Acute lymphoblastic leukemia pathophysiology
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Acute lymphoblastic leukemia Microchapters |
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Differentiating Acute lymphoblastic leukemia from other Diseases |
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Diagnosis |
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Acute lymphoblastic leukemia pathophysiology On the Web |
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Risk calculators and risk factors for Acute lymphoblastic leukemia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]Shivali Marketkar, M.B.B.S. [3]
Overview
The cause of most Acute lympoblastic leukemias is not known. In leukemias, including acute lymphoblastic leukemia chromosomal translocations occurs regularly and can trigger oncogenes. Some families have a hereditary predisposition. acute lymphoblastic leukemia is associated with exposure to radiation in animals and humans. Malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. There are specific markers for B-cell acute lymphoblastic leukemia and T-cell acute lymphoblastic leukemia
Pathophysiology
The cause of most acute lymphoblastic leukemia is not known. In general, cancer is caused by damage to DNA that leads to uncontrolled cellular growth and spread throughout the body, either by increasing chemical signals that cause growth, or interrupting chemical signals that control growth. This damage may be caused by environmental factors such as chemicals, drugs or radiation.
In leukemias, including acute lymphoblastic leukemia, chromosomal translocation occur regularly. It is thought that most translocations occur before birth during fetal development. These translocations may trigger oncogenes to "turn on", causing unregulated mitosis where cells divide too quickly and abnormally, resulting in leukemia.
Some families have a hereditary predisposition to acute lymphoblastic leukemia.[1]
Acute lymphoblastic leukemia is associated with exposure to radiation and chemicals in animals and humans. The association of radiation and leukemia in humans has been clearly established in studies of victims of the Chernobyl nuclear reactor and atom bombs in Hiroshima and Nagasaki. In animals, exposure to benzene and other chemicals can cause leukemia. Epidemiological studies have associated leukemia with workplace exposure to chemicals, but these studies are not as conclusive. Patients who are treated for other cancers with radiation and chemotherapy often develop leukemias as a result of that treatment.
Malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. Acute lymphoblastic leukemia causes damage and death by crowding out normal cells in the bone marrow, and by spreading (metastasizing) to other organs.
Markers
- B-cell Acute lymphoblastic leukemia:[2]
- T-cell Acute lymphoblastic leukemia:
Shown below is a bone marrow aspirate of a patient with Acute lymphoblastic leukemia (I think that this pic shoul be removed to gallery
Genetics
Cytogenetics, the study of characteristic large changes in the chromosomes of cancer cells, has been increasingly recognized as an important predictor of outcome in Acute lymphoblastic leukemia.[3]
- It has been recognized for many years that some patients presenting with acute leukemia may have a cytogenetic abnormality that is cytogenetically indistinguishable from the Philadelphia chromosome (Ph1). This occurs in about 20% of adults and a small percentage of children with Acute Lymphoblastic leukemia [2]
| Cytogenetic change | Risk category |
|---|---|
| Philadelphia chromosome | Poor prognosis |
| t(4;11)(q21;q23) | Poor prognosis |
| t(8;14)(q24.1;q32) | Poor prognosis |
| Complex karyotype (more than four abnormalities) | Poor prognosis |
| Low hypodiploidy or near triploidy | Poor prognosis |
| High hypodiploidy | Good prognosis |
| del(9p) | Good prognosis |
References
- ↑ New Engl J Med somewhere
- ↑ 2.0 2.1 "National Cancer Institute".
- ↑ Moorman A, Harrison C, Buck G, Richards S, Secker-Walker L, Martineau M, Vance G, Cherry A, Higgins R, Fielding A, Foroni L, Paietta E, Tallman M, Litzow M, Wiernik P, Rowe J, Goldstone A, Dewald G (2007). "Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial". Blood. 109 (8): 3189–97. PMID 17170120.