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Stem-cell mobilization for autografting in chronic myeloid leukemia

✍ Scribed by A.M. Carella; L. Celesti; E. Lerma; A. Dejana; F. Frassoni


Publisher
Elsevier Science
Year
1997
Tongue
English
Weight
602 KB
Volume
11
Category
Article
ISSN
0268-960X

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✦ Synopsis


In this article, the rationale for autografting in chronic myeloid leukemia is reviewed, and alternative therapeutic approaches to the use of granulocyte-colony stimulating factor and chemotherapymobilized peripheral blood stem cells are discussed. The data from patients treated using the original ICE (idarubicin, cytarabine, etoposide), or the shorter course mini-ICE protocols are considered, with special emphasis on those patients who received their chemotherapy regimens soon after diagnosis and prior to any treatment with interferon a.

The appropriate design of a trial to test the value of autografting in chronic myeloid leukemia is discussed, as is the optimal timing of collections to achieve the maximal yield and purity of Phnegative peripheral blood stem cells.

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease that is due to a unique gene rearrangement occurring within the pluripotent stem cell. Its main feature is the formation of a fusion gene (BCR-ABL) with increased tyrosine kinase activity generating a transforming activity for myelopoiesis. From a clinical point of view, CML develops from an initial chronic phase (CP) to accelerated and terminal blastic phases.

Allografting has proven to be the only therapeutic procedure capable eradicating the disease, even if it cannot be employed in all patients. In fact, most patients are beyond the recommended age limit or without a human leukocyte-antigen-(HLA-) matched or partially matched unrelated donor. Besides, one must consider the transplant-related mortality rate of approximately 40% within the first 100 days after transplantation.


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## Abstract Chronic Myeloid Leukemia (CML), a myeloproliferative disease of stem cell origin, is characterized by the presence of the Philadelphia (Ph) chromosome and the __bcr‐abl__ oncogene. The BCR‐ABL fusion gene product, thought to be causative in CML, has multiple effects on diverse cell func