functions or reveal whether they respond to a given drug. Engineered genetic variants associated with thousands of diseases can be tested at once to identify phenotypes for drug screening. These methods are widely shared, as are the datasets created by consortia led by the Carpenter—Singh lab, including JUMP, OASIS, and VISTA. Some of these technologies power techbio companies reaching clinical trials. Enjoy this glimpse into the cutting-edge intersection of AI, biotech, and several disease areas including neuroscience, metabolic disease, cancer, and rare diseases.

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Speaker

Ludmil B. Alexandrov, PhD
Professor
Department of Bioengineering
Department of Cellular and Molecular Medicine
UC San Diego

“Uncovering the Mutagenic Origins of Never-Smoking Lung Cancer and Early-Onset Colorectal Cancer”

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Kivanç Birsoy, PhD
Professor
Laboratory of Metabolic Regulation and Genetics
Rockefeller University

“Understanding the role of organellar metabolism in physiology and cancer”

Our research program develops single-cell and spatial technologies to study the genomic and epigenomic basis of human diseases. Human brain development is guided by gene regulatory programs that define neurogenic regions and give rise to diverse brain structures. Inhibitory interneurons and striatal medium spiny neurons (MSNs) originate from the ganglionic eminences (GEs), whereas excitatory neurons arise from the ventricular zone (VZ). The molecular programs that regionalize GE subtypes (MGE, LGE, CGE) and cortical areas remain poorly understood. We used single-nucleus methyl-3C sequencing (snm3C-seq), highly multiplex spatial transcriptomics, and chromatin+RNA MERFISH to investigate the 3D multi-omic architecture across GEs, the striatum, the hippocampus, and cortical regions spanning prenatal to adult stages. The study uncovers distinct 3D multi-omic programs in the three GE regions during brain development: MGEand CGE-derived interneurons show continuous subtypes and temporally separated trajectories of the DNA methylome and 3D genome, whereas LGE-derived MSNs display highly discrete subtypes with temporally synchronized multi-modal dynamics.

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Speaker

Chongyuan Luo, PhD
Assistant Professor
Human Genetics
University of California, Los Angeles

“Dissecting Human Brain Development and Prostate Cancer Evolution with Single-Cell and Spatial 3D-Multiomics”

Our research program develops single-cell and spatial technologies to study the genomic and epigenomic basis of human diseases. Human brain development is guided by gene regulatory programs that define neurogenic regions and give rise to diverse brain structures. Inhibitory interneurons and striatal medium spiny neurons (MSNs) originate from the ganglionic eminences (GEs), whereas excitatory neurons arise from the ventricular zone (VZ). The molecular programs that regionalize GE subtypes (MGE, LGE, CGE) and cortical areas remain poorly understood. We used single-nucleus methyl-3C sequencing (snm3C-seq), highly multiplex spatial transcriptomics, and chromatin+RNA MERFISH to investigate the 3D multi-omic architecture across GEs, the striatum, the hippocampus, and cortical regions spanning prenatal to adult stages. The study uncovers distinct 3D multi-omic programs in the three GE regions during brain development: MGEand CGE-derived interneurons show continuous subtypes and temporally separated trajectories of the DNA methylome and 3D genome, whereas LGE-derived MSNs display highly discrete subtypes with temporally synchronized multi-modal dynamics.

The ever-evolving cancer genome provides an exceptional opportunity to investigate the interaction between intratumoral genetic and epigenetic heterogeneity. We have developed computational approaches that integrate snm3C-seq and population-scale bulk profiles to determine the epigenomic and genomic subtypes of true single tumor cells. Using such unique experimental and computational strategies, we are investigating intra-tumoral, spatial, and subclonal methylome-genome evolution in prostate tumors.

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Speaker

Alison E. Ringel, PhD
Assistant Professor
Department of Biology
Massachusetts Institute of Technology and Ragon Institute

“Metabolic Circuits Linking Lipid Metabolism to T Cell Immunity”

Lipid metabolism is disrupted at many levels in the tumor microenvironment, which reflects the interplay between systemic metabolic state and local cellular processes. For T cells, the impact of different lipid species on anti-tumor functionality remains incompletely understood, even though effector T cells take up a wide range of extracellular lipids. This talk will focus on new roles for lipid metabolites in regulating T cell activities involved in tumor control, and how this may be manipulated to improve anti-tumor immune responses.

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Speaker

Jennifer Guerriero, PhD
Assistant Professor
Department of Surgery
Brigham and Women’s Hospital/Harvard Medical School

“Unraveling the complexities of tumor associated macrophages for anti-cancer therapy”

Tumor associated macrophages (TAMs) represent a significant proportion of solid tumors and enhance tumor cell growth, metastasis and importantly, inhibit anti-tumor responses of T cells. Our recent work has shown that removal or conversion of TAMs to an anti-tumor phenotype enhances chemo- and immuno-therapy establishing TAMs as targets for anti-cancer therapy. We recently revealed that some types of therapy such as poly(ADP-ribose) polymerase (PARP) inhibition (PARPi) can drive development of highly suppressive TAMs, restricting anti-tumor T cell function and survival. Murine models demonstrate that in the absence of TAMs, PARPi induce a robust recruitment of cytotoxic T cells and durable antitumor responses. Therefore, targeting TAMs is a promising strategy for improving PARPi treatment efficacy. However, while there is an urgent need to target TAMs during tumorigenesis and cancer therapy, to date, failure to fully characterize TAM biology and classify multiple subsets has hindered advancement in therapeutic targeting. Here we will the functional and phenotypic characterization of TAM subsets associated with cancer, before and after treatment, as well as novel TAM-modulating strategies and combinations that are likely to enhance current therapies and overcome chemo- and immuno-therapy resistance.

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Speaker

Elda Grabocka, PhD
Associate Professor
Departments of Pharmacology, Physiology and Cancer Biology & Surgery
Thomas Jefferson University and Jefferson Health

“The Dynamic Life of Stress Granules: Linking Cell Cycle, Metabolism, and Pancreatic Cancer”

This seminar will cover our research into stress adaptation in Pancreatic Ductal Adenocarcinoma (PDAC). We start with findings on molecular drivers of stress granule (SG) formation and their role in PDAC tumor development. Our investigation then revealed that SG composition and function are not static, but dynamically shaped by cell state, particularly the cell cycle. We’ll present novel findings on this cell-cycle-dependent heterogeneity and its consequences for tumor cell fate. We also touch on how systemic factors, like those in the metabolic syndrome-tumor axis, affect SG biology and cellular stress in PDAC.Finally, we integrate these multi-level insights—from molecular SG mechanics to cell-state modulation and systemic impacts—to illustrate their convergence in pancreatic tumorigenesis. We aim to highlight emerging therapeutic opportunities, such as phase-specific SG targeting, and foster discussion on new anti-PDAC strategies based on our findings.