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Dr Richard Clarkson

"That's why I think they're fascinating, because [cancer stem cells] are, by definition, the thing you will need to eliminate from a tumour to have an absolute cure for cancer. But they are elusive."

Who are you?

I'm Senior Lecturer in the School of Biosciences and have been in Cardiff for eight years, always in the mammary gland field. I was recruited into ECSCRI when it was opened in August last year and my remit when I arrived as a research fellow was in translational research in cancer. That means taking what I've found about normal mammary gland biology in my previous research and translating that into the cancer setting.

What do you think cancer stem cells are?

I think that fundamentally a cancer stem cell is a cell that has the ability to form a new tumour.  However, I'd define it as a property, or series of properties, rather than a specific cellular entity. You can't pick out a cell and say 'that is the original cancer stem cell'. It might be that it has those properties right now, but tomorrow it might not. I think it's a very plastic event.

Why do you think they're so interesting?

Because they are, by definition, the thing you will need to eliminate from a tumour to have an absolute cure for cancer. But they are elusive. They're very difficult to identify in the first place and ultimately to target therapeutically.

Tell me more about your current research here at the Institute

I came from Cambridge with a number of genes that we thought were responsible for regulating whether the cells of the mammary gland were maintained or whether they were lost.

We looked at these genes in more of a cancer setting when I came to Cardiff and extrapolated that any genes that have a role in telling a cell whether it should exist or not might have a consequence in breast cancer. Because that's the first step, I think, in cancer: a cell that goes wrong, and remains in place when it needs to be eliminated.

So we've now paired the genes down to two that are very important in cancer stem cells: Bcl3 and c-FLIP. We think that if we can inhibit Bcl3 we can prevent the cancer stem cells spreading around the body, a process called metastasis. And if we can suppress c-FLIP, we think we can sensitise the cancer stem cells to novel therapies that will allow them to be killed off.

How do you see your research being applied and influencing the bigger picture of cancer therapy?

My lab here is probably the most applied in terms of clinical therapies. Much of our focus involves seeing if new agents we've identified are actually useful for targeting our two genes and therefore the cancer stem cells.

We're currently doing this by using patients' tumours from clinics in Cardiff ex vivo, which means outside of the body, and looking at them live in the lab to see if we can kill off the tumour cells.

If that's successful, our next step is to move the drugs into the patients. Hopefully we're only a couple of years away from doing that.

What are you working on today?

I don't get in the lab anymore! Today, I talked with my collaborator, Andrea Brancale in pharmacy, about the scope for whether this inhibitor of c-FLIP that we've literally just identified could be adopted as a cancer therapy.

What can you gain as a researcher from working at the Institute?

The collaborations and the laboratory facilities. I'm five steps away from people who know what I'm talking about and five steps away from the tools that I need to do my job.

(Interviewer: Sophie Hopkins, final year Biosciences undergraduate student)