期刊
AMERICAN JOURNAL OF CLINICAL PATHOLOGY
卷 130, 期 4, 页码 635-641出版社
OXFORD UNIV PRESS INC
DOI: 10.1309/2450EGK3V0XK8D9D
关键词
p38 mitogen-activated protein kinase; myeloproliferative disorder; myelodysplastic syndrome
类别
The goal of the present study was to evaluate the activation patterns of p38 mitogen-activated protein kinase (MAPK) in myeloproliferative disorders (MPDs) and myelodysplastic syndromes (MDSs). Phosphorylated (activated) p38 MAPK was analyzed immunohistochemically in formalin-fixed decalcified bone marrow core biopsy specimens from 32 MPD, 33 MDS, and 11 control cases. Moderate p38 activation was commonly seen in MDS, whereas weak p38 activation was seen in all MPD cases and all control cases but I in the erythroid lineage. In myeloid and megakaryocytic lineages, strong p38 activation was more commonly observed in MDS compared with AIPD (myeloid, 22133 vs 2132; P < .0001; megakaryocytic, 18123 vs 5132; P < .0001) and control (myeloid, 22/33 vs 2/11; P = .012; megakaryocytic, 18/23 vs 3/9; P = .035) cases. Furthermore, weak p38 activation was observed in myeloid and megakaryocytic lineages in MPD compared with control (myeloid, 15/32 vs 1/11; P =.033; megakaryocytic, 16132 vs 019; P = .007) cases. Increased p38 MAPK activation may have a role in inhibiting hematopoiesis leading to cytopenias in MDS, and relatively decreased p38 activation in MPD might promote hematopoiesis, resulting in cytosis.
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