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.
