Research — Kim Lab | 3D Genome and Disease Mechanisms, KAIST

First, a 30-second primer

A single human cell holds roughly two meters of DNA, packed into a nucleus so small that thousands would fit across a pinhead. To fit, the genome folds — but not randomly.

Folding is guided by structural proteins (CTCF, cohesin) and a web of epigenetic marks. It pulls distant stretches of DNA into loops and neighborhoods called TADs, deciding which genes can reach their regulatory switches.

Change the fold, and you can change which genes turn on — and therefore what a cell becomes. When folding goes wrong, disease can follow.

Cancer · genome instability

Unstable genomes in cancer, read in 3D

The problem

Infection, nuclear instability, and other environmental insults trigger somatic changes in the genome — point mutations, copy-number variation, structural variants — that are among the leading causes of cancer.

The gap

These variations are directly connected to changes in 3D genome networks and epigenetic landscapes — yet the molecular mechanisms that drive them remain poorly understood.

Our approach

We build 3D genome folding maps of cancer samples with unstable genome structures, then dissect the key mechanisms behind them and what they mean for the clinic.

cancerSNP · CNV · SV3D contact mapsclinical implication

Instability rewires the contact map — new bright blocks mark rearranged regions

Cancer · genome stability

DNA damage, repair, and the broken fold

The problem

Our DNA is broken and repaired constantly. When repair fails, the errors that remain are a root cause of cancer — and repair does not happen on bare DNA, but on DNA that is folded into a complex 3D structure.

The gap

How the genome reorganizes its fold around a break, and whether that architecture helps or hinders faithful repair, is still poorly understood.

Our approach

We map how 3D folding changes at sites of DNA damage and during repair, and ask what goes wrong — structurally — when a cell takes the path toward cancer.

cancerDNA damage & repairgenome stability

Around a break, chromatin refolds and repair factors converge — we ask how that shape shapes the outcome

Technology · genome engineering

Learning to engineer 3D genome folding

The problem

The 3D genome is organized hierarchically — loops, TADs, compartments, chromosomes. The loop-extrusion model explains how loops form, but the cause-and-effect between loops, transcription, and epigenetic features is still unresolved.

The gap

Even how the genome's domain structures form in the first place remains elusive — which makes it hard to prove what folding actually does.

Our approach

We are developing new technology that can reshape 3D genome folding domains on demand, then test their function at target genes — turning correlation into causation.

genome engineeringloop extrusionsynthetic biologycause & effect

We build a loop where there wasn't one — and watch the target gene switch on

Why it matters

3D genome folding is woven into the mechanisms of many diseases — cancer and leukemia, medulloblastoma, schizophrenia, fragile X syndrome, immune dysregulation, and metabolic change — as well as fundamental biology like development. By understanding the rules of folding, and learning to rewrite them, we aim to turn a basic mechanism into a lever for health.

Curious enough to fold in?

We take students and researchers from biology, medicine, bioengineering, and computer science. No prior 3D-genome experience required — just curiosity and drive.

See open positions →