About Cancer

Like all warts, cervical warts are caused by a virus, the human papilloma virus (HPV). There are over 100 types of HPV, some types cause common skin warts, and others genital warts. There are about 30 types which can infect the cervix. If the cervix is infected with the virus this may cause visible warts but in many women infection can be only detected microscopically by a smear test.

Genital HPV is usually spread though direct sexual contact, including oral sex, but non-sexual infection, although rare, is also possible. The virus can also lie dormant in the body for many years. It would be wise not to assume anything about how you contracted the wart until you have had a full discussion with your husband about this. When transmission has occurred from an infected person, warts can take anything from a few weeks up to several months to appear. Generally the types of HPV that infect the skin of the hands and body don’t infect the genital area, so it would be very unusual to contract cervical warts in this way.
About half of the different types of HPV that can infect the cervix are associated with cervical cancer. The presence of the HPV infection in the cervix does increase the risk that mild abnormalities in the cervical tissue will progress to severe abnormalities and very occasionally to cervical cancer. However the overwhelming majority of HPV infections of the cervix never lead to cancer. Most HPV infections seem to go away by themselves, or with simple treatment from a specialist, without causing any cervical abnormalities. Cervical cancer can almost always be prevented by regular follow-up with cervical smears to detect and treat pre-cancerous changes before they go on to become invasive cervical cancer.

The most important thing to do now is to discuss the treatment and follow-up of the cervical wart with your specialist.


The short answer to your question is no, there is no link between sickle cell anaemia and cancer of any type.

Although sickle cell anaemia and cancer can both be serious illnesses, there is no link between the two conditions.  Sickle cell anaemia never turns into cancer, and people with sickle cell disease are not at any greater risk than other people of developing cancer.

Hydroxyurea is a drug sometimes used to treat sickle cell disease.  There are concerns that many years of treatment with hydroxurea can increase the risk of getting a ‘blood’ cancer but the risk is yet to be proven and appears to be small.

Sickle cell disease is due a faulty gene, which is inherited, so it runs in families.  It occurs mainly in people of African-Caribbean descent, and in some parts of central Africa is very common indeed.  It is also, much less commonly, found in people from parts of India, Saudi Arabia, Greece, Italy and North Africa.

If you inherit the sickle cell gene from just one parent then the condition is quite mild and usually causes no problems (this is called sickle cell trait), but if you inherit the gene from both your parents then this is sickle cell disease, which is much more serious.  However, over the last 25 years the treatment of the condition has improved a great deal and the outlook is very much better now than it used to be. 

For further information and support about sickle cell anaemia you may find it helpful to contact The Sickle cell society.


It may help to answer your question by starting with an explanation about lymphomas in general.

Lymphomas are cancers of the lymphoid tissue which is part of our body’s immune system.

Our immune system protects us from infection. It is a complex system made up of the bone marrow, the thymus gland (which lies behind the breast bone), the spleen and the lymph nodes (or lymph glands).

One of the most important cells in our immune system is a type of white blood cell called a lymphocyte. There are two types of lymphocytes: ‘B-cells’ and ‘T-cells’. All lymphocytes are produced in the bone marrow and start life as young, immature cells called stem cells. Some lymphocytes continue their development in the bone marrow or lymph nodes and these are called B-cells but others move to the thymus gland and they are called T-cells.

Many years ago it was thought that lymphomas could be divided into just two conditions: Hodgkin’s disease (named after Thomas Hodgkin, the London doctor who first described it over 100 years ago) and non-Hodgkin’s lymphoma (NHL). With the passage of time it has become clear that NHL is not a single illness but includes a number of cancers, which behave very differently.

The description and classification of the various types of NHL has developed over the years as more has been learnt both about the immune system and the cancers themselves. The most recent classification still recognises the difference between Hodgkin’s disease and NHL but then goes on to divide NHL into some fifteen different tumour types.

The cause for the great majority of these different types of NHL remains a mystery but in three types of the disease, all of which are very rare in the UK, a link with viruses has been established. These are Burkitt’s lymphoma, Burkitt-like lymphoma and post-transplant lymphom

In 1956 a British surgeon called Dennis Burkitt was working in equatorial AfricH described an unusual type of lymphoma which was very common in children in that region. This became known as Burkitt’s lymphomLater research showed that B-lymphocytes in these children became infected with a virus, the Epstein-Barr virus, or E-B virus. Epstein-Barr virus infections are common and usually cause no problems but in central Africa many of the children had chronic malaria infections which reduced their resistance to the virus. In some cases this allowed the virus to change the infected B-lymphocytes into cancerous cells leading to the development of the lymphom

In recent years it has been recognised that in the western world there is one type of NHL where the tumour cells have very similar appearances under the microscope to those of Burkitt’s lymphoma. This rare condition has been called Burkitt’s-like lymphoma. Further research has shown that a high proportion of patients with Burkitt-like lymphoma (but not all) are HIV positive and many have AIDS. It seems that in this condition once again an Epstein-Barr virus infection occurs and because the HIV has reduced the patient’s immunity the Epstein-Barr virus is able to survive and ‘transform’ the normal B-lymphocytes to cancerous cells.

The same situation has been seen in some patients who have had organ transplants. Often after organ transplantation drugs are given for some time, often years, to suppress the patient’s immunity in order to reduce the risk of rejection of the grafted organ. Some of these patients appear to develop E-B virus infections and once again, as their resistance is reduced, this may lead to the development of a B-cell lymphom

All three of these virally-related types of NHL behave in a very aggressive way and need immediate treatment.

In the African children with Burkitt’s lymphoma chemotherapy gives a high cure rate but the Burkitt-like lymphoma and post-transplant lymphomas tend to be more resistant to treatment. Although a variety of different drug combinations have been used cure is not possible in the majority of people. This means that a number of clinical trials are in progress to try and improve the results of treatment.

In conclusion, the likelihood of your husband’s NHL being one of those types with a known viral cause is very, very remote. Almost certainly he has one of the forms of lymphoma for which no definite cause is known.


Wart virus (also known as human papillomavirus or HPV) is known to be associated with abnormalities in the cervix known as CIN which if untreated can sometimes develop into cancer of the cervix. It is much less commonly associated with similar changes in the cells of the vagina known as VAIN (vaginal intraepithelial neoplasia) but this only very rarely leads to vaginal cancer. So once the cervix has been surgically removed (as it will have been if you have had cervical cancer), then there is no risk of getting a new cervical cancer and the chances of getting vaginal cancer are very slim indeed. There is always a very small risk of a recurrence of the original cervical cancer, but there is absolutely no evidence that having the wart virus in the vagina will increase this risk.

Although wart virus is known to be one of the factors in the development of most cervical cancers, it is also found in many other women who will never develop cervical cancer. So having the wart virus certainly does not mean a woman will develop cervical cancer. In fact only a very small number of women who ever have a wart virus will develop cancer or even pre-cancerous areas on the cervix.

There are over 80 different types of the wart virus, and some of these types are more likely to be associated with cancer development than others. For example some types are commonly found in women with cervical cancers, whereas other types just cause common skin warts. There are also other factors that may contribute to the risk of cancer; these include number of sexual partners, age, heavy smoking, number of children and other genital infections.

At this stage there is no known method for getting rid of the virus. It is likely to just go way on its own accord with the help of your natural body’s defences. It is certainly important, however, that you continue to have regular smears and examinations as follow up after your cancer.


Cancer of the vulva is a rare cancer. It usually affects women between the ages of 55 and 75, but can occur in younger or older women.

The cause of most vulval cancers remains unknown but there are a number of conditions that can affect the vulva which will sometimes lead to cancer after many years. These are: n VIN (vulval intraepithelial neoplasia) which can occur in the skin of the vulva and is linked to infection by some types of wart virus, known as human papilloma virus (HPV). There are three levels of abnormality: VIN1, VIN2 and VIN3. VIN3 is the most abnormal and, in some women, can develop into cancer of the vulva if left untreated. n vulval lichen sclerosus and vulval lichen planus. These are two non-cancerous conditions which cause inflammation of the skin of the vulva and occasionally can lead to the development of a cancer after a number of years.

Also there is evidence that cigarette smoking may increase the risk of developing both VIN and vulval cancer. This may be because smoking depresses the immune system.


The term VIN refers to particular changes which can occur in the skin that covers the vulva. VIN is not cancer and in some women it disappears without treatment. If the changes become more severe there is a chance that cancer might develop after many years, and so it is referred to as a pre-malignant condition. Although VIN used to be quite uncommon it is now being recognised and diagnosed more frequently. It can affect women of any age from the 20’s onwards.

The common type of VIN is associated with an infection in the skin of the vulva by some types of the genital wart virus known as human papilloma virus (HPV). HPV (often known as wart virus) is a very common infection. There are over 100 types of the virus and the commonest types can cause warts on the skin of the hands or verrucas on the feet. Some types can affect the genital area including the cervix, vulva and anus.

Genital HPV infection is spread by direct skin-to-skin contact during sex with someone who has the infection. HPV is so common that most sexually active women will be exposed to it at some time in their life. In most women their bodies own immune system will get rid of the HPV naturally without them ever knowing it was there. Some women notice genital warts. Some women have no visible warts, but the HPV can cause changes in the cells of the cervix or the vulv

Infection with HPV on its own is unlikely to cause VIN. Other factors that depress the bodys immune system may also need be presentsuch as smoking and much less commonlyparticular medicines (like those taken after transplant surgery)inherited immunity problems some rare bone marrow blood disorders.

The signs and symptoms of VIN vary and may include some or all of the following: n itching and soreness in the vulval area n burning, or a severe tingling sensation, that can become worse when passing urine n one or more areas of reddened or discoloured skin in the vulval area n raised areas of skin that can vary in size n a warty appearance of the skin

All these above symptoms can be caused by many conditions other than VIN. Sometimes there are no symptoms and some women are diagnosed with VIN whilst having medical tests for other health problems.

VIN is not cancer but the cells of the vulva have changed. If the cell changes are mild treatment may not be needed, but your mother will need to have the area checked regularly by her doctor. Treatment may be needed if the changes are more severe. The type of treatment that is most appropriate for your mother will depend on several things such as how abnormal the cells are and the size of the affected area.


Helicobacter pylori, or H pylori as it is also known, is a type of bacteria that is found in the lining of the stomach. A lot of different types of bacteria enter the stomach when we eat or drink. Most of this bacteria is killed by the acid contents of the stomach, but H pylori is not.

H pylori is a common bacterial infection and between 30-40% of people in Britain are infected, although the incidence is declining. H pylori can usually be successfully treated with antibiotics.

H pylori can cause inflammation of the stomach lining (gastritis) which may over time develop into stomach (gastric) cancer. As a result, H pylori has been recognized as a carcinogen (a substance that causes cancer) and people who are infected with H pylori are thought to have 3-6 times the risk of developing stomach cancer than people who are not infected. If the H pylori the treated with antibiotics this often stops the development of cancer as well.

The majority of people who are infected with H pylori will not develop stomach cancer and less than 3% of people actually do. Doctors have been looking in to why this happens but currently do not know why this is. It is thought that there may be some interaction with some of the other risk factors associated with the development of stomach cancer, such as smoking and poor diet.

In some situations H pylori is thought to protect against the development of cancer in the top of the stomach (the gastric cardia) and the lower end of the gullet (oesophagus) the tube that leads into the stomach.

There are different types of stomach cancer, named after the particular type of cell in the stomach that becomes cancerous and H pylori is more closely linked to some of these than others. The main types of stomach cancer are; adenocarcinoma, which develops in the glandular cells; sarcoma, which develops in the supporting structures of the stomach (such as the muscular wall) and lymphoma which is a cancer of the lymphatic tissue. H pylori is more closely associated with the development of stomach lymphomas, which are also known as MALT lymphomas. There is also an association between H pylori and adenocarcinoma.


In the past some studies suggested a possible increase in prostate cancer in men who had a vasectomy. Recent studies have looked at this question and found that there is no evidence that having a vasectomy increases the risk of developing prostate cancer.


Studies have suggested that there is a link between smoking and bowel cancer. The evidence suggests that people who smoke for many years have are between one and a half and three times more likely to get a bowel cancer than non-smokers.

The increased chance of getting a bowel cancer does seem to be associated with long-term smoking, with people who have smoked for more than 35 to 40 years being at risk.

Over the years there have been suggestions that drinking large quantities of coffee could lead to developing certain types of cancer. Breast cancer, cancer of the bladder and cancer of the pancreas have all been mentioned in this connection.

Careful studies, however, have failed to find any definite link between coffee drinking (even when the consumption has been heavy) and any of these cancers, or any other type of cancer.

So from the point of view of cancer risk coffee drinking seems safe.


This e-mail has been doing the rounds for a year or so and has caused a great deal of concern.

There is no evidence that deodorants or antiperspirants are linked to breast cancer.

One reason that the e-mail might have come about is that breast cancers can often spread to the lymph nodes (lymph glands) situated in the armpit and, of course, antiperspirants and deodorants are often used on the skin in this areBut there is absolutely nothing to link the use of these compounds with the spread of breast cancer to the lymph glands under the arm.

Also, deodorants and antiperspirants have been around for some time now and if they were causing breast cancer then a big increase in the number of women developing the condition might have been expected and this has not happened.

The only area of research that is looking at any connection between deodorants and antiperspirants and breast cancer is that many of them contain a preservative called parabens. It has been suggested that parabens can increase oestrogen levels in the body and if this were true then it could possibly have a small effect in increasing breast cancer risk. At the moment this is all theoretical, with nothing proven, and in the very unlikely event that it is shown that parabens stimulates oestrogen then the effect on breast cancer development is still likely to be very very small.


Hormone replacement therapy (HRT) involves taking supplements to replace the female hormone oestrogen which falls during the menopause.  The menopause is the time in a woman’s life when her ovaries, which normally produce oestrogen, stop working. Menopause usually happens around the age of 50 years.

During menopause most women get symptoms, which are caused by the fall in the levels of oestrogen and can include hot flushes, night sweats, vaginal dryness, mood changes and loss of concentration.  These vary from being mild to troublesome.

Also the hormone changes, which take place during menopause, mean that in the long-term women are at greater risk of bone thinning (osteoporosis) and heart disease than previously.

When it was first introduced it was hoped that HRT would ease menopausal symptoms and also reduce the risk of osteoporosis and heart disease in later life. However, recent evidence has shown that although there may be some benefits there are also risks associated with HRT. The other questions and answers in this section explore these risks and benefits in more detail.


There are three main types of skin cancer. These are rodent ulcers (also called basal cell carcinomas), squamous carcinomas and malignant melanomOf these rodent ulcers are far the commonest, making up nearly 4 out of every 5 skin cancers. Of the remainder most are squamous carcinoma with malignant melanomas being much less common (making up about 1 in 50 skin cancers).

For some time it has been known that people who have had transplants are more likely to develop rodent ulcers or squamous carcinomas of the skin than the rest of the population. This is because they usually take medication to stop rejection of the transplant which actually reduces their natural immunity (this is often called immunosuppressive therapy). It is thought that if this medication is continued long term, as is often necessary, then it reduces the body’s natural defences and one sign of this is an increased risk of skin cancer.

Steroid drugs, like prednisolone, do have an effect on the immune system with a tendency to reduce immunity. Indeed they are sometimes used as part of immunosuppressive treatments after transplants, as well as being used in many other medical conditions.

Because of this immunosppressive effect of steroids doctors have looked to see if there is an increased risk of skin cancer in people who take these drugs long term for other conditions (like rheumatoid arthritis). Their research has shown that there is virtually no effect as far as rodent ulcers and malignant melanomas are concerned but the likelihood of getting a squamous carcinoma is increased (being about double that of the rest of the population).

Although this may sound a little alarming it still means that the chances of actually developing a squamous cancer of the skin are small (and certainly would not be a reason for stopping your steroids). The other important thing to mention is that if these cancers do develop they are usually very treatable and highly curable with simple treatment, provided they are not neglected. So if you do develop any sore or ulcer or other skin problem which fails to heal after a week or two then do see your doctor for a check up just to be on the safe side.

One final thing to point out is that the research showed there was only a risk when steroids were taken as tablets, by mouth and that when they were used as inhalers (for example in treating or preventing asthma) then there was no problem.


Unfortunately lung cancer is very common. It is the most frequently occurring cancer in the UK with over 40,000 new cases diagnosed each year. Lung cancer that is discovered early may be cured with an operation but because the disease is often only discovered at a late stage and because it is often difficult to treat most people with lung cancer can’t be cured. On average over 100 people in the UK die from lung cancer every day!

The evidence for a link between smoking and lung cancer is overwhelming and estimates are that more than 90% of all lung cancers are due to smoking.

The risk of getting lung cancer increases with the number of cigarettes smoked. So someone who smokes 20 cigarettes a day is about 20 times more likely to get lung cancer than a non-smoker, whilst someone who smokes 30 cigarettes a day is about 30 times more likely to get the disease than someone who has never smoked.

The risk is also increased by the number of years you have been smoking and this is probably even more important than the number of cigarettes you actually smoke. For example, smoking 20 cigarettes a day for 40 years is 8 times more dangerous than smoking 40 cigarettes a day for 20 years.

Other things which affect the risk of lung cancer include:

  • the age at which you start smoking, the younger you start the greater the chance of lung cancer
  • the type of cigarette you smoke, low tar cigarettes do slightly reduce the risk of lung cancer
  • whether or not you inhale, as inhaling increase the cancer risk.

Although the more you smoke the greater the chance of getting lung cancer even smoking one or two cigarettes a day still increases your chance of getting the disease compared to a non-smoker so there really is no ‘safe’ level for smoking.

The safe message just has to be stop smoking!


Snuff is usually used in one of two ways: either as a powder that is sniffed into the nose, or small packets, which can be chewed or placed against the lining of the mouth. In each case nicotine from the snuff is absorbed by the lining of the nose, or mouth, and enters the blood stream, giving a chemical lift.

Taking snuff was widespread in Britain in the 1800s but then largely died out. There are signs, however, that it is starting to become popular again.

Although snuff, like cigarettes, contains nicotine, there is no evidence that taking snuff leads to an increased risk of getting lung cancer.

Putting snuff in your mouth does, however, increase the chances of developing cancers of the lining of the mouth. But the degree of risk is uncertain and quite a controversial issue with some people claiming there is almost no risk whereas others think there is a real danger.

Taking snuff can lead to nicotine dependence and addiction and putting snuff in the mouth can cause sores, reduce the flow of saliva and damage the gums. So even if it does not actually lead to cancer, taking snuff is not without its health hazards.


Unfortunately lung cancer is very common. It is the most frequently occurring cancer in the UK with over 40,000 new cases diagnosed each year. Lung cancer that is discovered early may be cured with an operation but because the disease is often only discovered at a late stage and because it is often difficult to treat most people with lung cancer can’t be cured

The evidence for a link between smoking and lung cancer is overwhelming and estimates are that more than 90% of all lung cancers are due to smoking.

The risk of getting lung cancer increases with the number of cigarettes smoked. So someone who smokes 20 cigarettes a day is about 20 times more likely to get lung cancer than a non-smoker, whilst someone who smokes 30 cigarettes a day is about 30 times more likely to get the disease than someone who has never smoked.

Starting smoking early in life also increases the risk. For example a person aged 60 who started smoking at 15 is three times more likely to get lung cancer than someone of the same age who started smoking at 25.

Smoking also causes other cancers and non-cancerous illnesses like heart disease. Taking all this into account current estimates are that about half of all regular smokers will be killed by their habit. Putting this another way, if you take 1,000 men in their 20s who smoke regular, 250 will die of smoking-related illnesses, including lung cancer, in middle age and another 250 will die of smoking-related illnesses in old age.

Overall the life expectancy of a regular smoker is 8 years less than that of a non-smoker and lung cancer is a major cause of this reduction in survival. The overwhelming message from all this is not to smoke!


We all begin life as a single cell, when the sperm from our father fertilizes the egg (ovum) from our mother.  The single cell divides into two, and those two cell divide into two, and this process of cell division goes on and on to make the countless billions of cells that make up an adult human being.

Even after we reach adulthood, and stop growing, many of our cell carry on dividing in order to provide new cells to replace those that have become worn out and died off.

The normal process of cell reproduction, when a single cell divides into two, is called mitosis.  

During the first part of mitosis the cell nucleus divides into two. The
cytoplasm surrounding the nucleus then divides so that two new daughter
cells are produced. 

During this division the chromosomes in the nucleus multiply to make two
identical sets of chromosomes. This means that the genetic blueprint
carried through to the two new cells, which are then identical to the old cell.

A variation of this process of cell division takes place in the cells which make the female eggs (ova) and the male sperm,  Here the new cells have a single set of 23 chromosomes in their nucleus, rather than the 23 pairs of
chromosomes in normal cells. This is so that when the egg and the sperm
fuse the new cell, that will go on to make the new baby, will have one set of
chromosomes from each parent. This sort of cell division, where the new
cells have only a single set of chromosomes, is called meiosis.


Proteins are large molecules that make up a vital part of every cell in our bodies.

Proteins are made up of amino acids.  Our cells use twenty different amino acids to make the proteins we need.  Different combinations of amino acids are grouped together to make polypeptides.  These polypeptides are then built up into proteins.  So a protein is made up of a number of polypeptides, and each polypeptide is made up of a number of different amino acids.

Our bodies contain countless different proteins.

Our own cells are able to make twelve of the twenty amino acids we need.  The other eight, which are called essential amino acids, come from the protein we take in our diet, from foods like meat, fish and eggs.

The proteins that a cell makes will control how that cell develops and behaves.  So a brain cell will make a different set of proteins from a liver cell, a muscle cell will make a different set of proteins to a skin cell. 

The proteins that a cell makes are controlled by the genes.  The genes send instructions to the cell to collect the amino acids to make the particular proteins that it needs.

One special group of proteins are called enzymes.  Enzymes are proteins that control the biochemical reactions that are essential for our bodies to work properly.  So, for example, enzymes are vital for the breakdown, and digestion, of our food, and they control the complex processes that turn our food into the energy we need to carry on living.


RNA is a nucleic acid.  The initials RNA stand for ribose nucleic acid.

RNA is one of two nucleic acids that are found in human cells.  The other is DNA (deoxyribose nucleic acid). DNA is the material that makes up the genes and chromosomes in our cells.  The genes and chromosomes carry the genetic blueprint that controls our bodies and makes each of us a unique individual.  

The way this works is that the DNA carries a code for making proteins, and the different proteins that it tells our cells to make lead not only to the differences between various types of cells, but also the differences between each and every one of us.

The DNA is in the nucleus of the cell, but the proteins are made in the ribosomes, which are microscopic structures in the cytoplasm of the cell, which surrounds the nucleus.  RNA carries the blueprint for making the proteins from the DNA in the nucleus to the ribosomes. 

So the RNA acts as a messenger carrying instructions from the DNA to the ribosomes. 

Once the ribosomes get the recipe from the RNA for the protein that is to be made, they collect the necessary amino acids together and build them up into polypeptides and proteins.

The  combination of the different proteins that RNA tells the ribosomes to make is different in each and every one of us, and this unique pattern of proteins makes each of us who and what we are.


DNA is a nucleic acid.  The initials DNA stand for deoxyribose nucleic acid.

DNA is the material that makes up the genes and chromosomes in our cells.  The genes and chromosomes carry the genetic blueprint that controls our bodies and makes each of us a unique individual.  

The way this works is that the DNA carries a code for making proteins, and the different proteins that it tells our cells to make lead not only to the differences between various types of cells, but also the differences between each and every one of us.

DNA is made up of building blocks called nucleotides.   Each nucleotide is itself made up of three parts: a phosphate, a sugar (which is deoxyribose) and a chemical called a ‘base’.  There are four different types of base in DNA nucleotides: thiamine, cytosine, adenine and guanine.

The actual structure of the DNA is a made up of two long strands.  Each strand is a bit like a very long comb.  The back bone, or spine, of each comb is made up by the phosphates and sugars and the different bases stick out from this spine, like the teeth sticking out on a comb.   The bases of the two strands link up with one another, so that the spine of the strands, or combs, is on the outside, with the bases, or teeth, of the comb joined together inside. 

The two strands are then coiled round one another, in a pattern a bit like a spiral staircase, called a double helix.

The DNA is very tightly coiled within the nucleus of our cells.  Although it is invisible to the naked eye and can only be seen under high powered microscopes, the DNA from a single human cell, if it was uncoiled, would be about 1m (just over 3 feet) long.

The way in which the four different bases, thiamine, cytosine, adenine and guanine, are  arranged along the DNA strands makes the blueprint for producing amino acids.  These amino acids are the building blocks that make up the different proteins the cell needs. 

So the pattern of the four bases on the strands of DNA is different in each and every one of us, and this unique pattern, in the nucleic acid in the nuclei of our cells, makes each of us who and what we are.


Cells are the tiny building blocks that make up our bodies.

Each cell is covered by a membrane, which is like a thin wall separating it from surrounding cells.  Inside the membrane is the nucleus and the cytoplasm.  The nucleus contains the genetic material, and is the control centre of the cell.   The cytoplasm is made up of fluid, called cytosol, and the organelles, which carry out the instructions from the nucleus.

All of us begin life as a single cell in our mother’s womb.  That single cell goes on to divide and multiply countless times to produce the many billions of cells that make up our bodies.

As this cell division takes place different types of cell develop – bone cells, brain cells, blood cells, skin cells and so on – which form all the different organs and tissues in our bodies. 

Cells are continually wearing out, and dying off, and have to be replaced.  So even when we have finished growing we still carry on making millions and millions of new cells every day, to make good the old cells that have been lost.

This process of cell replacement is very carefully controlled, so that the number of new cells being made is always the same as the number of old cells that have died off.

A cancer develops when this process goes wrong,  and too many new cells are produced.  Over time these build up to form a tumour.  So cancer is due to disordered, or abnormal, cell growth in  a particular part of the body.


hen treatments for cancer are being tested in a clinical trial there are a number of ways of measuring how successful the treatments are.

One obvious thing to do is to see how many people are cured by the treatment.  But sometimes it may be many years before you can tell for sure whether or not someone has been cured, which means it would take a very long time for the trial to give any answers.   So another way of looking at things is to see how many people are still alive after a particular length of time.

If a new drug is being used in a trial to treat a particular type of cancer, then one measure of its effectiveness might be to see how many people are still alive a year after the treatment started.   Suppose, for example, that in this trial 100 people were given the drug, and one year later 75 are still alive.  This gives an overall survival figure of 75 out of 100, or 75%.   But of those 75 people some may have had a very good response to the treatment, with complete disappearance of all signs of their cancer, whilst others may only have had a temporary benefit, with their cancer improving but then coming back, or have had very little change in their cancer, but still be alive one year later.  These latter individuals will still be alive one year after treatment, but will still have obvious signs of their cancer being present.  

At one year after treatment the number of people still surviving will be made up of those with no sign of cancer, and those who still have evidence of the disease being present.  Those people who have no trace of cancer are called ‘disease-free’, or ‘relapse-free’ survivors.   

So, the ‘overall survival’ figure for a trial, gives the total number of people who are still alive at a particular time after treatment.  But the ‘disease-free’, or ‘relapse-free’ survival figure gives only those people who are alive and have no trace of cancer.   This means that usually the overall survival figure will always be higher than the disease-free figure – unless the treatment is exceptionally good, when the two figure might be the same, but the ‘disease-free’ number can never be higher than the ‘overall’ figure.

This also means that the higher the proportion of ‘disease-free’ survivors the better the treatment.  So if two treatments, A and B,  have been compared and both give overall survival figures of 75% at one year after treatment, but the disease-free survival figure is 60% for treatment A, and only 30% for treatment B, then treatment A is likely to be better than treatment B.


With any treatment for cancer it is obviously very important to know whether or not that treatment has worked. Rather surprisingly, accurately scientifically measuring the outcome of cancer treatment can be very difficult.

Most assessments of the results of cancer treatment are based on things which can be counted or measured: for example, how long someone survives or how large a tumour is before and after a course of treatment. Even these apparently straightforward criteria can often be difficult to determine precisely and even if they are measurable they only give ‘objective’ information about what happened and give no idea of how the person who had the cancer actually felt.

The Karnofsky scale (sometimes called the Karnofsky index) was devised by two American doctors in the 1940s (David Karnofsky and Joseph Burchenal) as an attempt to try and measure the more ‘subjective’ side of the outcome of cancer treatment.

In fact the scale relates purely to physical ability and covers 11 points, from normal health to death, each scored as a percentage. The scale is:

Normal health 100%
Minor symptoms 90%
Normal activity with some effort 80%
Unable to carry on normal activity
but able to care for oneself 70%
Requires occasional help with
personal needs 60%
Disabled 50%
Requires considerable assistance and
medical care 40%
Severely disabled, in hospital 30%
Very sick, active support needed 20%
Moribund 10%
Death 0

Not all the definitions of each stage are very precise and they say nothing about the feelings and emotions of the individual. But the scale is simple and easy to use. Also, over the years, more complex ‘psychological’ tests have shown that generally well being and quality of life match the physical scores on the Karnofsky scale (so, if you have ‘normal health’ or ‘minor symptoms’ you tend to feel pretty good, but if you are ‘severely disabled’ or ‘very sick’ you feel very low indeed). For these reasons the Karnofsky scale has stood the test of time and is still widely used to help doctors decide how well someone is doing after treatment and sometimes used to help decide what treatment should actually be given.


Myelofibrosis is a very rare condition, occurring in 1 in 100,000 people each year.

Myelofibrosis is an illness where the normal cells of the bone marrow become replaced by scar tissue, or fibrosis.   This leads to progressive failure of the bone marrow.  The bone marrow is the factory that produces many of the cells in our blood, and so bone marrow failure causes anaemia (due to a lack of red blood cells), a higher risk of infection (due to a lack of white blood cells) and an increased risk of abnormal bleeding (because the number of platelets in the blood is reduced).

As the marrow begins to fail the liver and spleen try and make up for this, and start to fill with blood-making cells.  As a result of this they become swollen and  enlarged. They can become so big that they start to cause problems with pain, and swelling of the tummy.

As well as reducing the number of blood forming cells the presence of scar tissue in the bone marrow can also cause the bone marrow to become disordered, producing increasing amounts of primitive, abnormal, blood cells.  In somewhere between 1 in 5 to 1 in 20 people with myelofibrosis this process can turn into a form of acute leukaemia.  This transformation is more likely in people aged over 70, and those who have other risk factors such as quite severe anaemia, a very low platelet count, increased numbers of primitive white cells in their blood, or certain specific changes in the genes in their bone marrow cells.  

Unfortunately, even if this leukaemic transformation does not occur, myelofibrosis is still a serious condition, with an increased risk of major bleeding, severe infection, or blood clots, which can lead to strokes or heart attacks.

So it is important that you talk to your doctor about your concerns as they will have all the information about your own condition and can advise you fully about the risks in your case.


The stage of a cancer is a measure of how far it has progressed. So, a cancer that is small and in a single site is at an early stage, whereas one that has spread to many different parts of the body is at an advanced stage.

Over the years doctors have worked out staging systems for all the different types of cancer. Some of these are quite simple whilst others are very complicated. As an example, one of the simpler systems is the one used for bowel cancer. This is divided into four stages, A to D, with A being the earliest stage. The four stages are:

  • A – the cancer is confined to the wall of the bowel
  • B – the cancer has spread through the wall of the bowel
  • C – the cancer has spread to the nearby lymph glands
  • D – the cancer has spread to other organs, such as the liver or lungs.

Some staging systems use the numbers 1 to 4 for the various stages (often subdividing each stage into a, b or c), whilst another system uses the initial T, N and M, followed by a number to describe the primary tumour (T), any involved lymph nodes (N) and the presence or absence of any spread to other organs, or metastases (M). The situation is further complicated by the fact that there are often several different staging systems for a particular cancer and different doctors may use different systems.

Doctors use the results of tests and operation findings to decide the stage of a person’s cancer. Sometimes the stage will change as more results become available. For example, someone with bowel cancer might have examinations, x-rays and scans which suggest the tumour is confined to the bowel wall (stage A) but when an operation is done, and the tissues examined under a microscope, small seedlings of tumour may be found in the lymph glands, making it a stage C cancer.

Using a staging system has two main benefits. Firstly it gives an idea of how advanced a cancer is and so helps predict what the likely outcome of treatment will be. Secondly, ‘staging’ the cancer determines what the treatment should be, since often the treatment for an early stage cancer will be different from that for a more advanced tumour.

The grade of a cancer refers to the appearances of the tumour under the microscope. Depending on the appearances cancers may be given one of three grades. A ‘low’ grade is where the cancer cells look very like normal cells, with only slightly abnormal changes (these cancers are called ‘well-differentiated’. A ‘high’ grade is where the cells look very abnormal and show little or no resemblance to normal tissue (these cancers are called ‘poorly differentiated’). An ‘intermediate’ grade is somewhere between the high and low grades (these cancers are called ‘moderately differentiated’). For some cancers, such as breast cancer, the three different grades are often given numbers, so a low grade breast cancer is called Grade I, whereas a high grade breast cancer is called Grade III.

The grade of a cancer is considered to be a guide to how aggressive the tumour is: an intermediate grade cancer is likely to be more aggressive than a low grade and a high grade cancer is likely to be more aggressive than an intermediate grade tumour.

Taken together the stage and grade of a cancer do help doctors to predict how that cancer might behave, how it might respond to treatment, and what the chance of cure might be. But the stage and grade are only guides to what might happen and cancers do not always behave in the way that might be expected from their stage and grade.


Because each of us different, and because every cancer is slightly different, it is impossible for doctors to be absolutely certain whether or not someone will be cured of their cancer as a result of treatment.

Although they cannot give guarantees about what will happen, doctors can use their experience, and their knowledge of the particular type of tumour, and the results that have been published about the outcome of treatment, to make forecasts of how likely, or unlikely, it is that someone will be cured.

One way of giving these predictions is to talk about percentages.

What doctors are doing when they use these percentages is saying ’if we had a hundred people just like you, with a cancer just like yours, how many would we expect to be able to cure?’.  

If the chances of a cure are very good, then perhaps 90 or 95 people out every 100 might expect to get better.  This would be the same as saying that there is a 90 to 95 % chance of being cured.   In the same way, if there was only a small likelihood of a cure, with only 5 or 10 people out of every100 getting better, then the chance of a cure would be between 5 to 10%.

In your mother’s case what the doctor is saying is that if they saw a 100 people in a similar situation they would expect 60 of them to be cured.  This means that she has a better than 50/50 chance of cure, and that the doctor thinks it is more likely than not, that she will be cured.  But it does also mean that they cannot be certain of the outcome.

Without wanting to be gloomy, it is important to remember this uncertainty.  It is probably human nature to be positive and optimistic in this sort of situation and to focus on the 60% chance of a cure, rather than the 40% (or 40 out 100) chance that the treatment might not be completely successful.  But even if her doctor had told your mother there was a 95% chance of cure, this would still mean that there could be a small risk that treatment might not work.

At the end of the day, the figures that any doctor gives to their patient about the chances of successful treatment, are only a guide to what might happen and cannot be an absolutely certain prediction of the future.


There is a widespread public belief that stress can lead to cancer.

Over the last twenty years there have been many scientific studies looking at whether there really is a relationship between stress and cancer. These studies have used a number of different methods. Some have looked at women with benign and malignant (cancerous) breast lumps and compared the number of major stressful events in the five years or so before their condition was diagnosed, to see if the women with cancers had suffered more stress. Others have followed the lives of people who have been bereaved, or who were prisoners of war, to see if these stresses led to a greater chance of cancer developing in the future when compared to the normal population.

When the results of all these studies are analysed there is absolutely no evidence that stress does cause cancer.

At the end of the day stressful life events – bereavement, divorce, redundancy, moving house and so on are very very common and inevitably many people who do develop cancer will have experienced one or more of these in the few years before their tumour was discovered. Doctors often don’t know the cause of any particular cancer and people are distressed to find that there is no definite explanation as to why they developed cancer. They find it very plausible to believe that their cancer was caused by stress but there is no scientific evidence to suggest that these events are any commoner for cancer patients than for the population at large.

Cancer of the anus is quite rare with only about 300 new cases in the United Kingdom each year. Like most cancers the cause for the great majority of anal cancers is unknown.

A minority of anal tumours are, however, associated with infection by a virus called the human papilloma virus (HPV). This virus can cause warts in the genital area and very occasionally, often after many years, a cancer may develop in one of these warts. Anal cancer is commoner in the receptive partners of anal intercourse and HPV infection may be a factor in this.

Anal cancer is also commoner in people who have AIDS. No one is sure whether this is due to the presence of the HIV virus (the human immunodeficiency virus, which causes AIDS) or whether the reduced immunity of AIDS patients makes them ore at risk to the possible cancerous effects HPV.

Load More