Cancer Biology seminars

Wei Wei and Sizun Jiang discuss how spatial multiomics reveals interactions among cancer, immune and stromal cells and the cell states associated with treatment outcomes. Their findings connect melanoma and small-cell lung cancer with the organisation of local tumour ecosystems. The session considers how immune checkpoint blockade prepares melanoma tissue for combination treatment, coordinated macrophage and T-cell states, clonal evolution and lineage plasticity, and the relationship between spatial architecture and immune checkpoint pathways. It also examines the use of AI foundation models and agents in spatial-omics analysis and systems immunology to investigate immune responses and potential therapeutic targets.

Jang Hyun Park discusses how adaptive immunity monitors the central nervous system through lymphoid structures in skull bone marrow. The study identifies germinal-centre-like formations containing follicular-helper-like T cells that promote B-cell activation and humoral responses through CD40L, IL-21 and interferon-gamma signalling. In mouse models, these cells respond to CNS-derived antigens and contribute to anti-tumour immunity in the brain. The findings establish a local site of antigen-specific CNS surveillance and raise questions about its role across neurological diseases.

Anthony Letai discusses how understanding programmed cell death can guide the selection of cancer treatments. The seminar explains how apoptotic signalling can be measured and how these measurements can identify drugs capable of killing cancer cells. Hybrid: New Research Building Auditorium, Georgetown University Medical Center, Washington, DC, and Zoom. Monday 5 October 2026, 16:30–17:30 EDT (America/New_York; UTC−4). Use the attendance registration form or the event’s Zoom link on the organizer page. Organized by Georgetown’s Distinguished Scientist Seminar Series. Letai is Director of the National Cancer Institute. An in-person reception follows the seminar.

MIT Biology Colloquium Series talk by David Bilder (University of California, Berkeley), hosted by Yukiko Yamashita, on invertebrate oncology and the ancient evolutionary origins of tumor-host interactions.

Michelle M. Li examines how computational analyses can preserve the biological context of a proposed treatment, including cell type, disease state, genetic background and patient characteristics. She introduces Medea, an AI system that combines biological software, predictive models and literature retrieval while checking intermediate steps and reconciling evidence. The seminar presents evaluations involving cell-specific target selection, cancer-cell synthetic lethality and immunotherapy response. A separate yeast experiment tests predictions against previously unpublished measurements of gene-pair interactions under DNA-damaging treatments. The research addresses whether an agent can transfer useful evidence between contexts while recognizing when that transfer is unsupported. Reported comparisons cover predictive performance, computational failures and the ability to abstain. This recording retains the original seminar date.

Gladstone-UCSF Institute of Genomic Immunology Seminar by Christine Brown, PhD (Deputy Director, T Cell Therapeutics Research Laboratories) on developing and refining redirected CAR T cells for malignant brain tumors, including glioblastoma, tumor heterogeneity, immunosuppressive microenvironments, delivery routes, and manufacturing.

Emmanuelle Passegué examines why mechanisms that maintain blood-forming stem cells in early life can contribute to their deterioration with age. The lecture connects cell-cycle control, marrow support, inflammation, metabolic regulation and cellular memory to altered self-renewal and blood-cell production. It also considers genomic instability, clonal hematopoiesis and progression toward leukemia.

Blood production can be rapidly reorganised after infection or marrow injury. This lecture follows the molecular, cellular and metabolic responses of stem and progenitor cells that accelerate myeloid-cell output. It then examines how persistent or misdirected activation of these emergency mechanisms can contribute to chronic inflammatory disease and cancer.

Astrocytes release glutamate by regulated exocytosis in health and disease Vladimir Parpura, International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, P.R. China Parpura will present you with the evidence that astrocytes, a subtype of glial cells in the brain, can exocytotically release the neurotransmitter glutamate and how this release is regulated. Spatiotemporal characteristic of vesicular fusion that underlie glutamate release in astrocytes will be discussed. He will also present data on a translational project in which this release pathway can be targeted for the treatment of glioblastoma, the deadliest brain cancer.

Stephen Quake revisits the origins of genetic variation, connecting classic bacterial experiments with modern single-cell genomics. The lecture asks how mutations accumulate during human life, how they contribute to cancer and how tumour evolution can be reconstructed. It illustrates how measurements of individual cells help address these questions.

Studies of families with inherited breast-cancer risk led to BRCA1 and subsequently many other susceptibility genes. This seminar examines how large-scale sequencing and population studies have refined tumour associations and penetrance estimates. It moves from a simple dominant-inheritance model toward multifactorial risk, considering genetic and environmental modifiers that could support individualized surveillance and management.

The adult intestine is a major barrier epithelium and coordinator of multi-organ functions. Stem cells constantly repair the intestinal epithelium by adjusting their proliferation and differentiation to tissue intrinsic as well as micro- and macro-environmental signals. How these signals integrate to control intestinal and whole-body homeostasis is largely unknown. Addressing this gap in knowledge is central to an improved understanding of intestinal pathophysiology and its systemic consequences. Combining Drosophila and mammalian model systems my laboratory has discovered fundamental mechanisms driving intestinal regeneration and tumourigenesis and outlined complex inter-organ signaling regulating health and disease. During my talk, I will discuss inter-related areas of research from my lab, including:1- Interactions between the intestine and its microenvironment influencing intestinal regeneration and tumourigenesis. 2- Long-range signals from the intestine impacting whole-body in health and disease.

Cancer-related fatigue is a prominent and debilitating side effect of cancer and its treatment. It can develop prior to diagnosis, generally peaks during cancer treatment, and can persist long after treatment completion. Its mechanisms are multifactorial, and its expression is highly variable. Unfortunately, treatment options are limited. Our research uses syngeneic murine models of cancer and cisplatin-based chemotherapy to better understand these mechanisms. Our data indicate that both peripherally and centrally processes may contribute to the developmental of fatigue. These processes include metabolic alterations, mitochondrial dysfunction, pre-cachexia, and inflammation. However, our data has revealed that behavioral fatigue can persist even after the toxicity associated with cancer and its treatment recover. For example, running during cancer treatment attenuates kidney toxicity while also delaying recovery from fatigue-like behavior. Additionally, administration of anesthetics known to disrupt memory consolidation at the time treatment can promote recovery, and treatment-related cues can re-instate fatigue after recovery. Cancer-related fatigue can also promote habitual behavioral patterns, as observed using a devaluation task. We interpret this data to suggest that limit metabolic resources during cancer promote the utilization of habit-based behavioral strategies that serve to maintain fatigue behavior into survivorship. This line of work is exciting as it points us toward novel interventional targets for the treatment of persistent cancer-related fatigue.

Gliomas are brain tumors formed by networks of connected tumor cells, nested in and interacting with neuronal networks. Neuronal activities interfere with tumor growth and occurrence of seizures affects glioma prognosis, while the developing tumor triggers seizures in the infiltrated cortex. Oncometabolites produced by tumor cells and neurotransmitters affect both the generation of epileptic activities by neurons and the growth of glioma cells through synaptic-related mechanisms, involving both GABAergic / Chloride pathways and glutamatergic signaling. From a clinical sight, epilepsy occurrence is beneficial to glioma prognosis but growing tumors are epileptogenic, which constitutes a paradox. This lecture will review how inhibitory and excitatory signaling drives glioma growth and how epileptic and oncological processes are interfering, with a special focus on the human brain.