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Previous Volume 340:1330-1340 April 29, 1999 Number 17 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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In the past decade clinical and laboratory studies have led to important new insights into the biology of chronic myeloid leukemia (CML). Basic science has defined the molecular pathogenesis of CML as unregulated signal transduction by a tyrosine kinase. Clinical science has demonstrated that it is curable through immune-mediated elimination of leukemia cells by allogeneic T lymphocytes.

Clinical Features

CML is a malignant clonal disorder of hematopoietic stem cells that results in increases in not only myeloid cells but also erythroid cells and platelets in peripheral blood and marked myeloid hyperplasia in the bone marrow (Figure 1A, Figure 1B, . . . [Full Text of this Article]

Molecular Pathophysiology

Mechanism of Leukemogenesis

Treatment Options

Allogeneic Bone Marrow Transplantation

The Role of the Graft-Versus-Leukemia Effect in Curing CML

Interferon Alfa

Clinical Decision Making: Transplantation versus Interferon Alfa Therapy

Novel Treatments

Autografts

Molecular Therapy

Conclusions

Source Information

From the Division of Hematology and Oncology, Department of Medicine and Molecular Biology Institute, University of California at Los Angeles, Los Angeles.

Address reprint requests to Dr. Sawyers at 11-934 Factor Bldg., UCLA/Hematology–Oncology, 10833 Le Conte Ave., Los Angeles, CA 90095-1678, or at csawyers@med1.medsch.ucla.edu.

References

Related Letters:

Chronic Myeloid Leukemia
Nash I., Sawyers C. L.
Extract | Full Text  
N Engl J Med 1999; 341:765, Sep 2, 1999. Correspondence

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