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Study tracks leukemia's genetic evolution, may help predict disease course, tailor care
Date:2/14/2013

early in the disease's development, while others emerge over time. The researchers discovered that the initial driver mutations tend to be unique to malignancies that originate in immune system B cells (such as CLL), while those that arose later are often found in other malignancies.

  • In some cases, subgroups of cancer cells that had a fairly minimal presence before treatment came to predominate after treatment. "One way to think of this is that therapy 'leveled the field,' reducing the size of all the subgroups to the same basic level," Wu remarked. "The subgroups were then on an equal footing in competing with one another for survival. The ones that originally were somewhat rare may have gained a competitive advantage."

  • The instances where patients donated CLL samples several years apart proved particularly interesting. Cells from patients who received chemotherapy during those years underwent a great deal of genetic evolution, showing marked increases in some cell subgroups and decreases in others, whereas samples from patients who didn't undergo such therapy were remarkably stable. "This suggests that, in some patients, treatment can actually hasten the evolution of the disease and speed its recurrence," Wu observed.

  • Researchers were able to identify the cell subgroups that became more prominent in the later stages of the disease. In patients where these subgroups were particularly predominant, the disease was likely to worsen rapidly, requiring prompt therapy. "In other words, the faster the disease is evolving, the more likely it is to take an aggressive form," Wu explained.

  • From a practical point of view, advanced "sequencing" technology which analyzes genes into their most basic components combined with new analytical tools offers a feasible way to scan a large number of tissue samples, which is critical for finding links between gene mutations and the features of the disease itself and its response to treatment. The
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  • Contact: Teresa Herbert
    teresa_herbert@dfci.harvard.edu
    617-632-5653
    Dana-Farber Cancer Institute
    Source:Eurekalert  

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