Acute lymphoblastic leukemia pathophysiology: Difference between revisions
Carlos Lopez (talk | contribs) |
Carlos Lopez (talk | contribs) No edit summary |
||
| Line 5: | Line 5: | ||
== Overview == | == Overview == | ||
Generally cancer is caused by damage to [[Deoxyribonucleic Acid|DNA]] that leads to uncontrolled cellular growth causing the development of acute lymphoblastic leukemia. Genetic mutations involved in the pathogenesis of acute lymphoblastic leukemia are related with[[chromosomal translocation]]s. | Generally cancer is caused by damage to [[Deoxyribonucleic Acid|DNA]] that leads to uncontrolled cellular growth causing the development of acute lymphoblastic leukemia. Genetic mutations involved in the pathogenesis of acute lymphoblastic leukemia are related with[[chromosomal translocation]]s. B lymphoblastic leukemia/lymphoma with t(9;22)(q34;q11.2), t(v;11q23); MLL rearranged, t(12;21)(p13;q22) ''TEL-AML1'', t(5;14)(q31;q32)''IL3-IGH'' and t(1;19)(q23;p13.3) ''TCF3-PBX1''. According with the [[French-American-British classification | French-American-British (FAB) classification]] of acute lymphoblastic leukemia, leukemia is divided into 3 subtypes based on the type of cell from which the leukemia developed and its degree of maturity and morphological classification. This is the classification: ALL-L1: small uniform cells, ALL-L2: large varied cells, ALL-L3: large varied cells with [[vacuole]]s (bubble-like features). | ||
Revision as of 20:01, 28 August 2015
|
Acute lymphoblastic leukemia Microchapters |
|
Differentiating Acute lymphoblastic leukemia from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Acute lymphoblastic leukemia pathophysiology On the Web |
|
American Roentgen Ray Society Images of Acute lymphoblastic leukemia pathophysiology |
|
Directions to Hospitals Treating Acute lymphoblastic leukemia |
|
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] Carlos A Lopez, M.D. [4]
Overview
Generally cancer is caused by damage to DNA that leads to uncontrolled cellular growth causing the development of acute lymphoblastic leukemia. Genetic mutations involved in the pathogenesis of acute lymphoblastic leukemia are related withchromosomal translocations. B lymphoblastic leukemia/lymphoma with t(9;22)(q34;q11.2), t(v;11q23); MLL rearranged, t(12;21)(p13;q22) TEL-AML1, t(5;14)(q31;q32)IL3-IGH and t(1;19)(q23;p13.3) TCF3-PBX1. According with the French-American-British (FAB) classification of acute lymphoblastic leukemia, leukemia is divided into 3 subtypes based on the type of cell from which the leukemia developed and its degree of maturity and morphological classification. This is the classification: ALL-L1: small uniform cells, ALL-L2: large varied cells, ALL-L3: large varied cells with vacuoles (bubble-like features).
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On microscopic histopathological analysis, [feature1], [feature2], and feature3] are characteristic findings of [disease name]
[Disease name] is transmitted in [mode of genetic transmission] pattern.
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]
Development of [disease name] is the result of multiple genetic mutations.
Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
The progression to [disease name] usually involves the [molecular pathway].
The pathophysiology of [disease/malignancy] depends on the histological subtype.
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.
According with the World Health Organization (WHO) classification of acute lymphoblastic leukemia, B lymphoblastic leukemia/lymphoma with recurrent genetic abnormalities include:
- B lymphoblastic leukemia/lymphoma with t(9;22)(q34;q11.2), BCR-ABL1
- B lymphoblastic leukemia/lymphoma with t(v;11q23); MLL rearranged
- B lymphoblastic leukemia/lymphoma with t(12;21)(p13;q22) TEL-AML1 (ETV6-RUNX1)
- B lymphoblastic leukemia/lymphoma with hyperdiploidy
- B lymphoblastic leukemia/lymphoma with hypodiploidy
- B lymphoblastic leukemia/lymphoma with t(5;14)(q31;q32) IL3-IGH
- B lymphoblastic leukemia/lymphoma with t(1;19)(q23;p13.3) TCF3-PBX1
According with the French-American-British (FAB) classification of acute lymphoblastic leukemia is divided into 3 subtypes:
- ALL-L1: small uniform cells
- ALL-L2: large varied cells
- ALL-L3: large varied cells with vacuoles (bubble-like features)
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:[1]
- T-cell Acute lymphoblastic leukemia:
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.[2]
- 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 [1]
| 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 |
Gallery
References
- ↑ 1.0 1.1 "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.