Biologic characteristics of acute leukemia after myelodysplastic syndrome

Abstract

Ten patients with acute leukemia after primary myelodysplastic syndrome (MDS-AL) were examined to clarify the biologic nature of the leukemic cells in comparison with that of de novoacute myelocytic leukemia (AML). The morphologic and cytochemical features of the leukemic cells from all these patients corresponded well to those of de novo AML, and they were diagnosed with MDS-AML. Phenotypically, the frequent expression of the lymphocyte activation antigens, CD25 and CD30, was characteristic in MDS-AML. The in vitro response of MDS-AML cells to various growth factors was similar to that of de novo AML cells. Transforming growth factor ,81 (TGFj31) suppressed YELODYSPLASTIC syndrome (MDS) is recog-

CD90/Thy‐1 is preferentially expressed on blast cells of high risk acute myeloid leukaemias*

“…Taken together, our data indicated that the expression of CD90 was significantly higher in those AML subtypes usually characterized by a poor prognosis, such as sAML, elderly AML, de novo AML with unfavourable cytogenetics or unfavourable drug‐resistance profile. This corroborates the notion indicating these specific AML subsets as almost overlapping entities sharing several clinical and biological features, including a worse prognosis (Hann et al , 1997; Leith et al , 1997; Rosenfeld & Kantarjian, 2001), a phenotype of blast cells more often expressing CD34 (Masuya et al , 1993; Rosenfeld & Kantarjian, 2001) and, as shown here, CD90, as well as a pathogenesis characterized by progressive and multiple genetic damage, eventually leading to a complete dysregulation of cell growth and differentiation (Heaney & Golde, 1999). The close similarities of these diseases with MDS prompted us to investigate the expression of CD90 by the CD34‐expressing cell fraction of MDS.…”

Bone marrow ‐ mesenchymal stem cells impact on the U937 cells in the presence of staphylococcal enterotoxin B (SEB)

“…57 In the AML, blast cells escape from the negative impressions of TGFβ by making a noticeable reduction in the number of TGF-β1 high affinity binding sites. 58 Based on our results, hBM-MSCs and hBM-MSC-CM increase the transcription and expression of TGFβ in the U937 cells. The probable mechanism for this increment maybe through activation of P38 MAPK, ERK, and JNKcascades.…”

“…This soluble factor is generated by the cancer cells to block the growth of surrounding cells or lead to MSCs attraction and homing in on the tumour microenvironment . In the AML, blast cells escape from the negative impressions of TGF‐β by making a noticeable reduction in the number of TGF‐β1 high affinity binding sites …”

Identification and Hematopoietic Potential of CD45 − Clonal Cells with Very Immature Phenotype (CD45 − CD34 − CD38 − Lin − ) in Patients with Myelodysplastic Syndromes

“…One possible explanation for this failure is that the frequency of CD45 − CD34 − CD38 − Lin − cells in normal and de novo AML samples is too low to be detected. De novo AML has quite different biological characteristics from those of MDS and AL‐MDS [37, 38], and thus this failure in de novo AML is not surprising. A second possibility is that derangement of the cell‐surface antigens of malignant cells in MDS samples produces CD45 − CD34 − CD38 − Lin − cells, which do not exist in normal or de novo AML samples.…”