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The American Society of Hematology 2000 Education Program: 2000 Education Program Co-Chairs:
Nancy Berliner, M.D., Yale University School of Medicine, New Haven, CT
The 2000 Education Program will be held Saturday December 2, and Sunday, December 3, 2000 Chair: Hagop M. Kantarjian, M.D., M.D. Anderson Cancer Center, Houston, TX Speakers:
Rapid progress is occurring in research related to the biology and therapy of CML. Over the last 2 decades, 4 major therapeutic approaches have changed drastically the prognosis in CML: 1) allogeneic stem cell transplant (SCT); 2) interferon alpha (IFN-A) based regimens; 3) donor lymphocyte infusions (DLI); and 4) BCR-ABL tyrosine kinase inhibitors such as STI571 (signal transduction Inhibitor 571). Each modality has exploited and targeted different aspects of CML biology, and is associated with different risk-benefit ratios. Allogeneic SCT is associated with long-term event-free survival rates of 30% to 80% (depending on CML phase, patient age, donor matching, others) and with 1-year mortality rates of 10% to 60%. IFN-A with or without ara-C is associated with a median survival of 7 to 9 years, and with a 10-year survival rate of 70% to 80% among patients achieving a major cytogenetic response. DLI has proven the concept of graft-versus-tumor effect, inducing complete remissions in 70% of patients who relapse with active chronic phase CML post allogeneic SCT. STI571 may be the most important discovery yet in the treatment of CML. STI571 induces objective but transient responses in 40% to 50% of patients in CML blastic phase. In accelerated phase, the response rate with STI571 exceeds 70%, and these responses are durable. In chronic phase CML, STI571 given at greater than or equal to 300mg daily to patients who failed IFN-A produces a complete hematologic response (CHR) in over 90% of patients. Cytogenetic response rates are unknown yet, although early results suggest cytogenetic response rates of greater than or equal to 50%, which may be major in greater than or equal to 30%. The maturing results with STI571 may soon change current recommendations regarding the relative roles of established modalities such as allogeneic SCT and IFN-A. Important questions include: 1) whether STI571 therapy alone may be sufficient to induce long-term survival and event-free survival in CML, or whether it needs to be combined simultaneously or sequentially with IFN-A and ara-C; and 2) what would the indications for frontline allogeneic SCT be in relation to STI571 therapy? Other investigational modalities that will be discussed include: 1) PEG-interferon, 2) homoharringtonine, 3) decitabine, 4) intensive chemotherapy, and 4) CML vaccines. The new discoveries in CML biology will also be discussed in relation to potential new targets for CML therapy.
Source: American Society of Hematology
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