Chronic myeloid leukemia.

M W Deininger; J M Goldman

doi:10.1097/00062752-199807000-00010

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Chronic myeloid leukemia.

M W Deininger·J M Goldman

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Abstract

Progress has been made in understanding BCR-ABL-positive leukemias. A new transcript (p230BCR-ABL) has been characterized that is associated with Ph-positive chronic neutrophilic leukemia. The ATM protein appears to be a regulator of ABL activity in response to irradiation damage. Pathways linking BCR-ABL to the BCL-2 family of proteins may be active in Philadelphia-positive cells and inhibit apoptosis. The 62-kD protein constitutively phosphorylated in chronic myeloid leukemia progenitors has been cloned. Ph-negative long-term culture-initiating cells are detectable in many chronic myeloid leukemia patients. The combination of interferon alfa and cytarabine appears to be superior to interferon alfa alone. Autografting with in vivo-purged stem cells may induce prolonged remissions. Specific inhibitors of the BCR-ABL tyrosine kinase are becoming available.

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Antineoplastic Agents Apoptosis Fusion Proteins, bcr-abl Gene Expression Regulation, Neoplastic Humans Leukemia, Myelogenous, Chronic, BCR-ABL Positive Journal Article Research Support, Non-U.S. Gov't Review

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M W Deininger, J M Goldman. 1998. Chronic myeloid leukemia.. https://doi.org/10.1097/00062752-199807000-00010

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