A brief overview of the genetic basis of cancer and personalised medicine.
Cancer is a word which so many people associate with negativity, which is understandable; the media is filled with scare-stories (this headline in The Mirror would certainly strike fear into the hearts of many), and many people know someone who has died as a result of the big C-word. Modern treatments are advancing, meaning statistics are looking positive. Cancer is not something which should be feared, but understood.
I find that whilst newspapers will report on cancer stories, few actually clearly explain how cancer forms. Last summer, I attended a tissue engineering tour at the University of Manchester as part of the European City of Science 2016 celebrations. One woman on this tour sticks in my mind, as she was keen to bring cancer up at every opportunity, and yet could only describe it as “when cells grow and grow and grow and grow.” She was the perfect example of a member of the public trying to make sense of what many see as a death sentence. Cancer is something which everybody knows of, and yet very few know about.
The first thing which should clarified is that cancer is not just cells randomly growing out of control. Nor is it cells being triggered to grow as a result of excess radiation or another idea which could form the plot of a blockbuster film. Cancer is complex. Each cancer is unique, and while the basics are the same, treating Retinoblastoma is quite different to treating liver cancer, for example. There are two key types of gene which you need to have an understanding of to grasp cancer: oncogenes and tumour suppressor genes.
Oncogenes are versions of proto-oncogenes which can lead to tumour formation. Everyone has proto-oncogenes as they control cell growth and division. It is only when mutations occur that the oncogenes are formed which lead to rapid cell growth, as the cell growth is now no longer under control. There are many different proto-oncogenes in the body, and therefore many different oncogenes. Faults in different genes lead to different cancers.
Tumour suppressor genes do what they say on the tin. They’re essentially the opposite of proto-oncogenes in the sense that while they trigger cell growth, tumour suppressor genes stop it. When these are mutated, excessive cell growth cannot be stopped, hence tumours form. It is from these tumours that people then develop cancer.
This illustrates just why cancer treatments are difficult, and why personalised medicine is becoming the future. Different cancers are caused by different genes, and individual cancers can be caused by mutations in a range of genes (or multiple). Knowing exactly which gene is the difficult part, but now there are drugs for many cancers which aim to target specific genes so that there is a smaller chance of tumours forming again post-chemotherapy.
There is no denying that cancer is complex. But hopefully with this brief summary I have made the reasons behind this far more understandable. So next time you see a scary news article, or wonder why Friend A couldn’t have the same drugs as Friend B, you’ll have a better grasp of the basics of The Big C.
For those interested, Cancer Research UK has some interesting infographics and statistics here.