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Jun 11, 2026

Constraints spanning normal, precancer, to cancer transition in the colon

Speaker: Professor Ken Lau

Professor of Cell and Developmental Biology, Professor of Surgery, Department of Cell and Developmental Biology, Vanderbilt University

School of Biomedical Sciences cordially invites you to join the following seminar:

Date: 11 June 2026 (Thursday)
Time: 11:00 am – 12:00 pm
Venue: Seminar room 3, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Jason Wong

Biography

Professor Lau is internationally recognized in field of single-cell systems biology. His research focuses on gut biology, specifically the molecular events that occur at the intersection of mucosal damage, inflammation, and tumor initiation. His laboratory applies systems biology approaches to investigating interactions between cells and their microenvironment in modulating cellular identity, development, and the origins of cancer. Serving as co-chair of the NCI Human Tumor Atlas Network, he has led efforts to map human cancers at single-cell resolution, setting new standards for integrative cancer research. He is currently a full professor in the Department of Cell and Developmental Biology at Vanderbilt University, and the director of the Center for Computational Systems Biology.

Abstract

Across inflammation and premalignant progression of the proximal colon, epithelial damage unlocks conserved developmental programs that shift cellular identity and microenvironmental interactions. Using single-cell, clonal, and spatial analyses across mouse and human systems, we show that region-specific inflammatory injury in the ascending colon induces goblet-cell-dependent responses linked to microbial pathobionts. In parallel, lineage tracing and clonal reconstruction identify a rare fetal-like epithelial precursor population that persists into adulthood and becomes activated during regeneration after damage. These findings to colorectal tumorigenesis, where serrated tumorigenesis arise through gastric metaplasia after fetal reprogramming. We support a model in which proximal colonic injury drives fetal differentiation and gastric reprogramming that predisposes cells to neoplastic transformation.

 

All are welcome.

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