Over the past 15 years, important developments in the cell and molecular biology of chronic myeloid leukemia (CML) have produced significant changes in understanding of the pathophysiology of the disease. In this article we deal essentially with cell biology as a basis for autografting. The most important achievements of the past years are summarized. There is an exodus of normal hematopoietic cells from bone marrow at the beginning of leukemic invasion. Normal early hematopoietic progenitors (LTC-IC) are preserved at diagnosis and are much more frequent than the Ph-positive counterpart; however, PH-negative LTC-IC rapidly decline with time without a parallel increase of PH-positive LTC-IC. Therefore, probably leukemic stem cells are much fewer than previously thought. Nevertheless, a frequency of Ph-positive KTC-IC of 1/5 10(6) mononuclear cells corresponds with a remarkable tumor burden. Interferon preserves Ph-progenitors in cytogenic remitters. From these studies a new strategy for autografting patients with CML has been developed and is described here. Questions raised by these new techniques are also addressed.
|Number of pages||8|
|Journal||Current Oncology Reports|
|Publication status||Published - Mar 2000|
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