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.

JMML accounts for 1-2% of childhood leukemias each year; in the United States, an estimated 25-50 new cases are diagnosed each year, which also equates to about 3 cases per million children. There is no known environmental cause for JMML. Since about 10% of patients are diagnosed before 3 months of age, it is thought that JMML is a congenital condition in these infants

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.

CML accounts for 8% of all leukaemias in the UK, and around 680 people were diagnosed with the disease in 2011.

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.

Prognosis refers to how well a patient is expected to respond to treatment based on their individual characteristics at time of diagnosis. In JMML, three characteristic areas have been identified as significant in the prognosis of patients:

Without treatment, the survival [5 years?] of children with JMML is approximately 5%. Only Hematopoietic Stem Cell Transplantation (HSCT), commonly referred to as a bone marrow or (umbilical) cord blood transplant, has been shown to be successful in curing a child of JMML. With HSCT, recent research studies have found the survival rate to be approximately 50%. Relapse is a significant risk after HSCT for children with JMML. It is the greatest cause of death in JMML children who have had stem cell transplants. Relapse rate has been recorded as high as 50%. Many children have been brought into remission after a second stem cell transplant.

Although not yet formally incorporated in the generally accepted classification systems, molecular profiling of myelodysplastic syndrome genomes has increased the understanding of prognostic molecular factors for this disease. For example, in low-risk MDS, "IDH1" and "IDH2" mutations are associated with significantly worsened survival.

The American Cancer Society estimates that in 2014, about 5,980 new cases of chronic myelogenous leukemia were diagnosed, and about 810 people died of the disease. This means that a little over 10% of all newly diagnosed leukemia cases will be chronic myelogenous leukemia. The average risk of a person getting this disease is 1 in 588. The disease is more common in men than women, and more common in whites than African-Americans. The average age at diagnosis is 64 years, and this disease is rarely seen in children.

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.

Some people have a history of exposure to chemotherapy (especially alkylating agents such as melphalan, cyclophosphamide, busulfan, and chlorambucil) or radiation (therapeutic or accidental), or both (e.g., at the time of stem cell transplantation for another disease). Workers in some industries with heavy exposure to hydrocarbons such as the petroleum industry have a slightly higher risk of contracting the disease than the general population. Xylene and benzene exposure has been associated with myelodysplasia. Vietnam veterans exposed to Agent Orange are at risk of developing MDS. A link may exist between the development of MDS "in atomic-bomb survivors 40 to 60 years after radiation exposure" (in this case, referring to people who were in close proximity to the dropping of the atomic bomb in Hiroshima and Nagasaki during World War II).

Children with Down syndrome are susceptible to MDS, and a family history may indicate a hereditary form of sideroblastic anemia or Fanconi anemia.

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.

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.

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.

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

Taken together, haematological malignancies account for 9.5% of new cancer diagnoses in the United States and 30,000 patients in the UK are diagnosed each year. Within this category, lymphomas are more common than leukemias.

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

Chronic leukemia is an increase of abnormal white blood cells. It differs from acute leukemia, and is categorized as myelogenous or lymphocytic.

Chronic leukemia may refer to:

- Chronic myelogenous leukemia

- Chronic lymphocytic leukemia

- Hairy cell leukemia

Myeloid leukemia is a type of leukemia affecting myeloid tissue.

Types include:

- Acute myeloid leukemia

- Chronic myelogenous leukemia

T-LGLL is a rare form of leukemia, comprising 2-3% of all cases of chronic lymphoproliferative disorders.

Acute myeloid leukemia (AML) is a type of cancer affecting blood cells that eventually develop into non-lymphocyte white blood cells. The disease originates from the bone marrow, the soft inner portion of select bones where blood stem cells develop into either lymphocyte or in this particular condition, myeloid cells. This acute disease prevents bone marrow cells from properly maturing, thus causing an accumulation of immature myeloblast cells in the bone marrow.

Acute myeloid leukemia is more lethal than chronic myeloid leukemia, a disease that affects the same myeloid cells, but at a different pace. Many of the immature blast cells in acute myeloid leukemia have a higher loss of function and thus, a higher inability to carry out normal functions than those more developed immature myeloblast cells in chronic myeloid leukemia (O’Donnell et al. 2012). Acute in acute myeloid leukemia means that the amounts of blast cells are increasing at a very high rate. Myeloid refers to the type of white blood cells that are affected by the condition.

Acute myeloid leukemia is the most common acute leukemia that is affecting the adult population. The 5-year survival rate for the cancer stands at around 26% (ACS, 2016).

M2 acute myeloblastic leukemia with maturation refers to the subtype of acute myeloid leukemia characterized by the maturation stages of the myeloid cell development and the location of the AML1 gene. One of the hallmarks of M2 subtype acute myeloid leukemia is the formation of a fusion protein, AML1-ETO or RUNX1-RUNX1T1, due to a translocation of chromosome 8 to chromosome 21 or t(8;21) (Miyoshi et al., 1991, Andrieu et al., 1996). This cytogenetic abnormality has been found in 90% of M2 acute myeloblastic leukemia; while the other 10% constitutes a mix of M1 and M4 acute myeloid leukemia (GFHC, 1990).

Another translocation between chromosome 6p23 and chromosome 9q34 is also associated with the M2 subtype. The t(6;9) causes the formation of a fusion oncogene made of DEK (6p23) and CAN/NUP214 (9q34). This rare translocation has a poor prognosis compared to the t(8;21) because 70% of t(6;9) acute myeloid leukemia patients have the FLT3-ITD mutation (Schwartz et al., 1983, Kottaridis, 2001). The FLT-ITD mutation is one of the most lethal mutations in acute myeloid leukemia (Chi et al., 2008).

M2 acute myeloblastic leukemia with maturation, as classified by the FAB system, constitutes 25% of adult AML (Wiki Main article: AML).

As noted above, a leukemoid reaction is typically a response to an underlying medical issue. Causes of leukemoid reactions include:

- Severe hemorrhage (retroperitoneal hemorrhage)

- Drugs

- Use of sulfa drugs

- Use of dapsone

- Use of glucocorticoids

- Use of G-CSF or related growth factors

- All-trans retinoic acid (ATRA)

- Ethylene glycol intoxication

- Infections

- Clostridium difficile

- Tuberculosis

- Pertussis

- Infectious mononucleosis (lymphocyte predominant)

- Visceral larva migrans (eosinophil predominant)

- Asplenia

- Diabetic ketoacidosis

- Organ necrosis

- Hepatic necrosis

- Ischemic colitis

- As a feature of trisomy 21 in infancy (incidence of ~10%)

- As a paraneoplastic phenomenon (rare)

Acute eosinophilic leukemia is treated as other subtypes of AML. Response to treatment is approximately the same as in other types of AML.

Atypical chronic myeloid leukemia (aCML) is a type of leukemia. It is a heterogeneous disorder belonging to the group of myelodysplastic/myeloproliferative (MDS/MPN) syndromes.

In aCML many clinical features (splenomegaly, myeloid predominance in the bone marrow with some dysplastic features but without a differentiation block) and laboratory abnormalities (myeloid proliferation, low leukocyte alkaline phosphatase values) suggest the diagnosis of chronic myelogenous leukemia (CML). However the lack of the pathognomonic Philadelphia chromosome and of the resulting BCR-ABL1 fusion point to a different pathogenetic process. Since no specific recurrent genomic or karyotypic abnormalities have been identified in aCML, the molecular pathogenesis of this disease has remained elusive and the outcome dismal (median survival 37 months) with no improvement over the last 20 years. This sharply contrasts with the outcome for CML, for which the prognosis was dramatically improved by the development of imatinib as a specific inhibitor of the BCR-ABL protein and in particular for CML.

In 2012 "SETBP1" was identified as a novel oncogene in aCML; specific somatic mutations of this gene were discovered in people with aCML and related diseases. These mutations, which are identical to the ones present in SGS as germline mutations, impair the degradation of SETBP1 and therefore cause increased cellular levels of the protein.