Results 351 to 360 of about 1,006,148 (403)
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Hematology, 2002
AbstractIn this chapter, Drs. Keating and Willman review recent advances in our understanding of the pathophysiology of acute myeloid leukemia (AML) and allied conditions, including the advanced myelodysplastic syndromes (MDS), while Drs. Goldstone, Avivi, Giles, and Kantarjian focus on therapeutic data with an emphasis on current patient care and ...
Francis J, Giles +5 more
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AbstractIn this chapter, Drs. Keating and Willman review recent advances in our understanding of the pathophysiology of acute myeloid leukemia (AML) and allied conditions, including the advanced myelodysplastic syndromes (MDS), while Drs. Goldstone, Avivi, Giles, and Kantarjian focus on therapeutic data with an emphasis on current patient care and ...
Francis J, Giles +5 more
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Journal of the National Comprehensive Cancer Network, 2008
Approximately 13,290 people will be diagnosed with acute myeloid leukemia (AML) in 2008, and 8820 patients will die of the disease. As the population ages, the incidence of AML, along with myelodysplasia, appears to be rising. Clinical trials have led to significant treatment improvements in some areas, primarily acute promyelocytic leukemia.
Margaret R, O'Donnell +19 more
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Approximately 13,290 people will be diagnosed with acute myeloid leukemia (AML) in 2008, and 8820 patients will die of the disease. As the population ages, the incidence of AML, along with myelodysplasia, appears to be rising. Clinical trials have led to significant treatment improvements in some areas, primarily acute promyelocytic leukemia.
Margaret R, O'Donnell +19 more
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SEPHguarding acute myeloid leukemia
Cell Stem Cell, 2022Adaptive aberrant gene regulation is a hallmark of malignant growth and therapy resistance in acute myeloid leukemia (AML). In this issue of Cell Stem Cell, Eagle et al. identified oncogenic enhancer-driven overexpression of selenophosphate synthetase 2 (SEPHS2) as an opportunity for targeted mitigation of malignant cell growth in AML.
Malini, Gupta, Britta, Will
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Current Opinion in Hematology, 1998
Progress has been made in understanding BCR-ABL-positive leukemias. A new transcript (p230BCR-ABL) has been characterized that is associated with Ph-positive chronic neutrophilic leukemia. The ATM protein appears to be a regulator of ABL activity in response to irradiation damage.
M W, Deininger, J M, Goldman
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Progress has been made in understanding BCR-ABL-positive leukemias. A new transcript (p230BCR-ABL) has been characterized that is associated with Ph-positive chronic neutrophilic leukemia. The ATM protein appears to be a regulator of ABL activity in response to irradiation damage.
M W, Deininger, J M, Goldman
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Current Opinion in Oncology, 1992
Chronic myeloid leukemia is a clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia chromosome, involving myeloid, erythroid, megakaryocytic, B lymphoid, and sometimes T lymphoid cells but not marrow fibroblasts.
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Chronic myeloid leukemia is a clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia chromosome, involving myeloid, erythroid, megakaryocytic, B lymphoid, and sometimes T lymphoid cells but not marrow fibroblasts.
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New England Journal of Medicine, 1999
Over the past twenty years, clinical and laboratory studies have led to important new insights into the biology of chronic myeloid leukemia. Basic science has defined the molecular pathogenesis of chronic myeloid leukemia (CML) as unregulated signal transduction by the Bcr-Abl tyrosine kinase.
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Over the past twenty years, clinical and laboratory studies have led to important new insights into the biology of chronic myeloid leukemia. Basic science has defined the molecular pathogenesis of chronic myeloid leukemia (CML) as unregulated signal transduction by the Bcr-Abl tyrosine kinase.
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Curing Chronic Myeloid Leukemia
Current Hematologic Malignancy Reports, 2012The use of tyrosine kinase inhibitors (TKIs) targeted against the BCR-ABL1 oncoprotein has proven remarkably successful in chronic myeloid leukemia (CML) and long-term survival has become a reality. Despite this outstanding progress, detection of minimal residual disease precludes therapy termination in most TKI-receiving patients.
Delphine, Rea +4 more
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Current Opinion in Hematology, 1997
The molecular origin of the BCR-ABL chimeric gene is now reasonably well defined; a new breakpoint cluster region in the BCR gene, designated mu-bcr, has recently been identified. p210BCR-ABL binds with or phosphorylates a wide variety of intracellular proteins but the mechanism by which it exerts its oncogenic potential is not yet known.
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The molecular origin of the BCR-ABL chimeric gene is now reasonably well defined; a new breakpoint cluster region in the BCR gene, designated mu-bcr, has recently been identified. p210BCR-ABL binds with or phosphorylates a wide variety of intracellular proteins but the mechanism by which it exerts its oncogenic potential is not yet known.
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THERAPY-RELATED MYELOID LEUKEMIA
Hematology/Oncology Clinics of North America, 1996One of the most serious possible consequences of cancer therapy is the development of a second cancer, especially leukemia. Several distinct subsets of therapy-related leukemia can be distinguished currently. These include classic therapy-related myeloid leukemia, leukemia that follows treatment with agents that inhibit topoisomerase II, acute ...
M J, Thirman, R A, Larson
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Mayo Clinic Proceedings, 2006
Acute myeloid leukemia (AML) is a group of several different diseases, the treatment and outcome of which depend on several factors, including leukemia karyotype, patient age, and comorbid conditions. Despite advances in understanding the molecular biology of AML, its treatment remains challenging.
Elias J, Jabbour +2 more
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Acute myeloid leukemia (AML) is a group of several different diseases, the treatment and outcome of which depend on several factors, including leukemia karyotype, patient age, and comorbid conditions. Despite advances in understanding the molecular biology of AML, its treatment remains challenging.
Elias J, Jabbour +2 more
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