Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 96, Issue 2, Pages 153-163Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-012-1123-9
Keywords
AML; Cytogenetics; Molecular genetics; Minimal residual disease
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Funding
- National Institute for Health Research (NIHR) [RP-PG-0108-10093]
- Leukaemia & Lymphoma Research of Great Britain
- Guy's and St. Thomas' Charity
- MRD Work-package of the European LeukemiaNet [WP12]
- Deutsche Krebshilfe
- Medical Research Council [MR/J006742/1] Funding Source: researchfish
- National Institute for Health Research [RP-PG-0108-10093] Funding Source: researchfish
- National Institutes of Health Research (NIHR) [RP-PG-0108-10093] Funding Source: National Institutes of Health Research (NIHR)
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An increasing number of cytogenetic and molecular genetic aberrations have been identified in acute myeloid leukaemia (AML), highlighting the biological heterogeneity of the disease. Moreover, the characterisation of specific molecular abnormalities provides the basis for targeted therapies, such as all trans retinoic acid (ATRA) and arsenic trioxide treatment in acute promyelocytic leukaemia or tyrosine kinase inhibitors in AML with FLT3 mutations. Several cytogenetic and molecular genetic changes have been shown to be prognostically relevant and have been acknowledged in the latest WHO classification of AML as separate entities. A detailed marker assessment at diagnosis is crucial for risk-stratification of AML patients, allowing the identification of those at high risk of relapse, who may benefit from early allogeneic stem cell transplantation. Finally, molecular markers are important for the detection of minimal residual disease after initial therapy and during long-term follow-up, which enables a more tailored treatment approach for individual AML patients.
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