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Leukemia (2003) 17, 691–699. doi:10.1038/sj.leu.2402879

Perspectives on the treatment of chronic phase and advanced phase CML and Philadelphia chromosome positive ALL1

C A Schiffer1, R Hehlmann2 and R Larson3

  1. 1Division of Hematology/Oncology, Karmanos Cancer Institute, Wayne State University School of Medicine, Harper Hospital, Detroit, MI, USA
  2. 2III. Medizinische Klinik, Universitätsklinikum Mannheim, Universität Heidelberg, Mannheim, Germany
  3. 3Section of Hematology/Oncology, Department of Medicine and Cancer Research Center, University of Chicago, Chicago, IL, USA

Correspondence: CA Schiffer, Division of Hematology/Oncology, Karmanos Cancer Institute, Wayne State University School of Medicine, Harper Hospital, 505 Hudson 3990 John R, Detroit, MI 48201, USA. Fax: +1-313 993 0559

1These topics were discussed at the annual meeting of the American Society of Hematology, Orlando, FL, 7–11 December, 2001 in a CME session titled 'Controversies in the management of CML' (Moderator: SD Nimer).

Received 8 August 2002; Accepted 5 December 2002.

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Abstract

Chronic myeloid leukaemia (CML) is a malignant disease of the bone marrow characterised by the presence of the Philadelphia (Ph) chromosome. About 20% of acute lymphoblastic leukaemia (ALL) patients also show this genetic abnormality. A new drug, imatinib (Glivec®, Novartis Pharma AG, Basel, Switzerland, and formerly STI571) is having a profound effect on the treatment and management of all stages of CML and Philadelphia chromosome positive (Ph+) ALL. New treatment algorithms are being developed. Should imatinib replace or be combined with existing therapies? To address this question, we review the pros and cons of therapy with interferon-alpha (IFN-alpha), allogeneic transplantation, autologous transplantation, imatinib, and in the case of Ph+ ALL, chemotherapy and experimental approaches. Conservative and aggressive treatments will be discussed and new molecular methods of monitoring cytogenetic response and their significance will also be reviewed.

Keywords:

imatinib, IFN-alpha, SCT, CML, Ph+ ALL

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