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Treatment of acute lymphoblastic leukemia in adults focuses on the initial assessment of prognostic relevant genetic features as well as response-guided therapy based on molecular data. In at least half of adult acute lymphoblastic leukemia patients, clonal chromosomal abnormalities can be identified that deregulate candidate oncogenes or transcription factors by introducing a heterologous promoter or enhancer. Altered cell cycle progression or upregulated tyrosine kinase activity are other important mechanisms. Most of the translocations can lead to the generation of fusion genes that are translated into chimeric oncogeneic proteins, such as BCR-ABL, providing targets for novel therapeutic agents.