High amounts of ionizing radiation exposure can increase the risk of AML. Survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML, as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices. People treated with ionizing radiation after treatment for prostate cancer, non-Hodgkin lymphoma, lung cancer, and breast cancer have the highest chance of acquiring AML, but this increased risk returns to the background risk observed in the general population after 12 years.

Exposure to anticancer chemotherapy, in particular alkylating agents, can increase the risk of subsequently developing AML. The risk is highest about three to five years after chemotherapy. Other chemotherapy agents, specifically epipodophyllotoxins and anthracyclines, have also been associated with treatment-related leukemias, which are often associated with specific chromosomal abnormalities in the leukemic cells.

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, others have suggested the attributable risk, if any, is slight.

Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. How it is handled depends primarily on the type of leukemia. Nearly all leukemias appearing in pregnant women are acute leukemias. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester. Chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with Interferon-alpha hormones. Treatment for chronic lymphocytic leukemias, which are rare in pregnant women, can often be postponed until after the end of the pregnancy.

Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.

In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia.

Chronic myelogenous leukemia is associated with a genetic abnormality called the Philadelphia translocation; 95% of people with CML carry the Philadelphia mutation, although this is not exclusive to CML and can be observed in people with other types of leukemia.

Acute erythroid leukemia is rare, accounting for only 3–5% of all acute myeloid leukemia cases. One study estimated an occurrence rate of 0.077 cases per 100,000 people each year. 64–70% of people with this condition are male, and most are elderly, with a median age of 65.

The exact cause of most cases of childhood leukemia is not known. Most children with leukemia do not have any known risk factors. The immune system plays an important role in protecting the body's immune system. An alteration or defect in the immune system may increase the risk for developing cancer. The immune system can be damaged by different factors, such as exposure to different viruses, environmental factors, chemical factors and other various infections.

There also appears to be some evidence linking childhood leukemia to x-ray exposure. In a 2010 study by the University of California, Berkeley’s School of Public Health, researchers found that children with acute lymphoid leukemia (ALL) had almost twice the chance of having been exposed to three or more X-rays compared with children who did not have leukemia.

Information on prognosis is limited by the rarity of the condition. Prognosis appears to be no different to AML in general, taking into account other risk factors. Acute erythroid leukemia (M6) has a relatively poor prognosis. A 2010 study of 124 patients found a median overall survival of 8 months. A 2009 study on 91 patients found a median overall survival for erythroleukemia patients of 36 weeks, with no statistically significant difference to other AML patients. AEL patients did have a significantly shorter disease free survival period, a median of 32 weeks, but this effect was explained by other prognostic factors. That is, AEL is often associated with other risk factors, like monosomal karyotypes and a history of myelodysplastic syndrome. Prognosis is worse in elderly patients, those with a history of myelodysplastic syndrome, and in patients who had previously received chemotherapy for the treatment of a different neoplasm.

T-PLL is an extremely rare aggressive disease, and patients are not expected to live normal lifespans. Before the recent introduction of better treatments, such as alemtuzumab, the median survival time was 7.5 months after diagnosis. More recently, some patients have survived five years and more, although the median survival is still low.

Chloromas may occur in patients with a diagnosis of myelodysplastic syndrome (MDS) or myeloproliferative syndromes (MPS) (e.g. chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytosis, or myelofibrosis). The detection of a chloroma is considered "de facto" evidence these premalignant conditions have transformed into an acute leukemia requiring appropriate treatment. For example, presence of a chloroma is sufficient to indicate chronic myelogenous leukemia has entered its 'blast crisis' phase.

About four men are diagnosed with this disease for every three women. Despite its overall rarity, it is also the most common type of mature T cell leukemia.

At least one case of "FIP1L1-PDGFRA" fusion gene-induced eosinophilic leukemia presenting with myeloid sarcoma and eosinophilia has been reported. This form of myeloid sarcoma is distinguished by its highly successful treatment with imatinib (the recommended treatment for "FIP1L1-PDGRGA" fusion gene-induced eosinophilic leukemia) rather than more aggressive and toxic therapy.

This disease is rare, with fewer than 1 in 10,000 people being diagnosed with HCL during their lives. Men are four to five times more likely to develop hairy cell leukemia than women. In the United States, the annual incidence is approximately 3 cases per 1,000,000 men each year, and 0.6 cases per 1,000,000 women each year.

Most patients are white males over the age of 50, although it has been diagnosed in at least one teenager. It is less common in people of African and Asian descent compared to people of European descent.

It does not appear to be hereditary, although occasional familial cases that suggest a predisposition have been reported, usually showing a common Human Leukocyte Antigen (HLA) type.

Acute myelomonocytic leukemia (AMMoL) is a form of acute myeloid leukemia that involves a proliferation of CFU-GM myeloblasts and monoblasts.

It is classified under "M4" in the French-American-British classification (FAB).

It is classified under "AML, not otherwise classified" in the WHO classification.

Translocations have been observed.

Progression from myelodysplastic syndrome has been reported.

Acute myeloblastic leukemia (AML) is a group of malignant bone marrow neoplasms of myeloid

precursors of white blood cells. Acute myelomonocytic leukemia (AML-M4) is a common type of pediatric AML. However, the condition is rare and represents approximately 3% of all leukemias during childhood and has an incidence of 1.1 – 1.7 per million per year. The symptoms may be aspecific: asthenia, pallor, fever, dizziness and respiratory symptoms. More specific symptoms are bruises and/or (excessive) bleeding, coagulation disorders (DIC), neurological disorders and gingival hyperplasia. Diagnostic methods include blood analysis, bone marrow aspirate for cytochemical, immunological and cytogeneticalanalysis, and cerebrospinal fluid (CSF) investigations. A characteristic chromosomal abnormalityobserved in AML-M4 is inv(16). Treatment includes intensive multidrug chemotherapy and in selected cases allogeneic bone marrow transplantation. Nevertheless, outcome of AML remains poor with an

overall survival of 35-60%. Children with AML-M4 carrying the inv(16) abnormality have a better prognosis (61% 5-year overall survival). New therapeutics are required to increase the probability of cure in this serious disorder.

Despite decade-long remissions and years of living very normal lives after treatment, hairy cell leukemia is officially considered an incurable disease. While survivors of solid tumors are commonly declared to be permanently cured after two, three, or five years, people who have hairy cell leukemia are never considered 'cured'. Relapses of HCL have happened even after more than twenty years of continuous remission. Patients will require lifelong monitoring and should be aware that the disease can recur even after decades of good health.

People in remission need regular follow-up examinations after their treatment is over. Most physicians insist on seeing patients at least once a year for the rest of the patient's life, and getting blood counts about twice a year. Regular follow-up care ensures that patients are carefully monitored, any changes in health are discussed, and new or recurrent cancer can be detected and treated as soon as possible. Between regularly scheduled appointments, people who have hairy cell leukemia should report any health problems, especially viral or bacterial infections, as soon as they appear.

HCL patients are also at a slightly higher than average risk for developing a second kind of cancer, such as colon cancer or lung cancer, at some point during their lives (including before their HCL diagnosis). This appears to relate best to the number of hairy cells, and not to different forms of treatment. On average, patients might reasonably expect to have as much as double the risk of developing another cancer, with a peak about two years after HCL diagnosis and falling steadily after that, assuming that the HCL was successfully treated. Aggressive surveillance and prevention efforts are generally warranted, although the lifetime odds of developing a second cancer after HCL diagnosis are still less than 50%.

There is also a higher risk of developing an autoimmune disease. Autoimmune diseases may also go into remission after treatment of HCL.

The prognosis for BAL patients is not good which is worse than ALL and AML. Medical Blood Institute reported cases of CR rate was 31.6%, with a median remission are less than 6 months

The median survival time is only 7.5 months. The life quality is also low because the immune function of patient is damaged seriously. They have to stay in hospital and need 24h care.

In another study, the results showed that young age, normal karyotype and ALL induction therapy will have a better prognosis than Ph+, adult patients. The study shows median survival of children is 139 months versus 11 months of adults, 139 months for normal karyotype patients versus 8 months for ph+ patients.

Leukemia is usually described either as "acute", which grows quickly, or "chronic", which grows slowly. One main type of acute leukemia is acute lymphocytic leukemia (ALL), which accounts for about 3 out of 4 cases of leukemia in children. ALL is a form of leukemia that affects the lymphocytes, a type of white blood cells which fights infection. When a patient has ALL, the bone marrow makes too many immature white blood cells and they do not mature correctly. Therefore, the white blood cells over-produce, crowding the other blood cells. The white blood cells also do not work correctly to fight infection.

Another type of acute leukemia is acute myelogenous leukemia (AML). AML is cancer of the blood in which too many myeloblasts, immature white blood cells, are produced in the bone marrow. The marrow continues to produce abnormal cells that crowd the other blood cells and do not work properly to fight infection. Almost all childhood leukemia is acute.

Chronic leukemias are more common in adults than in children, and although they tend to grow more slowly than acute leukemias, they are harder to treat. These chronic leukemias are divided into two types: chronic myelogenous leukemia (CML) and chronic lymphocytic leukemia (CLL). CML is rare in children, but does occur and is treatable in children the same as in adults. CML patients have too many immature white blood cells being produced, and the cells crowd the other healthy blood cells.

A specific chromosome rearrangement is also found in patients with CML, among the 46 chromosomes in human cells. Part of chromosome nine breaks off and attaches itself to chromosome 22, meaning there is an exchange of genetic material between chromosomes 9 and 22. The rearrangement of the chromosomes changes the positions and functions of certain genes, which causes uncontrolled cell growth.

CLL is another form of chronic leukemia, but is extremely rare in children. Juvenile myelomonocytic leukemia (JMML) is a form of leukemia that is neither chronic nor acute and occurs most often in children under the age of four. JMML begins from myeloid cells, but is not as fast-growing as AML or as slow as CML.

Complete remission and long-term survival are more common in children than adults.

Prognosis depends upon the cause. One third of cases is associated with a t(1;22)(p13;q13) mutation in children. These cases carry a poor prognosis.

Another third of cases is found in Down syndrome. These cases have a reasonably fair prognosis.

The last third of cases may be heterogeneous, and carry a poor prognosis.

Myeloid leukemia is a type of leukemia affecting myeloid tissue.

Types include:

- Acute myeloid leukemia

- Chronic myelogenous leukemia

The 5 year survival has been noted as 89% in at least one study from France of 201 patients with T-LGL leukemia.

It is associated with GATA1, and risks are increased in individuals with Down syndrome.

However, not all cases are associated with Down syndrome, and other genes can also be associated with AMKL.

Another related gene is MKL1, which is also known as "MAL". This gene is a cofactor of serum response factor.

ANKL is treated similarly to most B-cell lymphomas. Anthracycline-containing chemotherapy regimens are commonly offered as the initial therapy. Some patients may receive a stem cell transplant.

Most patients will die 2 years after diagnosis.

Acute leukemia or acute leukaemia is a family of serious medical conditions relating to an original diagnosis of leukemia. In most cases, these can be classified according to the lineage, myeloid or lymphoid, of the malignant cells that grow uncontrolled, but some are mixed and for those such an assignment is not possible.

Forms of acute leukemia include:

- Acute myeloid leukemia

- Acute erythroid leukemia

- Acute lymphoblastic leukemia

- T-cell acute lymphoblastic leukemia

- Adult T-cell leukemia/lymphoma

- (Precursor)T-lymphoblastic leukemia/lymphoma

- "Blast crisis" of chronic myelogenous leukemia

Acute mast cell leukemia is extremely aggressive and has a grave prognosis. In most cases, multi-organ failure including bone marrow failure develops over weeks to months. Median survival after diagnosis is only about 6 months.

In the past 5 years, the research for the mechanisms of BAL does not have a great progress. Some new translocate case of BAL has been reported, such as t(15,17) and t(12,13). For t(15;17), the blasts with morphology of acute lymphoblastic leukemia co-expressed in B-lymphoid and myeloid lineages, and the cytogenetic study showed that the 4q21 abnormalities and t(15;17). However, promyelocytic-retinoid acid receptor rearrangement was not found by fluorescence in situ hybridization on interphase nuclei. Researchers also found some new chemotherapy method for specific cases. For example, The chemotherapy for ALL and gemtuzuab ozogamicin without all-trans-retinoic acid remain complete remission of the BAL patients with t(15,17) for more than 3.7 years.

The detection of BCR-ABL1 chimeric gene neutrophils was also found a good method for diagnosis some cases of BAL.

Totally, there is no breakthrough research for the therapy or mechanisms of BAL in recent years. For most of BAL patients, there is no good therapy method because we still don’t fully understand the mechanisms of BAL. Thus, we have to learn more about the different cases, do more research on the mutation that lead BAL. Beside chemotherapy, we should develop new method such as gene drug for BAL therapy.

Precursor B-cell lymphoblastic leukemia is a form of lymphoid leukemia in which too many B-cell lymphoblasts (immature white blood cells) are found in the blood and bone marrow. It is the most common type of acute lymphoblastic leukemia (ALL). It is sometimes additionally classified as a lymphoma, as designated "leukemia/lymphoma".

It consists of the following subtypes:

- t(9;22)-BCR/ ABL

- t(v;11q23)-MLL rearrangement

- t(1;19)-E2A/PBX1

- t(12;21)-ETV/ CBFα

- t(17;19)-E2A-HLF