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Increased expression of APAF-1 in low-risk myelodysplastic syndrome: a possible role in the pathophysiology of myelodysplasia.
- Source :
-
European Journal of Haematology . Jun2010, Vol. 84 Issue 6, p525-530. 6p. 1 Chart, 3 Graphs. - Publication Year :
- 2010
-
Abstract
- Objectives: APAF-1 is a central component of the intrinsic pathway of apoptosis, where APAF-1 dysregulation results in the development of diverse human neoplasms. The aim of this study was to characterize the mRNA expression levels of APAF-1 transcripts in low-risk and high-risk MDS and to elucidate whether the expression levels of APAF-1 transcripts are modulated with increased apoptosis in CD34+ MDS cells undergoing erythroid differentiation. Methods: APAF-1 ( ) expression was verified, by quantitative RT-PCR, in bone marrow aspirates from 33 patients with myelodysplastic syndromes (MDS), at the time of diagnosis, and in erythroid differentiation cultures from CD34+ from normal donors and patients with MDS. Results: APAF-1 expression was significantly higher in low-risk, compared to high-risk MDS, according to IPSS ( P < 0.0001), FAB ( P = 0.0265), and cytogenetic risk ( P = 0.0134). Low-risk MDS-derived differentiated erythroid cells demonstrated an increased expression of APAF-1, compared with normal cells, accompanied by an augmented rate of apoptosis. Conclusions: Increased expression of APAF-1 in low-risk disease and its positive correlation with the apoptotic rate observed during the erythroblast differentiation of low-risk MDS cells may indicate that the modulation of APAF-1, at the transcriptional level, participates in the pathophysiology of MDS. [ABSTRACT FROM AUTHOR]
- Subjects :
- *DYSPLASIA
*PATHOLOGICAL physiology
*APOPTOSIS
*CELL death
*BONE marrow
Subjects
Details
- Language :
- English
- ISSN :
- 09024441
- Volume :
- 84
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- European Journal of Haematology
- Publication Type :
- Academic Journal
- Accession number :
- 50516286
- Full Text :
- https://doi.org/10.1111/j.1600-0609.2010.01429.x