期刊
EUROPEAN JOURNAL OF HAEMATOLOGY
卷 75, 期 6, 页码 485-491出版社
WILEY
DOI: 10.1111/j.1600-0609.2005.00551.x
关键词
myelodysplastic syndromes; microvessel density; tumor necrosis factor-alpha; trephine bone marrow biopsy
类别
Objectives: An excessive intramedullar progenitor cell apoptosis, to which elevated expression of tumor necrosis factor-alpha (TNF-alpha) might contribute, is considered the main cause of inefficient hematopoiesis in myelodysplastic syndromes ( MDS). Enhanced bone marrow ( BM) angiogenesis is regarded as an essential cofactor in the progression of MDS to acute myelogenous leukemia ( AML) and microvessel formation may be induced by TNF-alpha as well. To investigate TNF-alpha signaling and neoangiogenesis as potential molecular pathways for therapeutic intervention in MDS with respect to the various MDS subtypes, we performed a morphological and clinico-pathological study on a large series of paraffin-embedded trephine BM biopsies. Methods: TNF-alpha expression and BM vessels were immunohistochemically analyzed on 89 paraffin-embedded BM biopsies from patients with MDS and secondary AML, including 12 control samples. Data were correlated with clinico-pathological and laboratory parameters and analyzed for their prognostic significance considering overall survival. Results: TNF-alpha was over-expressed in MDS patients, especially in those with refractory anemia and its expression correlated with BM cellularity and with magnitude of anemia as well as with microvessel density (MVD). TNF-alpha over-expression was associated with premature deaths. MVD was increased in MDS and secondary AML and correlated with marrow cellularity and expression of TNF-alpha, but was not of prognostic significance. Conclusions: TNF-alpha expression and MVD are elevated in MDS and secondary AML. TNF-alpha expression in BM progenitor cells appears to negatively impact erythropoiesis and overall survival in MDS, and may serve as a potential therapeutic target in patients with hypercellular MDS with marked anemia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据