Cancer divides on a knife edge.

Tumour cells survive inside a narrow band of mitotic instability — enough to keep evolving, not so much that division fails outright. Healthy cells sit nowhere near that edge. We are building a live-cell foundation model to find the perturbations that exploit the gap.

healthy cells tumour cells mitotic failure

The instability that makes a tumour dangerous is also what makes it fragile. A perturbation that adds a little mitotic stress can tip one population and not the other.

Chemotherapy already attacks cell division. It cannot tell whose.

Taxanes and vinca alkaloids are spindle poisons — they work by breaking mitosis. The trouble is that they break it in every dividing cell, so the dose is limited by what the patient can survive rather than by what the tumour needs. The suffering is not a side effect of one bad drug. It is what happens when a therapy cannot distinguish a tumour cell from a healthy one, and when finding one that can takes a decade.

1 in 5people develop cancer in their lifetime, with 20.6M new cases in 2024 rising to 34M by 2050.

3.4%of oncology programmes entering Phase 1 reach approval, after 10–15 years and upwards of $2B each.

~90%of solid tumours are aneuploid — already dividing under stress that healthy tissue never experiences.

We watch the same cell divide, before and after

Every existing method destroys the cell it measures. Sequencing lyses it; high-content imaging fixes and stains it. That means you can compare populations, but never a cell to itself — and the causal link between a perturbation and a fate is lost. Live-cell video keeps the cell alive, so we can follow one mitosis through to its own daughters.

  1. Step one

    Watch

    Live-cell video of mitosis — brightfield, H2B and tubulin, imaged every ten minutes. Lineage tracing links each baseline division to its own perturbed daughters.

  2. Step two

    Build

    A mitotic perturbation response atlas across four cell contexts, where every response is paired to its own control rather than to a separate population.

  3. Step three

    Model

    A foundation model trained on that pairing, learning the direction that moves a cell from a failing division toward a healthy one.

  4. Step four

    Rank

    Extrapolation across tens of thousands of genes and molecules, ranked by the gap between tumour and healthy response. Only the top of the list reaches the bench.

Why the existing toolkit falls short

Each alternative gives up at least one of the four properties you need in order to rank a perturbation by selectivity.

Same cell,
before & after
Mitotic
dynamics
Cell survives
measurement
Scales beyond
what’s measured
Brute-force wet-lab screening
Single-cell RNA-seq models
Fixed-cell high-content imaging
Live perturbation lineages

Who we work with

Lunenfeld-Tanenbaum Research Institute

Sinai Health in Toronto — named Canada’s first Nikon Center of Excellence for cellular imaging in 2021.

Creative Destruction Lab

Selected for the 2026–27 cohort, working with mentors through CDL’s objective-setting programme.

Second market: aging

Age-aware control cells extend the same platform into an atlas of rejuvenating perturbations and age-specific vulnerabilities.

What we are looking for

We are early, and the useful conversations right now are with people who know this problem from the inside.

hello@cliffside.bio