Live Event
Decoding Early Disease Risk Using Region-specific Genomics
February 19, 2026 04:00 PM (London)
Laurel Hiatt
Laurel is an M.D./Ph.D. candidate in Human Genetics at the University of Utah. Supported by an NCI fellowship, they explore how mutational patterns in normal colon tissue influence colorectal cancer. Their bioinformatics work spans short tandem repeat expansion disorders, pediatric rare disease diagnosis, and health disparities in transgender populations. Laurel serves on a Genetics Society of America subcommittee and anticipates a career as a physician-scientist in pediatric medical genetics.
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Learn how regionally resolved genomics can be used to uncover early, site-specific mutational processes that shape disease risk within tissues.
In this webinar, you will learn how:
Regional differences within a tissue or organ can shape disease development and clinical outcomes
To interpret common mutational signatures and link them to underlying biological or environmental mutational processes
A regionally resolved genomics workflow enables robust analysis of early mutational events
Disease risk is rarely uniform across a tissue or organ. Instead, specific regions often show higher susceptibility, shaped by local biology, environmental exposure, and early mutational events that occur long before pathology becomes visible.
Understanding how and where these mutations arise is a fundamental challenge across cancer biology, aging research, and studies of somatic mosaicism.
Colorectal cancer (CRC) provides a striking example of this problem. Tumors arise preferentially in defined segments of the colon, with location-linked differences in morphology, mutation profiles, and clinical outcomes. These patterns are particularly pronounced in early-onset disease. Yet, traditional organ-level analyses lack the resolution needed to connect regional biology with early mutagenic processes in otherwise normal tissue.
In this webinar, you’ll see how analyzing region-specific somatic mosaicism at single-structure resolution enables deeper insight into how mutations accumulate across an organ.
By profiling individual anatomical structures, you can quantify baseline mutation burden, compare regional differences in mutational accumulation, and extract signatures that point to underlying biological drivers, whether endogenous, environmental, or microbe-associated.
Using the colon as a model system in this case study, you will learn how regionally resolved genomics can be applied to test long-standing hypotheses about site-specific disease risk and early pathogenesis.
The workflow combines precise microdissection of intact tissue structures, minimal-artifact library preparation, and high-quality sequencing to generate data sufficient to resolve subtle yet biologically meaningful mutational patterns—an approach that can be applied beyond CRC to study early disease mechanisms across tissues and organ systems.
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