Hundreds of thousands of people are diagnosed with cancer every year in the UK. It is not one disease; there are over 200 different types, each with its own symptoms, methods of diagnosis and treatment.

What is cancer?

Cancer starts when cells in our bodies start to reproduce out of control, forming new, abnormal cells. These abnormal cells form lumps, known as tumours.

If the cells from tumours cannot spread, then the tumours are benign. They are not cancerous and can usually be removed.

If the cells are able to invade nearby healthy tissue and organs, or spread around the body through the blood or lymphatic system causing further tumours to grow, then the tumours are malignant or cancerous. These cancer cells are likely to spread if the tumour is not treated.

What causes cancer?

Every cell in our body contains DNA. It carries our genetic code and contains the instructions for all the cell’s actions.

If the DNA inside cells is damaged, these instructions go wrong. In fact damage to the DNA or “mutations” as they are known, constantly occur in our cells as they divide and reproduce. Most of the time, the cells recognise that a mutation has occurred and repair the DNA, or self-destruct and die.

When a number of mutations have occurred in the DNA of a cell, control of cell growth may be lost and the cells do not die. Instead they start to follow abnormal instructions that make them reproduce and grow, producing more and more of these mutated cells – this is the start of a cancer.

Many factors such as smoking or too much exposure to the sun can also trigger DNA damage – leading to a faster accumulation of the mutations which lead to cancer.

A family history of cancer can also increase chances of getting the disease, because it usually means that person starts their life already having inherited some of the DNA mutations that take them down the path to cancer.

Even when in remission, those who have had the disease have a higher risk of it developing again. In most cases however, the exact cause or sequence of events by which cancer develops, is not yet known

A recent study has found that there are more than 80 genetic markers (i.e. mutated genes) that can increase the risk of developing breast, prostate or ovarian cancer, for example. Scientists believe the results could soon lead to widespread use of DNA profiling for these cancers, though individual genetic testing for those likely to be at increased risk – such as when there is a strong family history of a type of cancer – is already in use.

Why is it so deadly?

Cancer cells are able to invade other parts of the body, where they settle and grow to form new tumours known as secondary deposits – the original site is known as the primary tumour. The cells spread by getting into the blood or lymph vessels and travelling around the body.

For example, if bowel cancer has spread through the wall of the bowel itself, it can start growing on the bladder. If cells enter the bloodstream they can travel to distant organs, such as the lungs or brain. Over time, the tumours will then replace normal tissue.

The process of cancer cells spreading is called metastasis. Once a cancer has started to spread, the chances of a cure often begin to fall, as it becomes more difficult to treat for a variety of reasons.

Cancer harms the body in a number of ways. The size of the tumour can interfere with nearby organs or ducts that carry important chemicals. For example, a tumour on the pancreas can grow to block the bile duct, leading to the patient developing obstructive jaundice. A brain tumour can push on important parts of the brain, causing blackouts, fits and other serious health problems. There may also be more widespread problems such as loss of appetite and increased energy use with loss of weight, or changes in the body’s clotting system leading to deep vein thrombosis.

Why is it so hard to stop?

Cancer is an extremely complex condition. Each type of cancer is biologically different from any other type. For example, skin cancer is biologically different from the blood cancer called lymphoma, of which there are then many different types.

That is then coupled with genetic differences between individuals and the often random nature of the DNA mutations that cause cancer.

All this makes it difficult to identify the way the particular cancer cells are behaving and how they are likely to spread or damage the body. Without a full understanding of the physiology of the cancer, effective treatments are hard to develop.

Early surgery to remove tumours can work. But the cancer can return if any cells are left behind. It can also return if cells have broken away from the primary tumour and formed microscopic secondary tumours elsewhere in the body before an operation to remove the primary.

And because cancer cells are our own body’s cells, many treatments to destroy them also risk destroying our healthy cells.

One controversial theory of why cancer is so hard to stop is that it is rooted in the ancient traits of our genes.

Prof Paul Davies from Arizona State University believes cancer may use tried-and-tested genetic pathways going back a billion years to the dawn of multicellular life, when unregulated cell growth would have been an advantage.

He argues that this tendency was suppressed by later, more sophisticated genes, but lies dormant in all living organisms. Cancer occurs when something unlocks these ancient pathways.

Other scientists disagree, saying that these pathways would not have survived millions of years of evolution.

One thing is for sure – our genes hold the key to understanding cancer and how to treat it.

The future of cancer research

The field of cancer research is moving away from defining a cancer by where it is in the body, as one type of breast cancer can have more in common with an ovarian cancer than another cancer in the breast.

Instead scientists are looking deeper at what is going wrong inside cancerous cells – a tumour can have 100,000 genetic mutations and these alter over time.

By pinpointing the mutations that can cause certain cancers, doctors hope to personalise treatment – choosing the drug most likely to work on a particular type of tumour.

Scientists are creating targeted cancer therapies using their latest insights into cancer at a molecular level. These treatments block the growth of cancer by interfering with genetic switches and molecules specifically involved in tumour growth and progression.

Clinical trials using gene therapy are also underway. This experimental treatment involves adding genetic material into a person’s cells to fight or prevent disease.

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