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What Is the Optimal Therapy for Childhood AML?

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The past 30 years have seen tremendous advances in the treatment of pediatric leukemia. What was once an invariably fatal diagnosis is now quite curable in close to 80% of cases. Unfortunately for children with acute myelogenous leukemia (AML), most of these developments have been in the treatment of acute lymphoblastic leukemia (ALL); even today, nearly half of all children diagnosed with AML will die of the disease.

The use of intensive therapy over a brief period of time has produced dramatic improvements in outcome for pediatric patients with acute myelogenous leukemia (AML), as has been demonstrated in studies by the major cooperative groups in the United States and Europe. Still, despite high-intensity chemotherapy and bone marrow transplantation, only about half of the children diagnosed with AML are cured. Future improvements are unlikely to come from further increases in chemotherapy intensity. Alternative approaches, such as risk-directed therapy based on different prognostic criteria; differentiation therapy with all-trans-retinoic acid (ATRA, Vesanoid), arsenic trioxide (Trisenox), or azacytidine; and immunotherapy with monoclonal antibodies, tumor vaccines, or cytokines may lead to further advances. [ONCOLOGY 16:1057-1070, 2002]

Improvement in pediatric acute myelogenous leukemia (AML) over the past 30 years has been only modest. Although rates of complete remission induction have climbed steadily to 85% or 90%, cure rates remain in the 50% to 60% range. These figures may inspire envy from medical oncologists treating adults with AML, but they lag far behind the successes in treating pediatric acute lymphocytic leukemia (ALL).

PORTLAND, Oregon-Giving erythropoietic therapy to chronic myelogenous leukemia (CML) patients does not appear to interfere with their response to imatinib mesylate (STI571, Gleevec) therapy, according to a retrospective study of 37 patients treated in the Leukemia Center at Oregon Health and Science University in Portland (ASCO abstract 106).

Gleevec Effective as First-Line Therapy of CML: IRIS Trial

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ASCO-In a phase III study, imatinib mesylate (Gleevec), formerly known as STI571, produced a 96% complete hematologic response rate and a 68% complete cytogenetic response rate in newly diagnosed chronic myeloid leukemia (CML) patients, Brian Druker, MD, said on behalf of the IRIS (International Randomized Interferon vs STI-571) Study Group at the 38th Annual Meeting of the American Society of Clinical Oncology (abstract 1).

IOM Reverses Finding of Childhood AML Link to Parent’s Vietnam Service

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WASHINGTON-After further review, a committee of the Institute of Medicine (IOM) has rescinded its earlier finding of a suggestive link between the exposure of veterans to herbicides used during the Vietnam War and an increased risk of their offspring developing acute myelogenous leukemia (AML). The committee’s reanalysis followed the finding that one study that it had relied on was in error.

Failure of treatment in chronic lymphocytic leukemia (CLL) is often characterized by increased expression of the antiapoptosis protein bcl-2. High levels of bcl-2 protein block the apoptotic death machinery at the mitochondrial level by maintaining the permeability transition pore (PTP) in the closed position.

Treatment of Acute Myelogenous Leukemia

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There have been significant advances in our understanding of the biology of acute myelogenous leukemia (AML), and to a lesser extent, in its treatment. Dr. Estey has provided an excellent overview of the current state of the clinical management of the disease. He has described both the standard therapeutic approaches, including allogeneic hematopoietic stem cell transplantation, as well as the role of investigational therapy. The present state of clinical research in AML is reviewed in some detail in the context of the broad clinical investigation of the disease at the M. D. Anderson Cancer Center. Dr. Estey makes a strong argument for the early consideration of investigational therapy, focusing on patients for whom "standard" therapy is demonstrably inadequate.

Treatment of Acute Myelogenous Leukemia

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Therapeutic strategies are evolving for the treatment of patients with newly diagnosed acute myelogenous leukemia (AML), as well as for those with relapsed or refractory disease. Clinical and laboratory studies have demonstrated that AML is not a single disease, but a heterogeneous group of diseases with different clinical features and natural histories. There are variable responses to therapy depending on both the biologic characteristics of the disease and the clinical characteristics of the patient. Nevertheless, studies evaluating the outcomes of relatively large numbers of patients with newly diagnosed AML show that the majority still die of their disease.[1-3]

These reports are written by oncologists from Pacific Shores Medical Group (a large group practice in Long Beach, California). The reports are primarily based on notes taken at the American Society of Clinical Oncology yearly meeting (San Francisco, May 2001). The reports include our impressions (shown in italic type) of the clinical significance of the studies. The information is intended to help you get updated on new developments in oncology. The coverage of the meeting is not meant to be comprehensive, but rather focused on highlights that we consider most interesting or relevant.

Treatment of Acute Myelogenous Leukemia

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The treatment of patients with acute myelogenous leukemia (AML) ranges from palliative care only, to standard therapy, to investigational approaches. Acute myelogenous leukemia is, in fact, several different diseases, and the percentage of clinical responses varies with disease and prognostic subsets.

R115777 Has Significant Activity in CML and Myelofibrosis

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HOUSTON-The farnesyl transferase inhibitor R115777 (tipifarnib, also known as Zarnestra) produced an overall response rate of 33% in patients with chronic myelogenous leukemia (CML) and decreased splenomegaly in most patients with myelofibrosis, but was not effective in multiple myeloma, reported Deborah Thomas, MD, at the 43rd Annual Meeting of the American Society of Hematology. Dr. Thomas is assistant professor in the Department of Leukemia at The University of Texas M. D. Anderson Cancer Center in Houston.

Long Survival Confirmed in CML Patients Who Respond to Interferon

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ORLANDO-Patients with chronic myelogenous leukemia (CML) who have a complete cytogenetic response (CCgR) to interferon-alfa have a long survival, and low-risk patients have a projected 10-year survival of more than 80%, Francesca

With Longer Follow-Up, Imatinib Continues to Improve Response Rates in CML

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ORLANDO, Florida-Updated data from two phase II trials show that imatinib mesylate (Gleevec, STI571) continues to improve response rates for patients with chronic myelogenous leukemia (CML) who did not respond to interferon therapy or are in blast crisis. With follow-up of 12 months or more, overall and complete response rates are proving to be durable and toxicities tolerable

Imatinib Produces Excellent Clinical Responses in Newly Diagnosed CML

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ORLANDO-Imatinib mesylate (STI-571, Gleevec) is showing excellent results in newly diagnosed patients with chronic myelogenous leukemia (CML) in the early chronic phase, scientists reported at the 43rd Annual Meeting of the American

Imatinib Plus Interferon Produces High Rate of Hematologic Response in CML

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ORLANDO, Florida-Two phase I/II studies indicate that combination treatment with imatinib mesylate (Gleevec, also known as STI571) produces a high rate of hematologic response in patients in the chronic phase of chronic myelogenous leukemia (CML). Dose-limiting toxicities were mainly hematologic, and researchers advocate further studies were recommended to establish efficacy and recommended dosing.

Molecular Studies Suggest Combining Imatinib With Other Agents in Resistant CML

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MANNHEIM, Germany-Despite encouraging initial responses, patients with chronic myelogenous leukemia (CML) frequently become resistant in the advanced, or blast crisis, phase of the disease after initially responding to selective inhibition of the Bcr-Abl tyrosine kinase by imatinib (Gleevec, also known as STI571).