Primary Thrombocytosis Clinical Trial
Official title:
The Role of Circ0014614 in the Formation and Development of ET
Research on the Role of Circ0014614 in the Formation and Development of ET
In recent years, tumor niche involved in the development of myeloproliferative disease（MPN）, which is remodelled by stem progenitor cells driving gene mutation, has attracted attention, but the reason and mechanism of remodelling microenvironment by mutated hematopoietic stem cells（ HSCs） are poorly understood. Our previous studies have shown that there is an obstacle in the transport of extracellular vesicles circ0014614 from MEPs in ET patients, which is enriched in the cytoplasm of megakaryocyte-erythroid progenitor（MEPs）, causing abnormal proliferation and reduced apoptosis of MEPs. The amplified MEPs affect the ossification of Mesenchymal stem cells（MCSs）. Based on this, we propose a hypothesis that circ0014614 may cause abnormal amplification of MEPs, reshape niche, induce ossification of MCSs, and abnormal amplification of osteoblasts（OBCs） through a certain pathway, promoting the formation and development of ET. This study will expand the collection of bone marrow samples from Essential thrombocytosis（ET） patients, detect the differences in circ0014614 levels in peripheral blood and bone marrow before and after treatment, and predict its downstream microRNA and mRNA through bioinformatics analysis to speculate its role in the occurrence and development of the disease. In recent years, tumor niche involved in the development of MPN, which is remodelled by stem progenitor cells driving gene mutation, has attracted attention, but the reason and mechanism of remodelling microenvironment by mutated HSCs are poorly understood. Our previous research has shown that there is an obstacle in the transport of extracellular vesicles circ0014614 from MEPs in ET patients, which is enriched in the cytoplasm of MEPs, causing abnormal proliferation and reduced apoptosis of MEPs. The amplified MEPs affect the ossification of MCSs. Based on this, we propose a hypothesis that circ0014614 may cause abnormal amplification of MEPs, reshape niche, induce ossification of MCSs, and abnormal amplification of OBCs through a certain pathway, promoting the formation and development of ET. This study will expand the collection of bone marrow samples from ET patients, detect the differences in circ0014614 levels in peripheral blood and bone marrow before and after treatment, and predict its downstream microRNA and mRNA through bioinformatics analysis to speculate its role in the occurrence and development of the disease. ;