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We talk to Professor Jo Morris, one of our researchers, about her career and her studies into the BRCA1 gene.
In 2006, Breast Cancer Now awarded Jo Morris a Scientific Fellowship. She has subsequently become a professor and, in November, gave her inaugural lecture at the University of Birmingham. We caught up with Jo to find out more about her research on the BRCA1 gene and the impact it could have for people affected by breast cancer.
In my childhood, I was always interested in how things worked. The more I learnt about biology, the more fascinated with it I became. Look at your hand and look closely at the fingerprints and the folds – how did they get there? It’s these kinds of questions I was asking as a child. And if you’re curious about the world, then science is the answer.
I then did a degree at university and then a PhD. After that, I went on to become a university researcher. Breast Cancer Now gave me a fellowship to support the breast cancer research I was doing, which helped me to move to the University of Birmingham to become a lecturer and to set up a lab. Since then, I got a permanent position at the University of Birmingham, and various projects in my lab have been funded by Breast Cancer Now and other funders, to the extent where the University has now made me a professor.
I think it was probably the idea that cancer is a very complicated disease. Breast cancer has many different types, and we know now that even the same type of breast cancer differs a lot between people.
When I started in research, we knew that breast and ovarian cancers were more common in some families than in the general population. We also knew that some of the genes in these families had changes in them. These were clues to understanding that, in at least some breast cancers, there might be a genetic cause, and this is what fascinated me. I wanted to study the genes that help protect us from breast cancer.
It came one day from looking through a microscope. I had been wondering whether a protein called ubiquitin might be important for breast cancer cells to repair their DNA.
I had been treating cells to damage their DNA, and I had labelled the ubiquitin proteins with coloured tags so that I could see it. When I looked through the microscope, there it was. I could see this protein going to the damaged DNA in these cells.
At that moment, I knew I had something important – and that no one else at that time knew it yet either. We now know that this protein is critical to the way that cells respond to damage and fix their DNA which prevents mutations and stops cancer developing.
BRCA1 stands for BREAST CANCER 1, and it was the first gene discovered that protects against breast cancer. We’re studying it because understanding it helps us understand how, most of the time, most of us don’t develop breast cancer.
We and others thought that BRCA1 only performs one role in preventing breast cancer development, but our current research suggests that there is another function.
The impact it could have is quite exciting. We think that cancer cells without this second BRCA1 function depend on weaker functions in the cell to survive. When BRCA1 stops working they are surviving using different genes with a similar function, but we think we will be able to target these genes to destroy the cancer cells in the future.
We hope it will be particularly useful regarding PARP inhibitors. These are a type of drug that stops that PARP molecule from repairing cancer cells, which is keeping cancer cells with BRCA1 mutations alive. We hope that in the next year PARP inhibitors will be approved for treating secondary breast cancer in the UK.
We also know that we need new ways to target cancer cells once they have become resistant. If we can find and target more than one function, it gives us more ways to stop them from coming back.
Some drugs, which are in early development, can block these other functions that cancer cells rely on when BRCA1 isn’t working well. Myself and those involved in the projects will be talking with pharmaceutical companies to ensure that new treatments are made to target these different functions.
But these other functions cancer cells depend on are not yet well understood. And what I find interesting is that cancer cells can survive without BRCA1. But if BRCA1 stops working properly in healthy cells, they die, which means that the cancer cells have found a way to survive without it. And this is what we want to understand further.
To find out whether targeting these remaining functions can prevent cancer recurrence and resistance to treatments.
We hope this work will give us knowledge that can help to improve breast cancer diagnosis and treatment. It might be that it helps us determine whether new treatments, such as ones given to prevent a recurrence, would benefit individual patients or not. Our work is investigating the functions of BRCA1 may also help doctors decide the right treatment for patients with certain changes in their genes.
If I wasn’t a researcher? Well, I like my job, and I’m lucky I get to do it. But if not this, maybe an artist? Science is creative within a framework, and sometimes it’s fun to remove the framework!
To find out more about Professor Jo Morris’ research, click here.
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