PRN: Can you tell us a little about your background and how you came to work in Paul Shore’s Lab?
I graduated with a BSc in Biology in 2000 from the University of Northumbria at Newcastle and decided to get some real world experience before continuing on to further education. I moved to Cambridge and began work at the Wellcome Trust Sanger Institute where I was lucky enough to work on the Human Genome Project. This was a really exciting time and I was there to see the project completion in 2003. I gained loads of experience from my years here and my second positon as a research assistant in the Mouse Genomics team gave me the push in needed to go back to education and get my PhD so I could work towards become a researcher in my own right.
In 2005 I moved to Manchester to complete a PhD at the Paterson Institute for Cancer Research. My project looked at breast cancer stem cells which are the cells which we believe are responsible for breast cancer initiation, progression, metastasis and recurrence following treatment. These cells make up a small subpopulation of cells within a breast tumour but they are extremely important and have been likened to the roots of a weed – if you cut the top of a dandelion away with your lawn mower it may appear the weed is gone but, as the roots remain intact under the soil, the plant will regrow just as before. The same is true in breast cancer, we can often treat the primary tumour but years later the cancer can regrow. It is vital that we understand as much as we can about the role cancer stem cells play in this so we can develop more successful breast cancer treatment in the future which will take out the “root” as well as the “plant”.
I stayed in Manchester after my PhD and took up a role as a post-doctoral research associate in the newly formed Breakthrough Breast Cancer Unit where I continued my studies into cancer stem cells. We know that breast cancer is not a single disease, there are many different sub-types with different prognosis and progression and each sub-type respond to different therapies. In this post I investigated the role that cancer stem cells have in different sub-types of breast cancer and investigated how these cancers and their stem cells respond to environmental signals.
PRN: What are you currently working on and how does this fit into the bigger picture of the work that the Shore Lab carries out?
In May of this year I joined Paul Shore’s lab, within the Faculty of Life Sciences at Manchester University, to carry out a 3 year project funded by Breast Cancer Campaign. The overall aim of the lab is to understand better the processes involved in breast cancer metastasis and how breast cancer cells can travel to, survive and grow in foreign environments like the bone. Paul’s lab has previously shown that, in some cases, breast cancers cells express two proteins, called Runx2 and CBFβ. These proteins are normally found in bone and when they interact they switch on genes and signalling pathways which basically tell bone cells to be bone cells. The finding that breast cancer cells express these proteins suggests that the reason breast cancer cells move towards and colonise the bone is because they’re being told they are bone. This is of great importance as we know that in around 3 in 4 patients with secondary disease the site of metastasis is the bone but we know relatively little about the processes involved in this progression.
The aim of my project is to look in more detail at the genes which are switched on by CBFb:Runx2 as this may offer us a method to target bone metastasis or, even better, may uncover a way to stop bone metastasis happening in the first place.
PRN: What will this mean for patients in the future who have breast cancer?
Breast cancer is the most common cancer in the UK with approximately 50,000 women and 350 men diagnosed each year. Amazing advances in treatments have meant that survival rates at 5 years have increased from around 50% 40 years ago to over 80% but there are still around 12,000 women and 80 men that die from the disease each year. When breast cancer has spread to other sites within the body, such as the bone, the disease can no longer be cured and can only be treated with the aim of slowing the disease or improving quality of life. It is this reason that it is so important that we study how progression occurs and try to find ways to treat or block it. One major problem we face is that we don’t know how to predict if and when the cancer will recur and where the likely site of recurrence will be. Research like ours will add to our understanding of the disease and how it progresses as well as uncovering possible targets to which new treatments can be developed.
PRN: Where do you think cancer treatment is heading in the future?
I think the most important thing for cancer treatment is the acceptance that we need personalised medicine - patient specific therapies which take into account the disease sub-type, the likely response to treatment and the likely path the disease will take. This isn’t a particularly new idea, drugs like Herceptin are already being used in patients with a specific sub-type of breast cancer as only these patients will respond to the drug. This will most likely mean that each patient will need a tailored program of drugs, over different time scales and with different surgical interventions but it should mean that the survival rates get even better.
PRN: What do you consider to be the greatest scientific breakthrough of all time?
Tough one …… I’m going to say the elucidation of the structure of DNA by Watson and Crick in 1953 (and their often forgotten research associate, Rosalind Franklin, who played a major role in this work) - I’m not sure it represents the single greatest scientific breakthrough of all time but it is certainly the one I feel is most important to me and my research.
The understanding of the structure of the “data storage” of cells very quickly led to our ability to read the sequence, copy it, manipulate it and begin to identify key regulators of processes. These are all huge leaps taken from that first finding just 60 years ago and they have made work like mine possible. We can now look at the genome of patients with breast cancer and identify mutations in the sequence which may lead to disease. We can then edit the genome in cells in our laboratories with so much accuracy that we can change a single base pair in much the same way as it may have occurred in a natural mutation. This not only facilitate studying these mutation in cells of interest but will perhaps allow us to find ways to correct unwanted genomic modification in patients in the future. The possibilities are endless.
PRN: What are your ambitions for your career?
I am in a great position at the minute - I enjoy the work and the team I work with and the University environment are great. I get to meet and talk with fundraisers and members of the public and I also get to take part in mentoring students through their undergraduate and graduate degrees.
I’m lucky to have a 3 year post as in science contracts are hard to come by and often quite short so my plan is to work hard for the next few years so I can learn as much as I can from my colleagues.
During this time I aim to develop my interests into an independent area of research so I can secure my own funding and go on to set up my own lab where I can continue to contribute to breast cancer research in the years to come.
Read a selection of Dr Harrison's papers: