FAQ - Leukemia, Myeloid
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What happens when a bone marrow transplant is needed for chronic myeloid leukemia?

My mother may have chronic myeloid leukemia, and one of the ways of treating it is a bone marrow transplant.

Who are usually the closest matches for donors? Can children be a close enough match (usually) to be a donor?

Once a donor is found, what happens?

I am very worried, and would like to know what my chances are of being able to help my mother. I would like to know what may be in store for her, and how I can help her prepare in every way. I would also like to know how the transplant affects the donor so I may prepare, if I am a match.

Thanks for any help.

There is a non invasive way to treat CML (chronic myeloid leukemia). This is with the use of a drug called Gleevac (Imantinib). This drug targets the receptors on the CML cells and prevents them from dividing.

CML occurs as a result of a translocation of a chromosome to produce a new chromosome called the philedelphia chromosome and to produce a active protein called BCR/abl. This is a tyrosine kinase receptor which actively stimulates cells to divide uncontrollably. Gleevac targets the receptor specifically and stops the cell division.

Good luck!  (+ info)

what is the cml (chronic myeloid leukemia)? and what is the best treatment for it?

a family member under going of chronic myeloid leukemia disease
and taking medicine by the guideance of doctor. is it medicine r ok ? or any other treatment?

Without knowing details of the specific case, I think most cml patients take gleevec to control the cml for as long as it works. That is the treatment that my great aunt as well as a friend are taking for their cml.  (+ info)

What is the difference between acute myeloid leukemia and acute lymphocytic leukemia?

Does AML start in premature blood cells and ALL start in mature blood cells?

Some immature blood cells (lymphoblasts) do normally mature into lymphocytes while other immature blood cells (myeoloblasts) normally mature into various types of "granulocytes" and monocytes. When the lymphoblasts become malignant it results in acute lymphocytic (same as lymphoblastc) leukemia. When the myeloblasts become malignant it results in acute myelocytic (same as myeloblastic) leukemia.  (+ info)

How is Acute myeloid leukemia different than chronic lymphoma leukemia?

acute leukemia characterized by proliferation of granular leukocytes; most common in adolescents and young adults

Acute myeloid leukemia (AML), also known as acute myelogenous leukemia, is a cancer of the myeloid line of white blood cells, characterized by the rapid proliferation of abnormal cells which accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age. While AML is a relatively rare disease overall, accounting for approximately 1.2% of cancer deaths in the United States,[1] its incidence is expected to increase as the population ages.

The symptoms of AML are caused by replacement of normal bone marrow with leukemic cells, resulting in a drop in red blood cells, platelets, and normal white blood cells. These symptoms include fatigue, shortness of breath, easy bruising and bleeding, and increased risk of infection. While a number of risk factors for AML have been elucidated, the specific cause of AML remains unclear. As an acute leukemia, AML progresses rapidly and is typically fatal in weeks to months if left untreated.

Acute myeloid leukemia is a potentially curable disease; however, only a minority of patients are cured with current therapy. AML is treated initially with chemotherapy aimed at inducing a remission; some patients may go on to receive a hematopoietic stem cell transplant.

Areas of active research in acute myeloid leukemia include further elucidation of the cause of AML; identification of better prognostic indicators; development of new methods of detecting residual disease after treatment; and the development of new drugs and targeted therapies.

The first published description of a case of leukemia in the medical literature dates to 1827, when a French physician named Alfred-Armand-Louis-Marie Velpeau described a 63-year-old florist who developed an illness characterized by fever, weakness, urinary stones, and substantial enlargement of the liver and spleen. Velpeau noted that the blood of this patient had a consistency "like gruel", and speculated that the appearance of the blood was due to white corpuscles.[2] In 1845, a series of patients who died with enlarged spleens and changes in the "colors and consistencies of their blood" was reported by the Edinburgh-based pathologist J.H. Bennett; he used the term "leucocythemia" to describe this pathological condition.[3]

The term "leukemia" was coined by Rudolf Virchow, the renowned German pathologist, in 1856. As a pioneer in the use of the light microscope in pathology, Virchow was the first to describe the abnormal excess of white blood cells in patients with the clinical syndrome described by Velpeau and Bennett. As Virchow was uncertain of the cause of the white blood cell excess, he used the purely descriptive term "leukemia" (Greek: "white blood") to refer to the condition.[4]

Further advances in the understanding of acute myeloid leukemia occurred rapidly with the development of new technology. In 1877, Paul Ehrlich developed a technique of staining blood films which allowed him to describe in detail normal and abnormal white blood cells. Wilhelm Ebstein introduced the term "acute leukemia" in 1889 to differentiate rapidly progressive and fatal leukemias from the more indolent chronic leukemias.[5] The term "myeloid" was coined by Neumann in 1869, as he was the first to recognize that white blood cells were made in the bone marrow (Greek: µυєλός, myelos = (bone) marrow) as opposed to the spleen. The technique of bone marrow examination to diagnose leukemia was first described in 1879 by Mosler.[6] Finally, in 1900 the myeloblast, which is the malignant cell in AML, was characterized by Naegeli, who divided the leukemias into myeloid and lymphocytic.[7]

Signs and symptoms
Most signs and symptoms of AML are due to an increased number of malignant white blood cells displacing or otherwise interfering with production of normal blood cells in the bone marrow. A lack of normal white blood cell production makes the patient susceptible to infections (while the leukemic cells themselves are derived from white blood cell precursors, they have no infection-fighting capacity).[8] A lack of red blood cells (anemia) can cause fatigue, paleness, and shortness of breath. A lack of platelets can lead to easy bruising or bleeding with minor trauma.

The early signs of AML are often non-specific, and may be similar to those of influenza or other common illnesses. Some generalized symptoms include fever, fatigue, weight loss or loss of appetite, shortness of breath with exertion, anemia, easy bruising or bleeding, petechiae (flat, pin-head sized spots under the skin caused by bleeding), bone pain and joint pain and persistent or frequent infections.[8]

Enlargement of the spleen may occur in AML, but it is typically mild and asymptomatic. Lymph node swelling is rare in AML, in contrast to acute lymphoblastic leukemia. The skin is involved about 10% of the time in the form of leukemia cutis. Rarely, Sweet's syndrome, a paraneoplastic inflammation of the skin, can occur with AML.[8]

Some patients with AML may experience swelling of the gums due to infiltration of leukemic cells into the gum tissue. Rarely, the first sign of leukemia may be the development of a solid leukemic mass or tumor outside of the bone marrow, called a chloroma. Occasionally, a person may show no symptoms, and the leukemia may be discovered incidentally during a routine blood test.[9]

A number of risk factors for developing AML have been identified, including:

"Pre-leukemic" blood disorders such as myelodysplastic or myeloproliferative syndromes can evolve into AML; the exact risk depends on the type of MDS/MPS.[10]
Exposure to anti-cancer chemotherapy, in particular alkylating agents, can increase the risk for the subsequent development of AML. The risk is highest about 3–5 years after chemotherapy.[11] Other chemotherapy agents, specifically epipodophyllotoxins and anthracyclines, have also been associated with treatment-related leukemia. These treatment-related leukemias are often associated with specific chromosomal abnormalities in the leukemic cells.[12]
Ionizing radiation exposure can increase the risk of AML. Survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML,[13] as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices.[14]
Occupational chemical exposure to benzene and other aromatic organic solvents is controversial as a cause of AML. Benzene and many of its derivatives are known to be carcinogenic in vitro. While some studies have suggested a link between occupational exposure to benzene and increased risk of AML,[15] others have suggested that the attributable risk, if any, is slight.[16]
Several congenital conditions may increase the risk of leukemia; the most common is probably Down syndrome, which is associated with a 10- to 18-fold increase in the risk of AML.[17]

Acute myeloid leukemia is a relatively rare cancer. There are approximately 10,500 new cases each year in the United States, and the incidence rate has remained stable from 1995 through 2005. AML accounts for 1.2% of all cancer deaths in the United States.[1]

The incidence of AML increases with age; the median age at diagnosis is 63 years. AML accounts for about 90% of all acute leukemias in adults, but is rare in children.[1] The rate of therapy-related AML (that is, AML caused by previous chemotherapy) is rising; therapy-related disease currently accounts for about 10–20% of all cases of AML.[18] AML is slightly more common in men, with a male-to-female ratio of 1.3:1.[19]

There is some geographic variation in the incidence of AML. In adults, the highest rates are seen in North America, Europe, and Oceania, while adult AML is rarer in Asia and Latin America.[20][21] In contrast, childhood AML is less common in North America and India than in other parts of Asia.[22] These differences may be due to population genetics, environmental factors, or a combination of the two.

A hereditary risk for AML appears to exist. There are numerous reports of multiple cases of AML developing in a family at a rate higher than predicted by chance alone.[23][24][25][26] The risk of developing AML is increased threefold in first-degree relatives of patients with AML.[27]

The malignant cell in AML is the myeloblast. In normal hematopoiesis, the myeloblast is an immature precursor of myeloid white blood cells; a normal myeloblast will gradually mature into a mature white blood cell. However, in AML, a single myeloblast accumulates genetic changes which "freeze" the cell in its immature state and prevent differentiation.[28] Such a mutation alone does not cause leukemia; however, when such a "differentiation arrest" is combined with other mutations which disrupt genes controlling proliferation, the result is the uncontrolled growth of an immature clone of cells, leading to the clinical entity of AML.[29]

Much of the diversity and heterogeneity of AML stems from the fact that leukemic transformation can occur at a number of different steps along the differentiation pathway.[30] Modern classification schemes for AML recognize that the characteristics and behavior of the leukemic cell (and the leukemia) may depend on the stage at which differentiation was halted.

Specific cytogenetic abnormalities can be found in many patients with AML; the types of chromosomal abnormalities often have prognostic significance.[31] The chromosomal translocations encode abnormal fusion proteins, usually transcription factors whose altered properties may cause the "differentiation arrest."[32] For example, in acute promyelocytic leukemia, the t(15;17) translocation produces a PML-RARα fusion protein which binds to the retinoic acid receptor element in the promoters of several myeloid-specific genes and inhibits myeloid differentiation.[33]

The clinical signs and symptoms of AML result from the fact that, as the leukemic clone of cells grows, it tends to displace or interfere with the development of normal blood cells in the bone marrow.[34] This leads to neutropenia, anemia, and thrombocytopenia. The symptoms of AML are in turn often due to the low numbers of these normal blood elements. In rare cases, patients can develop a chloroma, or solid tumor of leukemic cells outside the bone marrow, which can cause various symptoms depending on its location.[8]

The first clue to a diagnosis of AML is typically an abnormal result on a complete blood count. While an excess of abnormal white blood cells (leukocytosis) is a common finding, and leukemic blasts are sometimes seen, AML can also present with isolated decreases in platelets, red blood cells, or even with a low white blood cell count (leukopenia).[35] While a presumptive diagnosis of AML can be made via examination of the peripheral blood smear when there are circulating leukemic blasts, a definitive diagnosis usually requires an adequate bone marrow aspiration and biopsy

A bone marrow examination is often performed to identify the type of abnormal blood cells; however, if there are many leukemic cells circulating in the peripheral blood, a bone marrow biopsy may not be necessary. Marrow or blood is examined via light microscopy as well as flow cytometry to diagnose the presence of leukemia, to differentiate AML from other types of leukemia (e.g. acute lymphoblastic leukemia), and to classify the subtype of disease (see below). A sample of marrow or blood is typically also tested for chromosomal translocations by routine cytogenetics or fluorescent in situ hybridization.

The diagnosis and classification of AML can be challenging, and should be performed by a qualified hematopathologist or hematologist. In straightforward cases, the presence of certain morphologic features (such as Auer rods) or specific flow cytometry results can distinguish AML from other leukemias; however, in the absence of such features, diagnosis may be more difficult.[36]

According to the widely used WHO criteria, the diagnosis of AML is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by leukemic myeloblasts.[37] AML must be carefully differentiated from "pre-leukemic" conditions such as myelodysplastic or myeloproliferative syndromes, which are treated differently.

Because acute promyelocytic leukemia (APL) has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of leukemia. Fluorescent in situ hybridization performed on blood or bone marrow is often used for this purpose, as it readily identifies the chromosomal translocation (t[15;17]) that characterizes APL.[38]

The two most commonly used classification schemata for AML, as of 2006, are the older French-American-British (FAB) system and the newer World Health Organization (WHO) system.

French-American-British classification
The French-American-British (FAB) classification system divided AML into 8 subtypes, M0 through to M7, based on the type of cell from which the leukemia developed and its degree of maturity. This is done by examining the appearance of the malignant cells under light microscopy and/or by using cytogenetics to characterize any underlying chromosomal abnormalities. The subtypes have varying prognoses and responses to therapy. Although the WHO classification (see below) may be more useful, the FAB system is still widely used as of mid-2006.

The eight FAB subtypes are:[39]

M0 (undifferentiated AML)
M1 (myeloblastic, without maturation)
M2 (myeloblastic, with maturation)
M3 (promyelocytic), or acute promyelocytic leukemia (APL)
M4 (myelomonocytic)
M4eo (myelomonocytic together with bone marrow eosinophilia)
M5 monoblastic leukemia (M5a) or monocytic leukemia (M5b)
M6 (erythrocytic), or erythroleukemia
M7 (megakaryoblastic)

World Health Organization classification
The World Health Organization (WHO) classification of acute myeloid leukemia attempts to be more clinically useful and to produce more meaningful prognostic information than the FAB criteria. Each of the WHO categories contains numerous descriptive sub-categories of interest to the hematopathologist and oncologist; however, most of the clinically significant information in the WHO schema is communicated via categorization into one of the five subtypes listed below.

The WHO subtypes of AML are:[40]

AML with characteristic genetic abnormalities, which includes AML with translocations between chromosome 8 and 21 [t(8;21)], inversions in chromosome 16 [inv(16)], or translocations between chromosome 15 and 17 [t(15;17)]. Patients with AML in this category generally have a high rate of remission and a better prognosis compared to other types of AML.
AML with multilineage dysplasia. This category includes patients who have had a prior myelodysplastic syndrome (MDS) or myeloproliferative disease (MPD) that transforms into AML. This category of AML occurs most often in elderly patients and often has a worse prognosis.
AML and MDS, therapy-related. This category includes patients who have had prior chemotherapy and/or radiation and subsequently develop AML or MDS. These leukemias may be characterized by specific chromosomal abnormalities, and often carry a worse prognosis.
AML not otherwise categorized. Includes subtypes of AML that do not fall into the above categories.
Acute leukemias of ambiguous lineage. Acute leukemias of ambiguous lineage (also known as mixed phenotype or biphenotypic acute leukemia) occur when the leukemic cells can not be classified as either myeloid or lymphoid cells, or where both types of cells are present.


Chromosomal translocation (9;11), associated with AMLAcute myeloid leukemia is a curable disease; the chance of cure for a specific patient depends on a number of prognostic factors.[41]

Cytogenetics and prognosis in AML
The single most important prognostic factor in AML is cytogenetics, or the chromosomal structure of the leukemic cell. Certain cytogenetic abnormalities are associated with very good outcomes (for example, the (15;17) translocation in acute promyelocytic leukemia). About half of AML patients have "normal" cytogenetics; they fall into an intermediate risk group. A number of other cytogenetic abnormalities are known to associate with a poor prognosis and a high risk of relapse after treatment.[42][43][44]

The first publication to address cytogenetics and prognosis was the MRC trial of 1998:[45]

Risk Category Abnormality 5-year survival Relapse rate
Favorable t(8;21), t(15;17), inv(16) 70% 33%
Intermediate Normal, +8, +21, +22, del(7q), del(9q), Abnormal 11q23, all other structural or numerical changes 48% 50%
Adverse -5, -7, del(5q), Abnormal 3q, Complex cytogenetics 15% 78%

Later, the Southwest Oncology Group and Eastern Cooperative Oncology Group,[46] and later still, Cancer and Leukemia Group B published other, mostly overlapping lists of cytogenetics prognostication in leukemia[47]

Antecedent MDS and prognosis
AML which arises from a pre-existing myelodysplastic syndrome or myeloproliferative disease (so-called secondary AML) has a worse prognosis, as does treatment-related AML arising after chemotherapy for another previous malignancy. Both of these entities are associated with a high rate of unfavorable cytogenetic abnormalities.[48][49][50]

Other prognostic markers
In some studies, age >60 years and elevated lactate dehydrogenase level were also associated with poorer outcomes.[51] As with most forms of cancer, performance status (i.e. the general physical condition and activity level of the patient) plays a major role in prognosis as well.

FLT3 internal tandem duplications (ITDs) have been shown to confer a poorer prognosis in AML.[52] Treating these patients with more aggressive therapy, such as stem-cell transplantation in first remission, has not been shown to enhance long-term survival, so this prognostic feature is of uncertain clinical significance at this point.[53]

Researchers are investigating the clinical significance of c-KIT mutations[54] in AML. These are prevalent, and clinically relevant because of the availability of tyrosine kinase inhibitors, such as sunitinib and imatinib that can block the activity of c-KIT pharmacologically.

Other genes being investigated as prognostic factors or therapeutic targets include CEBPA, BAALC, ERG, and NPM1.

Overall expectation of cure
Cure rates in clinical trials have ranged from 20–45%;[55][56] however, it should be noted that clinical trials often include only younger patients and those able to tolerate aggressive therapies. The overall cure rate for all patients with AML (including the elderly and those unable to tolerate aggressive therapy) is likely lower. Cure rates for promyelocytic leukemia can be as high as 98%.[57]

Treatment of AML consists primarily of chemotherapy, and is divided into two phases: induction and postremission (or consolidation) therapy. The goal of induction therapy is to achieve a complete remission by reducing the amount of leukemic cells to an undetectable level; the goal of consolidation therapy is to eliminate any residual undetectable disease and achieve a cure.

As of 2006, all FAB subtypes except M3 are usually given induction chemotherapy with cytarabine (ara-C) and an anthracycline (such as daunorubicin or idarubicin).[58] Other alternatives, including high-dose ara-C alone, may also be used.[59][60] Because of the toxic effects of therapy, including myelosuppression and an increased risk of infection, induction chemotherapy may not offered to the very elderly. Induction chemotherapy usually requires a hospitalization of about 1 month to receive the chemotherapy and recover from its side effects.

Induction chemotherapy is known as "7 and 3" because the cytarabine is given as a continuous IV infusion for seven consecutive days, while the anthracycline is given for three consecutive days as an IV push. Up to 70% of patients will achieve a remission with this protocol.[61]

The M3 subtype of AML, also known as acute promyelocytic leukemia, is almost universally treated with the drug ATRA (all-trans-retinoic acid) in addition to induction chemotherapy.[62][63][64] Care must be taken to prevent disseminated intravascular coagulation (DIC), complicating the treatment of APL when the promyelocytes release the contents of their granules into the peripheral circulation. APL is eminently curable with well-documented treatment protocols.

The goal of the induction phase is to reach a complete remission. Complete remission does not mean that the disease has been cured; rather, it signifies that no disease can be detected with available diagnostic methods (i.e., <5% leukemic cells remain in the bone marrow).[58] Complete remission is obtained in about 50%–75% of newly diagnosed adults, although this may vary based on the prognostic factors described above.[65]

The durability of remission depends on the prognostic features of the original leukemia. In general, all remissions will fail without consolidation (post-remission) chemotherapy, and consolidation has become an important component of treatment.[66]

Even after complete remission is achieved, leukemic cells likely remain in numbers too small to be detected with current diagnostic techniques. If no further postremission or consolidation therapy is given, almost all patients will eventually relapse.[67] Therefore, more therapy is necessary to eliminate non-detectable disease and prevent relapse — that is, to achieve a cure.

The specific type of postremission therapy is individualized based on a patient's prognostic factors (see above) and general health. For good-prognosis leukemias (i.e. inv(16), t(8;21), and t(15;17)), patients will typically undergo an additional 3–5 courses of intensive chemotherapy, known as consolidation chemotherapy.[68][69] For patients at high risk of relapse (e.g. those with high-risk cytogenetics, underlying MDS, or therapy-related AML), allogeneic stem cell transplantation is usually recommended if the patient is able to tolerate a transplant and has a suitable donor. The best postremission therapy for intermediate-risk AML (normal cytogenetics or cytogenetic changes not falling into good-risk or high-risk groups) is less clear and depends on the specific situation, including the age and overall health of the patient, the patient's personal values, and whether a suitable stem cell donor is available.[69]

Relapsed AML
Despite aggressive therapy, however, only 20%–30% of patients enjoy long-term disease-free survival. For patients with relapsed AML, the only proven potentially curative therapy is a stem cell transplant, if one has not already been performed.[70][71][72] In 2000, Mylotarg (gemtuzumab zogamicin) was approved in the United States for patients aged more than 60 years with relapsed AML who are not candidates for high-dose chemotherapy.[73]

Patients with relapsed AML who are not candidates for stem cell transplantion, or who have relapsed after a stem cell transplant, should be strongly considered for enrollment in a clinical trial, as conventional treatment options are limited. Agents under investigation include cytotoxic drugs such as clofarabine as well as targeted therapies such as farnesyl transferase inhibitors, decitabine, and inhibitors of MDR1 (multidrug-resistance protein). Since treatment options for relapsed AML are so limited, another option which may be offered is palliative care.

For relapsed acute promyelocytic leukemia (APL), arsenic trioxide has been tested in trials and approved by the Food and Drug Administration. Like ATRA, arsenic trioxide does not work with other subtypes of AML.[74]

Chronic lymphocytic leukemia (CLL) is a cancer of white blood cells. In CLL, mature white blood cells of certain types, called lymphocytes, function abnormally and cause disease.


Chronic leukemia is a cancer that starts in the blood cells made in the bone marrow. The bone marrow is the spongy tissue found in the large bones of the body. The bone marrow makes precursor cells called "blasts" or "stem cells" that mature into different types of blood cells. Unlike acute leukemias, in which the process of maturation of the blast cells is interrupted, in chronic leukemias, most of the cells do mature and only a few remain as immature cells. However, even though the cells appear normal, they do not function as normal cells.

The different types of cells produced in the bone marrow are red blood cells (RBCs), which carry oxygen and other materials to all tissues of the body, and white blood cells (WBCs), which fight infection. Platelets play a part in the clotting of the blood. The white blood cells can be further subdivided into three main types: the granulocytes, monocytes, and the lymphocytes.

The granulocytes, as their name suggests, contain granules (particles). These granules contain special proteins (enzymes) and several other substances that can break down chemicals and destroy microorganisms such as bacteria. Monocytes are the second type of white blood cell. They also are important in defending the body against pathogens.

The lymphocytes form the third type of white blood cell. There are two main types of lymphocytes: T lymphocytes and B lymphocytes. They have different functions within the immune system. The B cells protect the body by making "antibodies." Antibodies are proteins that can attach to the surfaces of bacteria and viruses. The occurrence of this attachment sends signals to many other cell types to travel through the blood and destroy the antibody-coated organism. The T cell protects the body against viruses. When a virus enters a cell, it produces certain proteins that are projected onto the surface of the infected cell. T cells recognize these proteins and produce certain chemicals (cytokines) capable of destroying the virus-infected cells. In addition, T cells destroy some types of cancer cells.

Chronic leukemias develop very gradually. The abnormal lymphocytes multiply slowly, and in a poorly regulated manner. These lymphocytes live much longer than normal lymphocytes and, thus, their numbers build up in the body. In CLL, lymphocytes accumulate. The enlarged lymphocyte population congregates in the blood, bone marrow, lymph nodes, spleen, and liver. The two types of chronic leukemias can be easily distinguished under the microscope. Chronic lymphocytic leukemia (CLL) involves the T or B lymphocytes. B-cell abnormalities are more common than T-cell abnormalities. T cells are affected in only 5% of the patients.


Ninety percent of CLL cases are seen in people who are 50 years or older, with the average age at diagnosis being 65. Rarely is CLL diagnosed in a patient who is less than 35 years of age. The incidence of the disease increases with age. It is almost never seen in children. According to the estimates of the American Cancer Society (ACS), approximately 8,100 new cases of CLL were diagnosed in 2000, 4,600 in men and 3,500 in women.

CLL affects both sexes. Among patients younger than 65, the disease is slightly more common in men. However, among patients older than 75 years of age, CLL appears almost equally in men and women. Within the United States, CLL affects African-Americans as frequently as it does Caucasians. However, CLL appears more frequently among Americans than among people living in Asia, Latin America, and Africa.

In the United States and Europe, CLL accounts for more than one-quarter of all diagnosed leukemias. Over the past 50 years, the rate at which CLL has been appearing has increased significantly. However, many doctors think that this increase is not necessarily due to the disease actually being more common than in the past, but instead due to the fact that the disease is now more likely to be diagnosed when it does appear. Fifty years ago, only one out of ten CLL patients was diagnosed during the early stages of the disease. Now, half of all CLL patients are diagnosed during this early stage.

Causes and Symptoms

The cause of CLL is unknown. It is certain, however, that CLL is linked to genetic abnormalities and environmental factors. For example, close family members of patients with CLL are twice as likely to seven times as likely to be diagnosed with CLL as people in the general population. For another example, exposure to certain chemicals used in farming and other agricultural occupations may increase the risk that a person will develop CLL. In contrast, CLL is not associated with exposure to radiation known to cause other cancers. As of 2001, doctors were unsure whether people who have had certain virus infections are more likely to develop CLL than are people in the general population. If there does turn out to be such an association, it would not be with all viruses but with two human retroviruses (HTLVI and HTLV-II) or with Epstein-Barr virus (EBV).

The symptoms of CLL are generally vague and non-specific. One out of five patients with CLL has no symptoms at all, and the disease is discovered only through a routine blood test. A patient may experience all or some of the following symptoms:

chronic fatigue
a general feeling of malaise or of things being not quite right
swollen lymph nodes
an enlarged spleen, which could make the patient complain of abdominal fullness
a general feeling of ill health
frequent bacterial or viral infections.
unusually severe response to insect bites
night sweats
weight loss not due to dieting or exercise

There is no screening test for CLL. If the doctor has reason to suspect leukemia, he or she will conduct a very thorough physical examination to look for enlarged lymph nodes in the neck, underarm, and pelvic region. In addition, the doctor will look to see whether the liver and spleen are enlarged. Urine and blood tests may be ordered to check for microscopic amounts of blood in the urine and to obtain a complete differential blood count. This count will give the numbers and percentages of the different cells found in the blood. An abnormal blood test might suggest leukemia. Some authorities state that CLL may be diagnosed if the number of lymphocytes in the blood exceeds a certain level.

The doctor may perform a bone marrow aspiration and biopsy to confirm the diagnosis of leukemia. During the bone marrow biopsy, a cylindrical piece of bone and marrow is removed. The tissue is generally taken out of the hipbone. These samples are sent to the laboratory for examination. In many CLL patients, more than one-fourth of the bone marrow is made up of mature lymphocytes. In addition to diagnosis, bone marrow biopsy is also conducted during the treatment phase of the disease to see if the leukemia is responding to therapy.

Some CLL patients have a condition called hypogammaglobulinemia. Immunoglobulins are normal parts of the body's immune system, the system used to fight off infection. Patients with hypogammaglobulinemia have very low levels of all of the various types of immunoglobulins.

The doctor may also conduct immunophenotyping. This involves taking a sample of the blood and looking at what types of cells of the immune system are being affected by the CLL. Approximately 19 out of 20 CLL patients have the B-cell type of CLL. Far more rare is the T-cell type of CLL. In addition, the doctor may look for abnormalities in the chromosomes of the affected cells. Chromosomes are a unit of genetic material within cells. Patients exhibiting no chromosomal abnormalities have a better prognosis than those who do have such abnormalities. If the abnormalities become more complex over time, the patient's prognosis may worsen.

Standard imaging tests such as x rays, computed tomography scans (CT scans), and magnetic resonance imaging (MRI) may be used to check whether the leukemic cells have invaded other organs of the body, such as the bones, chest, kidneys, abdomen, or brain.

Clinical Staging, Treatments, and Prognosis


Usually one of two systems are used to stage CLL. One of these is the Binet system and the other the Rai system. According to the Rai system, patients at low risk have no enlargement of lymph nodes, spleen or liver. The occurrence of these marks entry into the intermediate stage, according to Rai. High risk patients have, in addition, anemia and a significant decrease in the number of blood platelets in their blood. Blood platelets help blood to clot. According to the Binet system, a patient's stage depends upon how much hemoglobin (part of red blood cells that carry oxygen) and how many platelets are in the blood, as well as how many other areas the disease has affected. According to both systems, patients at low risk usually survive more than ten years. Patients at intermediate risk usually survive about six years. Patients at high risk usually survive about 2 years. Other factors with important implications for prognosis include the pattern at which bone marrow is being affected by the CLL and the amount of time it takes for the number of lymphocytes to double.


Because the long-term prognosis for many patients with CLL is excellent, many patients receive no treatment at all at first. Many patients go for years before developing aggressive disease that requires treatment. Treatment for early stage CLL should be started only when one of the following conditions appears:

Symptoms of the disease are growing worse, for example, there is a greater degree of fever, weight loss, night sweats, and so forth.
The spleen is enlarging or enlargement of the spleen has become painful.
Disease of the lymph nodes has become more severe.
The condition of the bone marrow has deteriorated and there is anemia and a marked reduction in the number of blood platelets.
There is anemia or reduction in the number of blood platelets for reasons not specifically related to the condition of the bone marrow.
The population of lymphocytes is rapidly growing.
The patient is experiencing numerous infections caused by bacteria.
Therapy for CLL usually starts with chemotherapy. Depending on the stage of the disease, single or multiple drugs may be given. Drugs commonly prescribed include fludarabine, cladribine, chlorambucil and cyclophosphamide. Studies have also provided evidence that a combination of fludarabine and cyclophosphamide is effective. However, this combination has not yet been evaluated over periods of ten years or more. Another combination now being studied involves fludarabine and mitoxantrone (Novantrone). Yet another involves fludarabine and anthracyclines. Low-dose radiation therapy may be given to the whole body, or it may be used to alleviate the symptoms and discomfort due to an enlarged spleen and lymph nodes. The spleen may be removed in a procedure called a splenectomy.

Bone marrow transplantation (BMT) has produced some positive outcomes in patients with CLL, although it has not been the subject of sufficient systematic study to permit doctors to know how effective it is. In BMT, the patient's diseased bone marrow is replaced with healthy marrow. There are two ways of performing a bone marrow transplant. In an allogeneic bone marrow transplant, healthy marrow is taken from another person (donor) whose tissue is either the same or very closely resembles the patient's tissues. The donor may be a twin, a sibling, or a person who is not related at all. First, the patient's bone marrow is destroyed with very high doses of chemotherapy and radiation therapy. To replace the destroyed marrow, healthy marrow from the donor is given to the patient through a needle in the vein.

In the second type of bone marrow transplant, called an autologous bone marrow transplant, some of the patient's own marrow is taken out and treated with a combination of anticancer drugs to kill all the abnormal cells. This marrow is then frozen to save it. The marrow remaining in the patient's body is then destroyed with high-dose chemotherapy and radiation therapy. Following that, the patient's own frozen marrow is thawed and given back to the patient through a needle in the vein. The use of this mode of bone marrow transplant for the treatment of CLL is currently being investigated in clinical trials.

Allogeneic BMT has been successfully used with younger patients with CLL who have not responded positively to chemotherapy. Autologous BMT has produced some positive results in older CLL patients. However, BMT is generally not considered an option in treating most patients with CLL because they are too old to be considered good candidates for the procedure.

Other CLL therapies that are being investigated include monoclonal antibody-targeted therapy and interferons. Monoclonal antibodies (MoAbs) are laboratory-manufactured chemicals that closely resemble parts of the body's natural immune system. Studies of MoAbstargeted therapies have shown some positive results in CLL, although definitive studies have not been performed at the time of this writing in 2001. Interferon is a chemical normally made in the cells of the body. It helps protect the body against viruses and also seems to have some effect against certain cancers. The interferon used as medicine is a laboratory-manufactured copy of the interferon produced by the body. As of this writing in 2001, interferon therapy has produced some response in CLL patients. However, interferon therapy has not as yet been shown to be associated with prolongation of remission.

Radiation therapy is very effective for approximately one in three of those CLL patients for whom it is considered appropriate.

Because leukemia cells can spread to all the organs via the blood stream and the lymph vessels, surgery is not considered an option for treating leukemias.

Treatment of Cll and Its Complications

During therapy for CLL, complications frequently appear. Many patients develop infectious illnesses. Sometimes, two or more infectious diseases attack a patient at the same time. These infections should be treated with great care. Most people whose death has been directly attributed to CLL have actually died from bacterial infections. The patient should be involved in identifying symptoms of infection and reporting these to the doctor without delay. Doing so may save the patient's life.

Many patients develop anemia, which is treated with the drug prednisone. Patients who do not respond to prednisone therapy may have their spleen removed and may receive therapy with immunoglobulin, a component of the blood.

Treatment After Transformation of Cll

Between three and ten out of every hundred patients with CLL experiences transformation of the disease into large-cell lymphoma (LCL). When this happens it is called Richter's transformation. Its occurrence is often marked by fever, weight loss, and night sweats. Treatments for LCL are being studied, although outcomes have not been very good. Very infrequently, CLL may transform into another disease, called prolymphocytic leukemia. Attempts to develop adequate therapies for this disease are ongoing.


For many CLL patients, the prognosis is excellent. Using the Binet and Rai staging systems, patients at low risk usually survive more than ten years. Patients at intermediate risk usually survive about six years. Patients at high risk usually survive about two years. The average patient survives approximately nine years following diagnosis. Factors with important implications for prognosis that are not included in the Binet or Rai systems are the pattern at which bone marrow is being affected by the CLL and the amount of time it takes for the number of lymphocytes in the blood to double. It is uncertain whether BMT may prolong the lifespan of CLL patients. Many of the chemotherapy agents used to treat disease do effectively control the leukemia and its effects but, as yet, the more established chemotherapy agents have not been shown to increase the life span of patients.

Coping With Cancer Treatment

Since many CLL patients die from infection, it is essential that patient be very alert to the signs of infection. If patients perform this role and seek medical attention as soon as symptoms of infection appear, then treatment can be started early. This may save a life.

It is very difficult for some patients to be not only informed that they have leukemia but then to also be told that they do not need treatment. This may be very confusing, unless the patient realizes that treatment may be necessary at some future time and that starting therapies too soon may be counterproductive.

Because nutritional alteration, weight loss, and psychosocial problems may accompany CLL, it may be prudent for patients to consult with a registered dietitian.

Cancer patients need supportive care to help them come through the treatment period with physical and emotional strength in tact. Many patients experience feelings of depression, anxiety, and fatigue, and many experience nausea and vomiting during treatment. Studies have shown that these can be managed effectively if discussed with the attending physician.


Although some cancers are related to known risk factors, such as smoking, in leukemias, there are no known risk factors. Therefore, at the present time, there is no way known to prevent the leukemias from developing. Everyone should undergo periodic medical checkups.

chronic lymphocytic leukemia
Chronic lymphocytic leukemia
Classification & external resources
Peripheral blood smear showing CLL cells
ICD-10 C91.1
ICD-9 204.1
DiseasesDB 2641
eMedicine med/370
MeSH D015462
Chronic lymphocytic leukemia (or "chronic lymphoid leukemia"), known for short as CLL, is a type of leukemia in which too many lymphocytes are produced. Although the malignant lymphocytes in CLL may look normal and mature, they are not and these cells may not cope effectively with infection.

CLL is the most common form of leukemia in adults. Men are twice as likely to develop CLL as women. However, the key risk factor is age. Over 75% of new cases are diagnosed in patients over age 50. More than 7,000 new cases of CLL are diagnosed in the U.S. each year.

CLL is an abnormal neoplastic proliferation of B cells. The cells accumulate mainly in the bone marrow and blood. CLL is closely related to (and most consider it the same as) a disease called small lymphocytic lymphoma (SLL), a type of non-Hodgkin's lymphoma which presents primarily in the lymph nodes. In the past, cases with similar microscopic appearance in the blood but with a T cell phenotype were referred to as T-cell CLL. However, it is now recognized that these so-called T-cell CLLs are in fact a separate disease group and are currently classified as T cell prolymphocytic leukemias.

The diagnosis of CLL is based on the demonstration of an abnormal population of B lymphocytes in the blood, bone marrow, or tissues that display an unusual but characteristic pattern of molecules on the cell surface. This atypical molecular pattern includes the co-expression of cells surface markers CD5 and CD23. In addition, all the CLL cells within one individual are clonal, that is genetically identical. In practice, this is inferred by the detection of only one of the mututally exclusive antibody light chains, kappa or lambda, on the entire population of the abnormal B cells. Normal B lymphocytes consist of a stew of different antibody producing cells resulting in a mixture of both kappa and lambda expressing cells. The lack of the normal distribution of kappa and lambda producing B cells is one basis for demonstrating clonality, the key element for establishing a diagnosis of any B cell malignancy (B cell Non-Hodgkin lymphoma).

Recent publications have indicated that two types of CLL exist based on the maturational state of the cell. This distinction can be discerned by the presence of certain marker molecules such as CD38 and ZAP-70. Their expression correlates with a more immature cellular state and a more rapid disease course. The cellular DNA also differs between the two groups. The group with the immature cell pattern shows few changes in the DNA in the antibody gene region whereas the mature group contains considerable alterations of the DNA in the antibody gene region. Since assessment of the DNA changes is difficult to perform, most physicians rely on the pattern of marker molecule expression to determine the subtype of CLL.

In addition to the maturational state, the prognosis of patients with CLL is dependent on the genetic changes within the neoplastic cell population. These genetic changes can be identified by fluorescent probes to chromosomal parts using a technique referred to as fluorescent in situ hybridization (FISH). Four main genetic aberrations are recognized in CLL cells that have a major impact on disease behavior. Deletions of part of the short arm of chromosome 17 (del 17p) which target the cell cycle regulating protein p53 are particularly deleterious. Patients with this abnormality have significantly short interval before they require therapy and a shorter survival. This abnormality is found in 5-10% of patients with CLL. Deletions of the long arm on chromosome 11 (del 11q) are also unfavorable although not to the degree seen with del 17p. The abnormality targets the ATM gene and occurs infrequently in CLL (5-10%). An additional chromosome 12 (trisomy 12) is a relatively frequent finding occurring in 20-25% of patients and imparts an intermediate prognosis. Finally, deletion of the long arm of chromosome 13 (del 13q) is the most common abnormality in CLL with roughly 50% of patients with cells containing this defect. These patients have the best prognosis and most will live many years, even decades, without the need for therapy. The gene targeted by this deletion is a segment that likely produces small inhibitory RNA molecules that affect expression of important death inhibiting genes.

Hematologic disorders that may resemble CLL in their clinical presentation, behavior, and microscopic appearance include mantle cell lymphoma, marginal zone lymphoma, B cell prolymphocytic leukemia, and lymphoplasmacytic lymphoma. Hairy cell leukemia is also a neoplasm of B lymphocytes but differs significantly from CLL by its morphology under the microscope (hairy cell leukemia cells have delicate, hair-like projections on their surface) and marker molecule expression. All the B cell malignancies of the blood and bone marrow can be differentiated from one another by the combination of cellular microscopic morphology, marker molecule expression, and specific tumor-associated gene defects. This is best accomplished by evaluation of the patient's blood, bone marrow and occasionally lymph node cells by a pathologist with specific training in blood disorders. A sophisticated instrument called a flow cytometer is necessary for cell marker analysis and the detection of genetic problems in the cells may require visualing the DNA changes with fluorescent probes by fluorescent in situ hybridization (FISH).

Whilst generally considered incurable CLL progresses slowly in most cases. Many people with CLL lead normal and active lives for many years - in some cases for decades. Because of its slow onset, early-stage CLL is generally not treated since it is believed that early CLL intervention does not improve survival time or quality of life. Instead, the condition is monitored over time.

The decision to start CLL treatment is taken when the patient's clinical symptoms or blood counts indicate that the disease has progressed to a point where it may affect the patient's quality of life. Clinical "staging systems" such as the Rai 4-stage system and the Binet classification can help to determine when and how to treat the patient.

CLL treatment focuses on controlling the disease and its symptoms rather than on an outright cure. CLL is treated by chemotherapy, radiation therapy, biological therapy, or bone marrow transplantation. Symptoms are sometimes treated surgically (splenectomy removal of enlarged spleen) or by radiation therapy ("de-bulking" swollen lymph nodes).

Initial CLL treatments vary depending on the exact diagnosis and the progression of the disease, and even with the preference and experience of the health care practitioner. There are dozens of agents used for CLL therapy, and there is considerable research activity studying them individually or in combination with each other. For example, although the purine analogue fludarabine was shown to give superior response rates than chlorambucil as primary therapy,[1] there is no evidence that early use of fludarabine improves overall survival, and some clinicians prefer to reserve fludarabine for relapsed disease. Combination chemotherapy regimens such as fludarabine with cyclophosphamide, FCR (fludarabine, cyclophosphamide and rituximab) and CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) are effective in both newly-diagnosed and relapsed CLL. Allogeneic bone marrow (stem cell) transplantation is rarely used as a first-line treatment for CLL due to its risk.

"Refractory" CLL is a disease that no longer responds favorably to treatment. In this case more aggressive therapies, including bone marrow (stem cell) transplantation, are considered. The monoclonal antibody, alemtuzumab (directed against CD52), may be used in patients with refractory, bone marrow-based disease.[2] There is increasing interest in the use of reduced intensity allogeneic stem cell transplantion, which offers the prospect of cure for selected patients with a suitable donor.[3]

Determining when to start treatment and by what means is often difficult; studies have shown there is no survival advantage to treating the disease too early. The National Cancer Institute Working Group has issued guidelines for treatment, with specific markers that should be met before it is initiated.  (+ info)

How long can a person live with Acute Myeloid Leukemia when it is left untreated and treated. (cont below)?

I would like to have a round-about answer. Thanks for your answers. Thanks for taking the time to read and answer this. :]

Average survival without treatment ranges from weeks to few months.
With treatment, for either AML or ALL, cure is possible (though altogether too uncommon), so a person could live a "normal" life span. Going through treatment is rigorous, no doubt, and can be fatal. Unfortunately, most patients with adult AML who enter remission will relapse within 2 years.

Blessings  (+ info)

what is the survival rate of acute myeloid leukemia?

can u plz suggest some sites that offer help regarding treatment?
what is the approximate cost of treatment for AML in India?
Hope some doctors in India can answer this.

Cancer of any kind is dangerous - there is no such thing as a good cancer. Leukemia takes lives of children and adults every day but at the same time, there are many survivors that are in remission and doing very well. How well a patient does depends on so many different factors including age, cell counts, what type and subtype of leukemia he or she has, the will to fight, and so many other factors.

My son E was diagnosed with a Wilms' Tumour as a newborn, won his battle, and was recently diagnosed with Secondary Acute Myelogenous Leukemia (AML). His cancer is most likely a secondary cancer caused by the chemotherapy his first time when he fought Wilms. E somehow passed his screenings he has every 3 months back in October but in the end of November we started to notice he wasn't quite himself, and he was diagnosed December 19th.

There are lots of symptoms of leukemia but each individual is different. Some display some symptoms while others display other ones. E had a cold in November that he just couldn't kick. We took him to the doctor and he was given an antibiotic. He got a little better but as soon as he finished the antibiotic he got sick again. He usually has a couple bruises here and there since he is a 2 year old. His walking was greatly affected from one of the drugs in his first chemo cocktail so he trips and falls pretty often. But the bruising he had was more than usual - he bruised at the slightest bump. That's when we really knew something was wrong and took him to the doctor again. Once he was diagnosed we found out that his spleen and liver were enlarged - also symptoms of leukemia. Due to the extent of enlargement of his spleen, he had it removed after a round of chemotherapy. So far he has had 3 strong doses of chemo, a round of consolidation chemo, he's on his 2nd round of consolidation chemo and he's labeled as being in remission! He still has 3-5 rounds of consolidation chemo left just to make sure all of the cancerous cells are gone then a bone marrow transplant down the road when a donor becomes available.

A leukemia diagnosis is absolutely not a death sentence. It's treatable but you have to keep in mind that it does take lives. I know many children and adults that have gone on to live completely normal lives after getting their No Evidence of Disease (NED) status. Sometimes a patient does relapse but it is absolutely possible that he or she can reach remission and eventually NED status.

AML has an overall long-term survival rate of 21.3%. Because children (under 15) typically do better, their long-term survival rate is around 55.2%. Between the different subtypes there are different survival rates. Again, every cause is different, every patient is different. The treatment given also has an impact on the survival of the patient - some cases respond to treatment better than others. Certain factors also impact the survival rate. There are some genetic mutations that increase the likelihood of survival and some genetic mutations that greatly decrease the likelihood of survival. Previous chemotherapy and radiation or previous battles with cancer generally lead to a smaller percentage of survivals compared to a first-time diagnosis.

We live in Canada so I can't estimate the costs of treatment in India.

I hope this helped you out some. If you have any more questions feel free to email me ([email protected]) or IM me (crazycanuckj).  (+ info)

What is the difference between Myelodysplastic syndrome and chronic myeloid leukemia?

Myelodysplastic syndromes are bone marrow stem cell disorders that cause inefficient blood production. CML is unregulated growth of myeloid cells in the bone marrow and the accumulation of these cells in the blood. It is also a marrow stem cell disorder.  (+ info)

what are the chances of a 17 year olld with cml(chronic myeloid leukemia?

my friends brother has cml and shes like really messed up about it and i was just wondering what are his chances?and whaqt can i do to cheer her up?

Gleevec (imatinib) has revolutionized CML therapy. Most patients went 3 years on average a decade ago before blast crisis developed. I have had patients now on Gleevec (and similar meds) now 10 years who remain stable in chronic phase. We are not sure (and really do not believe) that Gleevec can cure CML.

For patients this young, doctors usually look for match-related donors fpr allogeneic transplant, as this is potentially curative therapy. If only unrelated donors are available, my experience is transplant doctors usually recommend medicine therapy like Gleevec and reserve the more toxic unrelated transplant until absolutely needed.

Blessings  (+ info)

can you have a baby if you have acute myeloid leukemia?

Will it be a high risk pregnancy or would the baby not be affected?

You mean pregnant with AML now? If so, then if less than 12 weeks, usually if patient does not terminate pregnancy there would be a very high risk of defects or more likely early spontaneous abortion due to toxicity of chemotherapy to fetus. If after 12 weeks, then chance for defects much lower if chemo given, but risk for complications remains higher than average (prematurity, low weight, miscarriage).

If you had AML previously, then your child overwhelmingly likely will be fine. There are very rare AML hereditary syndromes, but these are extremely rare. Biggest trouble can be just getting pregnant in the first place for patients.

God bless, best wishes  (+ info)

My daughter was just diagnosed with Acute Myeloid Leukemia?

How Do I cope with this, she was complaining about being sick, I feel like its my fault. She was complaining about not feeling good, then she was diagnosed. I know it's not my fault that she got this but, still. How do I cope?

You'll find your own routine. At first it's pure shock, Leukemia is the last thing from most parents minds, and its certainly the last thing you wanted to hear. If every parents first thought when their child was sick was "LEUKEMIA" the oncology departments would be in disarray.

When something like this happens, first instinct is to find someone to blame, often people blame the doctors or themselves for not spotting it sooner, usually, this couldn't be further from the truth.

Make sure you keep thinking positively, i'm not sure how old your daughter is, but i'd try not to keep things from her, kids with cancer spend a lot of time thinking about things, they end up far more mature for their age than they might have been otherwise.

I'll bet you and your family will be amazed at how much strength you'll give each other at this time, it's hard now, but keep fighting and you'll do it.

A few hours ago, 30 odd people stood in the playroom of this hospital corridor and sang, cheered and cried, because an 13 year old girl, who'd been fighting Acute Myeloid Leukemia since she was 10 years old has been declared cancer free. And it happens all the time.

Kids are tough, i didn't think my daughter was strong enough to beat this, btu she's doing it. And i bet yours will too.

Best wishes, god bless.  (+ info)

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