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Target Leukaemia
Questions and answers about Leukaemia and other blood disorders
  1. What is cancer?
  2. What is leukaemia?
  3. Is leukaemia a single disorder?
  4. What is the difference between chronic and acute leukaemia?
  5. Why are there so many different forms of leukaemia?
  6. What causes the damage to bone marrow cells?
  7. Can DNA damage be detected?
  8. Why should a translocation or mutation cause leukaemia?
  9. Are translocations and other genetic defects found in other leukaemias?
  10. Does leukaemia run in families?
  11. Why does chronic leukaemia sometimes turn into the acute form?
  12. How common is leukaemia?
  13. Who gets leukaemia?
  14. What is hairy cell leukaemia?
  15. What are the major symptoms of leukaemia?
  16. How is leukaemia diagnosed?
  17. What are multiple myeloma and non-Hodgkin's lymphoma?
  18. How common are multiple myeloma and non-Hodgkin's lymphoma?
  19. What are the signs and symptoms of multiple myeloma?
  20. Is there genetic damage in multiple myeloma and NHL?
  21. How are blood malignancies treated?
  22. What traditional medicines are available for treating blood malignancies?
  23. What role does radiotherapy have in blood cancer?
  24. What role does bone marrow and stem cell transplantation play?
  25. What progress has been made in the treatment of blood cancer?
  26. Can leukaemia and lymphoma be cured?
  27. What help is available for people with leukaemia and their families?

What is cancer?
Almost everyone knows somebody who has cancer, or has had it. It is widely understood to mean the uncontrolled growth of cells and tissues in an organ to form lumps and bumps. Cancer is also known as a tumour (from the Latin for swelling), or a malignancy, meaning malicious. As an overall cause of death, cancer is second only to cardiovascular disease.
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What is leukaemia?
Leukaemia is a cancer of the blood which arises from an excessive and uncontrolled growth of cells in the bone marrow. Leukaemia differs from solid cancers, because the faulty cells are released from the bone marrow into the blood, rather than forming a solid mass. Examination of a leukaemic blood sample will often reveal an excess (sometimes a massive excess) of circulating malignant white cells. These often look abnormal and may be unable to carry out their usual functions. As their numbers increase, they often accumulate in organs such as the spleen and lymph nodes, causing secondary swellings and pain. In advanced leukaemia, the bone marrow itself may be almost packed solid with abnormal white cells. When seen in the scanning electron microscope, most types of leukaemia cell look rather similar to each other.
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Is leukaemia a single disorder?
There are many different kinds of leukaemia, depending on which type of bone marrow cell is out of control. Some leukaemias occur much more frequently than others, and some are extremely rare. They are often divided into two main groups called the myeloid leukaemias and the lymphoid leukaemias. These in turn are often classified as either chronic or acute. In this website, we will consider acute lymphoblastic and chronic lymphocytic leukaemia (ALL and CLL), acute myeloblastic and chronic myelocytic leukaemia (AML and CML), and hairy cell leukaemia. Two related disorders, multiple myeloma and non-Hodgkin’s lymphoma (NHL) will also be discussed.
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What is the difference between chronic and acute leukaemia?
Chronic illnesses are those that persist and progress over prolonged periods of time, in contrast with acute illnesses that have a sudden onset and usually rapid progression. These terms also apply to leukaemia. Chronic leukaemias are often found by chance during a routine medical examination. They may 'smoulder' for years without the need for treatment, though in most cases, symptoms eventually develop. With acute leukaemias, onset and progression are often rapid and are characterised by symptoms that emerge early and progress quickly.
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Target Leukaemia

Why are there so many different forms of leukaemia?
There is strong evidence that leukaemia arises when damage occurs to the genes or chromosomes contained within bone marrow cells. The cells in blood arise from stem cells that divide repeatedly throughout life. The daughter cells may remain as stem cells, but if they are influenced by chemicals called growth factors or colony stimulating units, they become committed to a particular line of development. The first step would be for them to become either a lymphoid stem cell or a myeloid stem cell. Under the influence of further growth factors in the bone marrow or in organs such as the thymus, they will become further specialised, forming T-cells, B-cells or myeloid cells, and so on.

The many forms of leukaemia reflect the stage along these pathways at which chromosome damage occurs.

  • Damage in the pluripotent stem cell can lead to the development of either acute lymphoblastic leukaemia (ALL) in adults or chronic myelocytic leukaemia (CML), depending on the exact location and type of damage.
  • If the damage occurs in the myeloid stem cell, then acute myeloblastic leukaemia (AML) may occur.
  • Cells in the T-cell pathway can give rise to acute lymphoblastic leukaemia (T-ALL,) or chronic lymphocytic leukaemia (T-CLL).
  • Damage to early B-cells can result in B-cell acute lymphoblastic leukaemia.
  • If damage occurs further down the B-cell pathway, the resulting disease may be non-Hodgkin's lymphoma (NHL) or multiple myeloma (MMy).

There are many other variants of leukaemia, and even the common forms are classified into many sub-types, each with slightly different characteristics and likely outcomes.
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What causes the damage to bone marrow cells?
Because most types of leukaemia become more common as we get older, it seems likely that damage accumulates as the years pass because of something in the environment. Such damage occurs throughout life, but can be repaired by enzymes within cells, especially when we are young. As we age, the repair process becomes less effective and damage gradually accumulates until it reaches a trigger level for disease.

A well-established environmental factor is radiation. This was clearly shown in studies comparing the incidence of leukaemia in people exposed to radiation in Hiroshima with those not exposed. Here the risk in those exposed was over 100 times that in those not exposed.

In radiation terms, Hiroshima was a catastrophic event, but everyone is continuously exposed to low levels of radiation arising from rocks and outer space. No doubt these high energy particles account for some chromosome damage if they collide with DNA molecules.

Another cause of cancer (including leukaemia) is exposure to substances (carcinogens) that can attack DNA and chemically modify it. Many such substances are known and no doubt there are many others yet to be found. We can be exposed to such agents in the air we breathe and in the food we eat - both in the home and at work. A good example is cigarette smoke, which contains a number of carcinogens. It has been shown to increase the risk of leukaemia by 50 per cent. Some herbicides have also been implicated in some blood disorders.
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Relationship between the stage of maturation of white blood cells and various common forms of blood cancer
Relationship between the stage of maturation of white blood cells and various common forms of blood cancer
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Can DNA damage be detected?
Using sophisticated laboratory techniques, gene mutations and chromosome damage can often be detected, but studies in large numbers of people are necessary to confirm a definite link with any particular disease. Just occasionally, the damage is sufficiently marked to be detectable using a microscope.

This is the case with CML, where an unusual chromosome pattern was reported in 1960. We each have 46 chromosomes, made up of 23 pairs, in every cell of our body (except sperm and egg cells). These are numbered 1 to 22, plus an X chromosome and a Y chromosome. Females have a pair of X chromosomes and males have an X and a Y chromosome. The chromosomes can be stained during cell division for viewing under a microscope and appear as short filaments with bands that remain constant for any given chromosome. By photographing such a preparation, it is possible to align them in their pairs.

When this was done for CML cells, it was found that one of the pair of chromosome 9 had an extra piece attached to it and that chromosome 22 - now called the Philadelphia chromosome - lacked a piece. Research showed that there had been an exchange of material between chromosomes 9 and 22 - called a translocation. Studies on many patients proved that this translocation was present in 95 per cent of CML patients.
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Why should a translocation or mutation cause leukaemia?
Molecular gene mapping studies show that the break point for the 9-22 translocation in CML, often written as t(9:22), is close to several genes involved in the control of cell division. The translocation disrupts these genes, the regulation of cell division is lost and the cells multiply out of control. Genes of various kinds associated with cancers are widespread, and over 100 have now been detected. Many forms of blood cancer are associated with damage of this kind.
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Are translocations and other genetic defects found in other leukaemias?
Many leukaemic cells show genetic damage. For instance, in acute lymphoblastic leukaemia, a t(9:22) translocation similar to chronic myelocytic leukaemia is often found together with other translocations and genetic abnormalities in up to one-third of patients. In non-Hodgkin's lymphoma, several translocations have also been found and in multiple myeloma, there are often numerous chromosome defects, but they vary greatly between patients. By contrast, translocations are rare or unknown in chronic lymphocytic leukaemia (CLL). However, other genetic defects such as gene mutations may be present. In a recent study of CLL patients, 65 per cent had one gene abnormality, 25 per cent had two and 10 per cent had three or more.
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Does leukaemia run in families?
Despite these gene abnormalities, leukaemia does not seem to have a strong inherited component or to run in families to any great extent. However, the risk of developing CLL is slightly higher if close relatives have it.
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Why does chronic leukaemia sometimes turn into the acute form?
In the early stages of chronic leukaemia, only a single type of translocation or a specific gene mutation may be present. At this stage, the illness may 'smoulder', with few symptoms or even none at all. Eventually though, in most types of leukaemia, damage at other chromosomal sites appear and the illness enters what is called an accelerated phase which becomes harder to control. Eventually, the cumulative damage becomes so severe that almost all control of cell division is lost and vast numbers of leukaemic cells arise, precipitating the blast phase. By way of an example, CML cells in the blast phase often have a whole extra chromosome 8 and a translocation between chromosomes 15 and 17 (t15:17). These grossly abnormal cells can easily overwhelm the body, often with fatal consequences.
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How common is leukaemia?
In comparison with many solid tumours, leukaemia is relatively uncommon. The risk to an individual of getting any kind of leukaemia during their lifetime is less than one per cent, though the risk is slightly higher in males.

To measure how common any particular leukaemia is, scientists calculate the number of new cases that are diagnosed each year for every 100,000 of the population - called the incidence. Acute myeloblastic leukaemia is the most common acute leukaemia, but is quite uncommon in people below 50. After that, the incidence rises steeply. In children, the commonest leukaemia is acute lymphoblastic leukaemia. The incidence is low in the young adult and in middle age but rises again in the over-65 age group. Chronic lymphocytic leukaemia is uncommon in children and teenagers, but rises steadily in the over-50s, while chronic myelocytic leukaemia affects all age groups but increases with age. In CLL, there are about twice as many males affected, while in CML the rate is much closer in the two sexes.
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Incidence of Leukaemia in individuals exposed (pink) and not exposed (purple) to radiation after the atomic bombing of Hiroshima (1946-1965) (Based on Wantrobe M, Blood Pure and Eloquent. McGraw Hill, 1980, p.528 - with permission)
Incidence of Leukaemia in individuals exposed (pink) and not exposed (purple) to radiation after the atomic bombing of Hiroshima (1946-1965) (Based on Wantrobe M, Blood Pure and Eloquent. McGraw Hill, 1980, p.528 - with permission)
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The 46 chromosomes from a patient with CML lined up as 23 pairs. The presence of an X and a Y pair show that it is a male. The additional fragment on 9 and the missing part on 22 are arrowed, showing the t(9:22) translocation
The 46 chromosomes from a patient with CML lined up as 23 pairs. The presence of an X and a Y pair show that it is a male. The additional fragment on 9 and the missing part on 22 are arrowed, showing the t(9:22) translocation
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Diagram showing the t(9:22) chromosome translocation in CML
Diagram showing the t(9:22) chromosome translocation in CML
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Additional chromosome damage is present by the time that CML enters the blast phase. An extra chromosome number 8 and another translocation t(15:17) in addition to t(9:22) are shown
Additional chromosome damage is present by the time that CML enters the blast phase. An extra chromosome number 8 and another translocation t(15:17) in addition to t(9:22) are shown
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Who gets leukaemia?
Most people with leukaemia are adults, often in the older age group, but a minority are children. However, the pattern of risk is different under the age of 15, where acute leukaemia is by far the most common. For example, ALL accounts for more than 80 per cent of childhood leukaemia, AML for 17 per cent and others about 3 per cent. Once early adulthood is reached, the risk of ALL falls significantly, but from the mid-40s onwards, the rate rises again.

Adults are much more likely to have chronic leukaemia (CLL, CML or less often, hairy cell leukaemia) than acute types, though there is a risk that they may progress to acute blast-stage disease. Most cases of CML occur in the 50 to 70 age group but tail off after that. In adults, most leukaemia and related disorders such as non-Hodgkin's lymphoma generally rise steadily with increasing age. Multiple myeloma is rare below 40 and most common in the over 60s.
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What is hairy cell leukaemia?
This is an uncommon disease accounting for about 3 to 4 per cent of all leukaemias. It is most frequent in people over the age of 50. Biochemical studies suggest that the abnormal cells are of B-cell origin. Hairy cells are so called because their cytoplasm has long projections or ridges which give them a very distinctive 'hairy' appearance under the microscope.
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What are the major symptoms of leukaemia?
Acute leukaemia: The symptoms of all types of acute leukaemia are similar, but with small variations in adults and children; both groups will have a combination of the signs below.

Symptoms prompting a visit to the doctor arise commonly in children at around 4 to 5 years of age and most are caused by changes in the bone marrow that cause anaemia, pallor, defects of blood clotting due to too few platelets, recurrent infections and bone pain (especially in the long bones). The person may also be generally unwell, have a fever, and sometimes mouth ulcers. With children, if the brain is involved, there may be headache and a stiff neck. The doctor may also be able to detect enlarged lymph nodes, spleen and liver, and be able to find tiny skin haemorrhages.

The bones may be sensitive to pressure. Examination of a blood sample will often reveal a raised white blood cell count and the presence of immature blast cells. In adults, there is a greater likelihood of a mass of leukaemic cells below the breast bone.

Chronic leukaemia: Symptoms in CLL are absent in a quarter of people - they are usually diagnosed during routine medical examination. The remainder may have lymph node enlargement, experience lack of energy due to anaemia, have infections that are hard to shake off, possibly pain due to an enlarged spleen and a tendency to bruise easily due to a lack of platelets. Blood samples will show a raised total white cell count.

In CML, a similar range of symptoms will be present, but 95 per cent have an enlarged spleen, 70 per cent bone tenderness, 80 per cent will feel tired and unwell, 60 per cent have loss of weight, 50 per cent an enlarged liver, 40 per cent have bruising, bleeding or abdominal pain. The white cell count will often be markedly raised from normal. Platelet count may be very raised or depressed, depending on the stage of the illness.
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How is leukaemia diagnosed?
There is considerable overlap between the symptoms of acute and chronic leukaemia. A clear diagnosis between the many different kinds of leukaemia will require a detailed examination of the type of white cells circulating in the blood or located in the bone marrow. This is done by specialist staff who microscopically examine cell samples smeared onto glass slides. They may use stains that reveal the size and shape of the cell's different parts, or special fluorescent stains that selectively pick out markers carried on the surface of leukaemic cells. Translocations for specific forms of leukaemia may be detectable by special preparations of the chromosomes during cell division. The results obtained are very important, because the treatment required will differ according to the type and stage of the leukaemia detected.
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Risk of developing a leukaemia during a normal lifetime in comparison with some other forms of cancer
Risk of developing a leukaemia during a normal lifetime in comparison with some other forms of cancer
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Incidence of acute lymphoblastic leukaemia (ALL) and acute myeloblastic leukaemia (AML) in different age groups (From 3rd National Cancer Survey, USA)
Incidence of acute lymphoblastic leukaemia (ALL) and acute myeloblastic leukaemia (AML) in different age groups (From 3rd National Cancer Survey, USA)
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Number of cases per 100,000 per year (incidence) of chronic lymphocytic leukaemia (CLL) in males and females (from SEER Database of the US National Cancer Institute)
Number of cases per 100,000 per year (incidence) of chronic lymphocytic leukaemia (CLL) in males and females (from SEER Database of the US National Cancer Institute)
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Age distribution of onset of CML, showing the peak occurrence on the 50-70 age group. Typically, 45 per cent of people with CML will be female and 55 per cent male
Age distribution of onset of CML, showing the peak occurrence on the 50-70 age group. Typically, 45 per cent of people with CML will be female and 55 per cent male
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What are multiple myeloma and non-Hodgkin's lymphoma?
Multiple myeloma, like leukaemia, is also a disorder in which white cells proliferate out of control. In this case, the malignant cells are related to B-cells but have undergone a further stage of maturation into what are known as plasma cells - the antibody-producing factories of the immune system.

In a healthy person, B-cells are released from bone marrow and patrol the body looking for foreign materials or infecting agents. Many also congregate as resting clusters in the lymph nodes, spleen and other lymphatic tissue. If the wandering B-cells find bacteria or viruses, they become activated, which causes them to multiply and transform within two or three days into plasma cells. These are quite a lot bigger than B-cells and have many internal fibre-like strands. Plasma cells make large quantities of antibody that attacks and eliminates the invaders. Most plasma cells soon die, but some remain as 'memory cells' and provide long-lasting immunity.

In multiple myeloma, plasma cells appear to take up residence in the bone marrow - usually at many sites within the skeleton. Here they are stimulated to keep dividing and remain alive (normally they are quite short-lived), so that they continue to secrete antibody which gradually builds up in the blood. This causes damage to other organs such as the kidney, and kidney failure is a frequent cause of death in this illness. Plasma cell accumulation also results in the release of materials (IL-1ß, VEGF) that destroy the surrounding bone and stimulate the growth of many new blood vessels in the area (a process called angiogenesis) - both of which weaken the bone structure.

Non-Hodgkin's lymphoma is the name given to a group of disorders that share certain clinical features. The most common forms are known as diffuse large B-cell lymphoma and follicular lymphoma. As in multiple myeloma, the cell types involved shows many of the characteristics of B-cells, but at an immature stage of development. They often have antibodies and other common tell-tale surface markers of B-cells. Non-Hodgkin's lymphomas usually arise in the lymph nodes - often in the neck - but may begin in a wide variety of other sites in the body, making diagnosis difficult.
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Some of the events that take place in the bone in multiple myeloma. The Y-shaped objects emerging from the plasma cell represent antibodies (IL = interleukin, VEGF = vascular endothelial growth factor)
Some of the events that take place in the bone in multiple myeloma. The Y-shaped objects emerging from the plasma cell represent antibodies (IL = interleukin, VEGF = vascular endothelial growth factor)
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How common are multiple myeloma and non-Hodgkin's lymphoma?
Multiple myeloma is mainly a disease of older people and has an overall incidence of about four per 100,000. However, frequency increases rapidly in later life, reaching about 25 per 100,000 in the over-80s. This disorder is very uncommon in anyone under the age of 40. Men are affected about twice as often as women, and black-skinned people are more susceptible than white people. There is a definite link with radiation exposure.

Non-Hodgkin's lymphoma is really a mixed group of related disorders which, taken together, are the fifth and sixth most common cancers in women and men respectively and a major cause of cancer deaths. It is the third most common cancer of children, with a peak in the early teens, but cases are few. The incidence rises steadily from about the age of 50 onwards to a maximum of about 20 per 100,000 in those aged 80 and over. It appears that NHL is rapidly becoming more common, but the reason for this is still uncertain.
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What are the signs and symptoms of multiple myeloma?
Multiple myeloma may be present for many years without symptoms. Eventually, though, the build-up of plasma cells in the bone will begin to cause dull aching pains in the spine, ribs and pelvis. There is often a tendency for bone fractures to occur without obvious severe trauma. Patients often complain of being very tired and at that time, clinical tests usually show that they are anaemic (lacking red blood cells). The blood may also become very viscous because of a massive build up of abnormal circulating antibody fragments. Many secondary symptoms may arise from this, including recurrent infections, a tendency to bleed, and damage to vision and kidneys.
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Is there genetic damage in multiple myeloma and NHL?
Multiple myeloma: Studies have shown that the plasma cells of pretty well everyone with multiple myeloma have chromosomal abnormalities. Three-quarters have unusual rearrangements in chromosome 14, but there may also be others involved. The rearrangements are quite numerous and complex, so that there are many different sub-types of this disorder. However, this damage is not inherited and there is only a slightly increased risk of multiple myeloma even when family clusters occur.

Non-Hodgkin's lymphoma: Although there are well-established chromosomal abnormalities in some sub-types of lymphoma, in others they are inconsistent and no clear pattern has so far emerged. Inheritance of NHL is uncommon, but studies have suggested that there was a two-to threefold increased risk of NHL in both men and women whose immediate family had experienced the disease.
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Incidence of multiple myeloma and non-Hodgkin's lymphoma in different age groups
Incidence of multiple myeloma and non-Hodgkin's lymphoma in different age groups
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How are blood malignancies treated?
Some people with chronic leukaemia, myeloma or follicular lymphoma but no symptoms are placed on a regular monitoring regime and do not require immediate treatment. For the remainder, nearly all will require some form of chemotherapy with anti-cancer medicines. The aim of treatment is twofold: firstly, to bring the disease under control (remission) and then to keep the patient disease-free (maintenance).

During chronic phase disease, single medicines are usually used to achieve and then maintain remission. If a relapse occurs, the treatment may be repeated and additional medicines given, but gradually, most patients find they relapse more and more quickly with successive cycles. At this stage, they may be considered for a bone marrow transplant.

In acute leukaemia in younger people, medicines are often used aggressively in multiple combinations to bring the cell count under control. In older people, the side effects from aggressive treatment have to be weighed against the possible benefits. Once remission has been gained, the medicines may be changed to different ones that maintain the remission. Bone marrow transplantation may be considered if a suitable donor is available. In children, it has been common to irradiate the brain, as this has been shown to prevent the build up of leukaemic cells inside the skull.

Combinations of chemotherapy medicines are also used to induce remission in patients with diffuse large B-cell lymphoma and patients achieving a remission at this stage have a good chance of cure. It has been shown that the addition of the monoclonal antibody rituximab to initial chemotherapy improves the chance of long-term survival and this now forms part of the standard treatment for this disease.

During most of these procedures, any signs of infection will be treated very actively, using a range of antibiotics. This is very important, because anti-leukaemia medicines markedly reduce the level of immunity in most people, making them especially vulnerable to infection.
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What traditional medicines are available for treating blood malignancies?
In the past 50 years many medicines have been discovered which help fight blood cancer. The exact choice will depend on the type of malignancy, its stage, and the age and general health of the patient. They are often used in a variety of combinations. Almost all except the steroids and biomolecules act by interfering either directly or indirectly with DNA synthesis, and hence cell division.

In addition to these medicines, others with a supportive function may be used in some conditions. For example, treatments that stimulate red or white blood cell formation may be used to combat anaemia or to boost white cell count prior to collecting cells for transplant. Special medicines called bisphosphonates may also be given to try to protect the bone from damage in multiple myeloma. Treatment with chemotherapy invariably lowers the resistance of patient to infection, necessitating antibiotic treatment and special precautions to avoid passing on infections.
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What role does radiotherapy have in blood cancer?
Radiotherapy has an important part to play in many blood cancers. It is used in three main ways. Firstly, well-defined localised concentrations of cancer cells (e.g. bone in multiple myeloma or the spleen in CLL) can be irradiated to eliminate them or reduce their bulk to relieve pain. Secondly, whole body irradiation can be used to destroy the cancer cells within the whole bone marrow prior to transplanting healthy replacement cells. Finally, radioactivity can be targeted very precisely to tumour cells by coupling radioactive elements to monoclonal antibodies.
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What role does bone marrow and stem cell transplantation play?
This is outside the scope of this booklet, but is so important that at least a brief mention is necessary. For further details, you should refer to publications from charities such as Leukaemia Care and Cancer BACUP, which have more detailed leaflets.

Bone marrow transplants can be curative, but are not suitable for everyone or for every kind of leukaemia. In lymphoma, they are often only used for patients who relapse after other treatment. Their aim is to provide the patient with a healthy source of blood cell types that can replace the defective cancerous cells. There are two main types of bone marrow transplants:

  • Allogeneic - which means that someone else donates the bone marrow cells
  • Autologous - where the patient's own bone marrow (or more often, stem cells) is used. Stem cells are immature blood cells which retain the potential to develop into red or white blood cells or platelets. They are usually collected from the blood.

In allogeneic bone marrow transplants, the best kind of donor is a brother or sister, whose cells will closely match the patient's. Cells from a non-relative can be used if a suitable match can be found. The cells are collected from the spongy cavity inside a bone, often the crest of the pelvis. Before transplantation, the existing faulty bone marrow has to be destroyed by high dose chemotherapy, often combined with radiotherapy. After this treatment, the donated marrow cells are given through a drip into a vein. It will take a few weeks for the transplanted cells to 'take' and during this period, there is an increased risk of infection due to low levels of immunity. To counter this, the patient will be given antibiotics and monitored very carefully.

For an autologous transplant, the cells are taken from the patient, collected during a period of remission. These may be bone marrow cells, but more often are stem cells collected from the blood and separated by a special machine. Before collection, a growth factor will be given to boost the number of stem cells in circulation. Otherwise, the basic procedure is rather similar to allogeneic transplant, but the cells may 'take' more quickly.
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The stages in treating leukaemia (illustrated here by reference to AML) may involve chemotherapy to induce remission followed by different medicines to keep the patient in remission (maintenance therapy). Bone marrow transplantation is an option depending on the individual and type of leukaemia
The stages in treating leukaemia (illustrated here by reference to AML) may involve chemotherapy to induce remission followed by different medicines to keep the patient in remission (maintenance therapy). Bone marrow transplantation is an option depending on the individual and type of leukaemia
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Some types of medicine traditionally used in blood malignancies
Some types of medicine traditionally used in blood malignancies
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What progress has been made in the treatment of blood cancer?
Fifty or sixty years ago, most blood cancers were rapidly fatal. Life span in chronic leukaemia was nearly always longer than in acute disease, but sooner or later, most cases entered the blast phase, leading eventually to death. The medicines available today greatly extend the life of most patients and have improved the quality of life beyond measure. A fuller understanding of the immune system also means that bone marrow transplantation is available to a greater number of people.

An area where progress has been especially dramatic is leukaemia in children under 15. Ten-year survival from all kinds of childhood cancer has risen from just over 20 per cent in the mid-60s to about 70 per cent today. In 1960, children with acute lymphoblastic leukaemia lived for only about 4 months. Data from the Childhood Cancer Research Group at Oxford University show a remarkable improvement in survival from diagnosis in the last 33 years in both childhood ALL and non-ALL.

In ALL, numbers surviving for seven years after diagnosis has risen from around 35 per cent in 1971 to nearly 80 per cent in 1997. In non-ALL, only about seven per cent survived for seven years in 1971, compared to over 65 per cent of those diagnosed in 1997. If survival for five to six years can be achieved, extended survival is much more likely. These advances are a direct result of new medicines, more intensive combinations and an increased use of bone marrow transplantation.
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Can leukaemia and lymphoma be cured?
The answer depends on the definition of 'cured'. Many people enter remission after treatment, recover their health and lead a normal life. For all practical purposes, they could be said to be cured. However, many of them still harbour small numbers of leukaemic cells in their bone marrow or blood. Sometimes these cells regrow and the disease returns. Depending on the leukaemia type, this may occur after just a few months or may not occur for many years. In a few, it may never happen - their cure is complete.
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What help is available for people with leukaemia and their families?
The diagnosis of any serious illness is likely to cause great concern, stress and upheaval of normal life patterns. Many questions will arise and will need to be answered. Often they will be of a personal nature rather than medical - issues such as diet, sex life, exercise, work and career, sources of financial support, and psychological help when needed. Such questions are outside the scope of this booklet, but some answers may come from GPs and consultants to whom patients are referred. But such people are often very busy and alternative sources of information are required.

There are several excellent charities in the UK which can provide leaflets, booklets, telephone helplines and, most importantly, contacts with local support groups. Some deal with cancer in general, such as Cancer BACUP, while others focus mainly on leukaemia and related diseases. Leukaemia CARE is one of the major ones in the UK. Contact details of these and other charities can be found here.
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Ten year survival for all cancers (children under 15). In 40 years this has risen from around 20 per cent to 70 per cent today. (Courtesy of the UK Child Cancer Study Group)
Ten year survival for all cancers (children under 15). In 40 years this has risen from around 20 per cent to 70 per cent today. (Courtesy of the UK Child Cancer Study Group)
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Improvement in survival after diagnosis of children under 15 with ALL or non-ALL between 1971 and 1997. Results from the National Registry of Childhood Tumours, provided by the childhood Cancer Research Group, University of Oxford
Improvement in survival after diagnosis of children under 15 with ALL or non-ALL between 1971 and 1997. Results from the National Registry of Childhood Tumours, provided by the childhood Cancer Research Group, University of Oxford
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