[Pathobiology of acute myeloid leukemia].
Acute myeloid leukemia (AML) arises from the clonal expansion of primitive myeloid precursor cells. A series of genetic alterations leads to a perturbation of normal developmental programs affecting growth, maturation and differentiation of hematopoietic cells. As a consequence, immature leukemic cells that have the ability to divide and proliferate, but lack normal differentiation mechanisms, accumulate in the bone marrow. This, in turn, leads to a severe impairment of normal hematopoiesis. Over the last several years, a number of clinical and basic research studies have elucidated important pathogenetic mechanisms leading to the initiation of AML. The identification of numerous chromosomal aberrations and mutations specific for AML has deepened our insights into the biology of AML and has allowed to improve our diagnostic tools, the definition of prognostic subgroups and therapeutic concepts.
Christ
Oliver
O
Medizinische Klinik und Poliklinik III, Klinikum der Universität München-Grosshadern.
Feuring-Buske
Michaela
M
Hiddemann
Wolfgang
W
Buske
Christian
C
D014408:Biomarkers, Tumor / Q000235:genetics; D001853:Bone Marrow / Q000473:pathology; D002454:Cell Differentiation / Q000235:genetics; D002455:Cell Division / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000473:pathology; D002869:Chromosome Aberrations; D006410:Hematopoiesis / Q000235:genetics; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000175:diagnosis / Q000235:genetics / Q000473:pathology*; D009154:Mutation / Q000235:genetics; D023461:Myeloid Progenitor Cells / Q000473:pathology; D011379:Prognosis
D014408:Biomarkers, Tumor