An accumulation of cytogenetic and molecular genetic events characterizes the progression from MDS to secondary AML: an analysis of 38 paired samples analyzed by cytogenetics, molecular mutation analysis and SNP microarray profiling

Growth and Differentiation Effects of Homer3 on a Leukemia Cell Line

“…Gene-expression detection technology in the hematopoietic cell of AML patients have been applied in scientific research and clinical testing, in hope of identifying candidate genes which may refer to the development and progression of AML and marker of diagnosis or prognosis (Delaunay et al, 2003;Weltermann et al, 2004;Gonzalez Garcia et al, 2006;Foran, 2010;Flach et al, 2011). For example, in the passed several years, the nucleophosmin (PNM1) mutations with normal cytogenetics has been identified a prognostic factors in AML patients (Schnittger et al, 2005), more and more genes would probably provide biomarkers in the future.…”

Gene mutation patterns and their prognostic impact in a cohort of 1185 patients with acute myeloid leukemia

“…[5][6][7][8][9][10][11] For example, acute promyelocytic leukemia (APL, AML-M3) with t(15;17) translocation is associated with a favorable prognosis, [12][13][14] and core-binding factor (CBF) leukemias with t(8;21) translocation in AML-M2 variant (M2v) or inv(16) rearrangement in AML-M4 with eosinophilia (M4eo) have also been reported to have relatively good outcome. 5,7,15 Nevertheless, ϳ 1/2 of AML patients lack typical prognostic karyotypic changes. To improve clinical outcome, it is important to identify specific and accurate predictors in this group of patients using molecular approaches.…”

Molecular Genetic Biomarkers in Myeloid Malignancies

“…85 Approximately a third of MDS cases eventually transform into AML, and new genetic lesions (molecular or cytogenetic) become detectable in more than half of these cases. 99 The spectrums of acquired genetic lesions in de novo and secondary MDS are similar, but their frequencies vary. [99][100][101] Myeloproliferative/myelodysplastic overlap disorders, including chronic myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia, are characterized as having both MDS and MPN-like features.…”

“…99 The spectrums of acquired genetic lesions in de novo and secondary MDS are similar, but their frequencies vary. [99][100][101] Myeloproliferative/myelodysplastic overlap disorders, including chronic myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia, are characterized as having both MDS and MPN-like features. Chronic myelomonocytic leukemia shows persistent peripheral blood monocytosis (.10 9 /L), dysplasia in at least 1 myeloid lineage, fewer than 20% blasts, and lacks BCR-ABL1 and PFGFR rearrangements.…”