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Reversibility of acute B-cell leukaemia induced by BCR-ABL1.

Cancer is thought to arise from multiple genetic events that establish irreversible malignancy. A different mechanism might be present in certain leukaemias initiated by a chromosomal translocation. We have taken a new approach to determine if ablation of the genetic abnormality is sufficient for reversion by generating a conditional transgenic model of BCR-ABL1 (also known as BCR-ABL)-induced leukaemia. This oncogene is the result of a reciprocal translocation and is associated with different forms of leukaemia. The most common form, p210 BCR-ABL1, is found in more than 90% of patients with chronic myelogenous leukaemia (CML) and in up to 15% of adult patients with de novoacute lymphoblastic leukaemia (ALL). Efforts to establish a useful transgenic model have been hampered by embryonic lethality when the oncogene is expressed during embryogenesis, by reduced penetrance or by extremely long latency periods. One model uses the 'knock-in' approach to induce leukaemia by p190 BCR-ABL1(ref. 10). Given the limitations of models with p210, we used a different experimental approach. Lethal leukaemia developed within an acceptable time frame in all animals, and complete remission was achieved by suppression of BCR-ABL1expression, even after multiple rounds of induction and reversion. Our results demonstrate that BCR-ABL1is required for both induction and maintenance of leukaemia.

Pubmed ID: 10615128


  • Huettner CS
  • Zhang P
  • Van Etten RA
  • Tenen DG


Nature genetics

Publication Data

January 10, 2000

Associated Grants


Mesh Terms

  • Adult
  • Animals
  • Bone Marrow Cells
  • Burkitt Lymphoma
  • Fusion Proteins, bcr-abl
  • Humans
  • Immunoblotting
  • Mice
  • Mice, Transgenic
  • Neoplasm Transplantation