Chronic Myeloid Leukemia: A Cancer Not Meant for Children
Chronic Myeloid Leukemia (CML) is a cancer of the white blood cells that forms in the bone marrow and travels through the cardiovascular system. With this particular type of leukemia, it takes much longer to develop symptoms. In fact, it may be a few years before symptoms are showing, according to The American Cancer Society. CML can move into and damage organs such as the spleen. It is rarely seen in children, but is more common in adults.
When leukemia is being diagnosed, it is important to consider whether the abnormal blood cells look mature or immature (like stem cells). In chronic leukemia, the cells have partially matured, but still do not look fully grown. These cells do not fight infection well but are able to survive longer, divide more, and take over the space of normal, healthy cells.
Chronic leukemias take longer to develop and patients may live for years with the disease. CML, however, is more difficult to cure than acute leukemias, which consist of the production and build up of immature cells.
Leukemia is also classified by the specific bone marrow cells affected. CML occurs in early myeloid cells, which are supposed to become platelets, red blood cells, or white blood cells as they mature. Lymphoblastic leukemias, however, start in the preliminary cells that become lymphocytes.
A common indication of CML is pain in the upper stomach region. Often, CML leads to an enlarged spleen or liver, which is the cause of the pain. Weight loss, mild fever, night sweats, and a loss of appetite are also common symptoms of CML. If CML is not diagnosed early on, the symptoms common to later stages include bleeding, infection, and bruises.
In order to diagnose any type of leukemia, a blood test needs to be taken. CML is determined based on increased levels of granulocytes (and is sometime called chronic granulatocytic leukemia) — a category of white blood cells. A bone marrow biopsy is also commonly performed to determine the type of leukemia a patient may have.
Additionally, 95% of patients with CML have the Philadelphia chromosome, the result of a chromosomal translocation between chromosomes 9 and 22 (designated t(9;22)(q34;q11)). The resulting Philadelphia chromosome is significantly smaller than a normal chromosome 22, which is how it was first discovered. As a result of this translocation, is the juxtaposition and fusion of 2 proto-oncogenes, BCR and Abl1. The resulting fusion protein (BCR-ABL) is oncogenic and causes the affected cells to become cancerous.
There are two curative treatments for CML: a bone marrow transplant and an allogenic stem cell transplant. Both of these treatments are relatively intensive and often require long term use of immunosuppressive drugs to prevent complications associated with mis-matched immune systems. Other common treatments include splenectomy, myelosuppressive or leukopheresis therapy, tyrosine kinase inhibitors regimen, and interferon alfa-2b therapy, all of which are designed to reduce the tumor burden
In 2001, the U.S. Food and Drug Administration approved the marketing of the medication imatinib mesylate to treat CML. The research shows that this drug was able to stop the progression of the disease in at least 65 percent of patients. This allowed the production of normal bone marrow stem cells in patients with CML.
This disease is still in need of additional curative treatments and the preclinical research sector focuses their efforts on using tumor models to study innovative medications.
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