We’re bringing together leaders in cancer research.
Denis Guttridge, PhD
Professor, Department of Pediatrics
Director, Darby Children’s Research Institute
Associate Director of Translational Science, Hollings Cancer Center
Medical University of South Carolina
“Evolving Insights into Cancer Cachexia: Lessons Learned from the Muscle Microenvironment“
We’re bringing together leaders in cancer research.
William A. Weiss, MD, PhD
Evelyn and Mattie Anderson Endowed Chair in Cancer Research
Professor, Departments of Neurology, Pediatrics, and Neurological Surgery
UC San Francisco
Co-Leader, Pediatric Malignancies Program
UCSF Helen Diller Family Comprehensive Cancer Center
“Models and vulnerabilities for brain cancers”
Medulloblastoma is the most common tumor of childhood. Glioblastoma is the most common tumor of adulthood. I will present new models of human group 3 medulloblastoma. We differentiate human induced pluripotent stem cells cells to neuroepithelial stem (NES) cells, transduce NES cells with MYC, alone and in combination with other gain of function effectors, and transplant orthotopically into the hindbrain. I will discuss characterization and developmental therapeutics in resulting models. I will also present developmental therapeutic studies in glioblastoma, focusing separately on molecular glues targeting RAS and bi-steric inhibitors of mTORC1. I will discuss screens to identify combination therapies that improve efficacy, as well as separate screens and approaches to enhance delivery to the brain while abrogating peripheral toxicity.
Distinguished Cardiovascular and Muscular Diseases Seminar Series
Mark Mercola, PhD
Joan and Sanford I. Weill Scholar
Professor of Cardiovascular Medicine
Stanford Cardiovascular Institute
Seminar Abstract: Very few new medicines are approved for heart disease, even though heart disease is the largest cause of human mortality. Many investigational drugs fail to show effectiveness – driving up the development cost and discouraging investment – and use of human induced pluripotent stem cells (hiPSC) offer a promising way to improve heart disease drug discovery. This talk will cover a) how hiPSC-cardiomyocyte phenotypes predict clinical outcomes from myopathic gene variants, b) using hiPSC models to refine oncology drugs to limit cardiovascular toxicities, and c) combining hiPSC and animal models to develop new treatments for cardiomyopathy and myocardial infarction.
Distinguished Cardiovascular and Muscular Diseases Seminar Series
Helen Blau, PhD
Donald E and Delia B Baxter Foundation Professor
Director, Baxter Laboratory for Stem Cell Biology
Stanford University School of Medicine
Seminar Abstract: Blau discovered a pivotal molecular determinant of stem cell and tissue dysfunction with aging, 15-hydroxyprostaglandin dehydrogenase. This enzyme, which she termed a ‘gerozyme’, modulates Prostaglandin E2 levels and can be targeted therapeutically with a small molecule to promote muscle and cartilage regeneration and rejuvenation. This treatment holds promise as a therapy for sarcopenia and for osteoarthritis.
Distinguished Cardiovascular and Muscular Diseases Seminar Series
James L. Kirkland, MD, PhD
Professor of Medicine and Director
Center for Advanced Gerotherapeutics
Cedars-Sinai Medical Center
Seminar Abstract: Cellular senescence is a cell fate entailing essentially irreversible replicative arrest and resistance to apoptosis that can occur in most cell types across the age range in response to damage-related signals. Senescent cells can acquire a senescence-associated secretory phenotype that includes release of multiple proteins, peptides, bioactive small molecules, and coding and non-coding nucleotides. Persisting senescent cells not removed by the immune system can become pro-inflammatory, spread senescence locally and systemically, release aggregated proteins, reshape the extracellular matrix, and sometimes escape senescence to emerge as cancer cells. Transplanting senescent cells or organs containing senescent cells can induce multiple disorders and diseases. Conversely, senolytics, agents that selectively eliminate pro-inflammatory senescent cells, appear to delay, prevent, alleviate, or treat multiple conditions in preclinical models. Clinical trials of senolytics are currently underway, with some indicating safety, tolerability, and target engagement and with a few early phase clinical trials suggesting efficacy. Much remains to be done to determine if senolytics will enter clinical practice.
We’re bringing together leaders in cancer research.
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.
We’re bringing together leaders in cancer research.
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.
We’re bringing together leaders in cancer research.
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”
We’re bringing together leaders in cancer research.
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.
We’re bringing together leaders in cancer research.
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.