By Mhairi Morris, Loughborough University
Current estimates state that nearly half of us will develop cancer at some point during our lifetime, either a benign tumour that doesn’t require treatment or a more aggressive malignant tumour with the potential to kill.
Around a fifth of all cancers are linked to an infectious agent, and according to the World Cancer Research Fund (WCRF), an estimated 30-40% of cancers could be prevented by making better dietary and lifestyle choices, for example, quitting smoking, consuming less alcohol, wearing sunscreen, eating less processed red meats, maintaining a healthy weight, and eating a diet rich in leafy green vegetables.
I’m sure none of this comes as any great surprise: we all know to avoid getting sunburnt and we know that copious amounts of bacon and burgers are probably not going to do our bodies any good. But what if I told you that participating in physical activity could alter your risk of developing cancer? Would that affect your lifestyle choices any more than knowing you should maintain a healthy weight, or consume alcohol in moderation? Things we all know, but don’t necessarily adhere to….
In all honesty, it’s not something I had given much consideration to in my research career to date. I was always more interested in the cellular processes that govern cancer progression and metastasis. For example, did you know that it’s rarely the primary tumour that kills? Around 90% of all cancer-related deaths are caused by the secondary metastasis – that is to say, the little bunch of cancer cells that break away from the primary tumour and migrate to another site in the body. For this reason, I was always interested to learn how cancer cells move around, what made them “decide” to break away from the primary site, and how did they “know” where to go to?
All my research up to this point has focused on the role that a certain tumour virus, Epstein-Barr virus (EBV), plays in promoting a specific type of head and neck cancer called nasopharyngeal carcinoma (NPC). The virus, most notorious for its causal role in glandular fever, infects over 90% of the world, yet in certain geographical populations, has been linked to particular cancers, including NPC. One of the ways this virus can directly cause cancer is through expression of an oncogene called latent membrane protein 1 (LMP1). LMP1 helps the cancer cells to move around by breaking down the adherens junctions that connect the epithelial cells lining the nasopharynx, found at the back of the nose and throat. It then causes the cells to secrete enzymes called matrix metalloproteinases (MMPs) which chew up the extracellular matrix underlying the epithelial cells, thereby allowing the cancer cells to move down through the dermis and enter into the blood vessel system, where they hitch a ride to a new site. LMP1 can also cause the cells to spew out extracellular matrix proteins, such as one called fibronectin, which acts a bit like a train track for the cells to travel along. You can read more about this phenomenon here.
In February of this year, I started a new chapter in my research career when I took up a lectureship at Loughborough University. Based in the School of Sport, Exercise and Health Sciences, I’m now looking to expand my research to a “whole systems physiology” level – in other words, as well as looking at the cellular processes involved in cancer metastasis, I want to see what factors may be produced during exercise that could help prevent cancer spreading. I’m also interested in looking at whether physical activity could be used as a treatment option for patients in remission to prevent the tumour recurring later on.
One of the ways I’m looking to do this is by creating a 3D cell culture model system. Using a system that already exists in house, I can then look at the invasiveness of cancer cells in response to treatment with conditioned culture medium taken from “exercised” skeletal muscle cells. In time, I hope that this will shed some new insights into the molecular level processes of how cells, and in particular cancer cells, respond to varying levels of exercise intensity, which could then be translated into the whole body physiology with recommendations on the amount, frequency and intensity of exercise that may lower global cancer risk.
You can find out more about me and what I do at: www.perspectivesoncancer.com