Every day in the UK there are more than 400 people diagnosed with cancer that will survive the disease for more than 10 years thanks to research.
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 is the name given to a collection of related diseases. In all types of cancer, some of the body’s cells begin to divide without stopping and spread into surrounding tissues.
Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and divide to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.
When cancer develops, however, this orderly process breaks down. As cells become more and more abnormal, old or damaged cells survive when they should die, and new cells form when they are not needed. These extra cells can divide without stopping and may form growths called 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?
The body is made up of trillions of living cells. These cells grow, divide, and die in an orderly fashion. This process is tightly regulated and is controlled by the DNA behaviour within the cell. In a baby or a child normal cells divide rapidly to allow for growth. After the person becomes an adult, most cells divide only to replace worn-out or dying cells or to repair injuries.
When cells of the body at a particular site start to grow out of control, they may become cancerous. Cancer cell growth is different from normal cell growth. Instead of dying, cancer cells continue to grow and form new, abnormal cells. In addition, these cells can also invade other tissues. This is a property that normal cells do not possess.
Cancer cells originate from normal cells when their DNA (deoxyribonucleic acid) or blue prints within the cell nucleus is damaged. DNA is in every cell and it directs all the cell’s actions, growth, death, protein synthesis etc. when DNA is damaged in a normal cell the cell either repairs the damage or the cell dies.
Normally, the body safeguards against cancer via numerous methods, such as: apoptosis or a process by which abnormal cells die on their own accord, helper molecules (some DNA polymerases), possibly senescence or ageing, etc.
In cancer cells, the damaged DNA is not repaired, and the cell does not die. Instead it gives rise to more such abnormal cells with abnormal DNA. These new cells all have the same defective DNA of the original cancer cell.
DNA damage may be inherited from parents or may be a spontaneous problem that occurs during the lifetime of a person. This is called a mutation. DNA damage may also be triggered by exposure to certain environmental toxins such as those present in cigarette smoke. There are, however, multiple factors that may cause cancer and it is difficult to pin point an exact cause.
Every cell in our body contains DNA. It carries our genetic code and contains the instructions for all the cell’s actions.
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 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.
A cancer that has spread from the place where it first started to another place in the body is called metastatic cancer. The process by which cancer cells spread to other parts of the body is called metastasis.
Metastatic cancer has the same name and the same type of cancer cells as the original, or primary, cancer. For example, breast cancer that spreads to and forms a metastatic tumour in the lung is metastatic breast cancer, not lung cancer.
Under a microscope, metastatic cancer cells generally look the same as cells of the original cancer. Moreover, metastatic cancer cells and cells of the original cancer usually have some molecular features in common, such as the presence of specific chromosome changes.
Treatment may help prolong the lives of some people with metastatic cancer. In general, though, the primary goal of treatments for metastatic cancer is to control the growth of the cancer or to relieve symptoms caused by it. Metastatic tumours can cause severe damage to how the body functions, and most people who die of cancer die of metastatic disease.
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.
How common is cancer?
Unfortunately, around one in four (25%) people in the UK already face poor health or disability after treatment for cancer. If this number continues to rise by over 3% a year, this could see four million people living with cancer by 2030. The proportion of people living longer after cancer is increasing, and the number of people alive and more than 5 years from initial diagnosis is predicted to more than double between 2010 and 2030 to 2.7 million.
And by the end of 2016, more than a thousand people will be diagnosed with cancer every day in the UK.
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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