Research Themes
Cancer Stem Cells: Finding the Cells That Start It All
Not every cancer cell is a threat. Within a tumour, the vast majority of cells are dead ends — but a rare few have the power to start a new tumour from scratch, resist treatment, and drive the disease forward. We call these cancer stem cells, and finding them is one of the biggest open challenges in cancer biology. Our lab is working to identify exactly which cells these are, what keeps them alive, and — most importantly — how to stop them.
What we’re trying to answer:
- Out of billions of cells in a tumour, which ones actually have the power to start a new one?
- What allows these rare cells to persist and regenerate, generation after generation?
- Do these cells have a hidden weakness — a vulnerability we could target without harming everything else?
Cell State Plasticity: A Moving Target
Cancer cells aren’t locked into a single identity. The same tumour cell can shift between different functional states — becoming more invasive, more drug-tolerant, or more stem-like — and then shift back again. This flexibility, called cell state plasticity, may be one of the reasons cancer is so hard to eliminate: even if a treatment kills every cell in one state, surviving cells can simply switch into another. Our lab studies how and why cells make these switches, with the goal of closing off the escape route entirely.
What we’re trying to answer:
- Can we block the switch itself, rather than chasing each state one at a time?
- How do tumour cells change identity — and what triggers the switch?
- Which of these cellular states help a cancer cell adapt and survive treatment?
Treatment Resistance & Metastatic Dissemination
Beating cancer isn’t just about shrinking a tumour — it’s about eliminating every cell capable of bringing it back, wherever it ends up. Our most recent work shows that chemotherapy doesn’t just kill cancer cells; it actively reshapes which cells survive, selecting for a rare population of “persister” cells that enter a stress-tolerant, dormant-like state rather than dying. These are the cells most likely to survive treatment, travel to distant organs, and eventually re-emerge as relapse or metastatic disease — sometimes years later. Understanding how these cells persist and where they go is central to preventing recurrence, not just treating the original tumour.
What we’re trying to answer:
- Which specific tumour clones survive chemotherapy, and why?
- What genetic programs allow a cell to enter — and later exit — a drug-tolerant “persister” state?
- Which of these surviving clones go on to seed metastatic disease elsewhere in the body?
Together, we can accelerate discoveries that reveal the hidden cells responsible for cancer progression. Your support enables innovative research at the intersection of cancer stem cells, cell-state plasticity, and tumour evolution.