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A recent article published in The New England Journal of Medicine indicates that the detection of specific genetic alterations may help to individualize therapy for patients with chronic lymphocytic leukemia. Through individualized therapy, patients who are at an increased risk of a cancer recurrence can receive more aggressive treatment to improve survival, while patients with less aggressive cancer can be spared from the side effects caused by extensive treatment.

Chronic lymphocytic leukemia (CLL) is a cancer involving the lymph (immune) system, which includes lymph nodes, blood, and blood vessels found throughout the body, as well as the spleen, thymus, and tonsils. This cancer is found in large amounts in circulating blood and bone marrow (spongy material inside large bones that produces blood forming cells). Chronic lymphocytic leukemia is characterized by the production of atypical lymphocytes. Lymphocytes are specialized immune cells, of which there are 2 types: B and T-cells. These cells are produced in the bone marrow and each has a very specific function in aiding the body to fight infection. The large majority of CLL cases involve mature B-lymphocytes that tend to live much longer than normal, accumulating in the blood, bone marrow, lymph nodes and spleen. This results in overcrowding of these areas, suppressing the formation and function of blood and immune cells that are normally present. Additionally, the cancerous lymphocytes themselves do not function normally, leading to a further decrease in the ability of the body to fight infection. Chronic lymphocytic leukemia is considered to be a slow-growing, or low-grade cancer.

A recent clinical trial assessed the presence of genetic abnormalities in over 300 CLL patients and the prognostic indication of these specific abnormalities. Four specific genetic abnormalities were present in a large percentage of patients, including abnormalities on chromosome bands 13q, 11q, 12q, and 17p. Patients with each genetic abnormality were followed throughout the course of their disease to determine if specific disease characteristics existed in direct association with a genetic abnormality.

Patients in the 17p and 11q groups had more advanced disease upon diagnosis than those in the other groups. Patients with a 17p abnormality had the shortest average treatment-free interval (9 months), and those with the 13q abnormality had the longest average treatment-free interval (92 months). Additionally, patients with the 17p and 11q abnormalities had the shortest average survival time, 32 and 79 months, respectively. Patients with 12q and 13q abnormalities had the longest average survival time, 111 and 133 months, respectively.

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These results appear to indicate a clear association between specific genetic abnormalities and disease characteristics in CLL patients. Researchers conducting this trial report that these genetic aberrations are important independent predictors of the aggressiveness of this disease and patient survival times. Patients with 17p or 11q abnormalities may benefit from more extensive therapy in order to improve survival. Conversely, patients with 12q or 13q abnormalities may be spared from destructive side effects associated with more aggressive therapy.

Patients with CLL may wish to speak with their physician about the risks and benefits of participating in a clinical trial further evaluating genetic testing and the effects these results may have on treatment strategies. Two sources of information about ongoing clinical trials include comprehensive, easy-to-use listing services provided by the National Cancer Institute ( and also provides personalized clinical trial searches on behalf of patients. (The New England Journal of Medicine, Vol 343, No 26, pp 1910-1916, 2000)

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