The Role of Circ0014614 in the Formation and Development of ET

Status

UNKNOWN

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT05921838

Enrollment

120

Registered

2023-06-27

Start date

2021-01-01

Completion date

2023-12-31

Last updated

2023-06-27

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Primary Thrombocytosis

Brief summary

Research on the Role of Circ0014614 in the Formation and Development of ET

Detailed description

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.

Interventions

None listed

Study design

Observational model

OTHER

Time perspective

CROSS_SECTIONAL

Eligibility

Sex/Gender

ALL

Age

18 Years to 64 Years

Inclusion criteria

1. According to the classification and diagnostic criteria of hematological myeloid tumors by WHO 2016, patients diagnosed as ET are standardized 2. Voluntary signing of informed consent form 3. Age ≥ 18 years old, regardless of gender 4. No pregnancy plan during treatment

Exclusion criteria

1.The researcher judged that it was not suitable to participate in this study

Design outcomes

Primary

Measure	Time frame	Description
Circ0014614 copies in ET patients treated with interferon for 8 months	8months	Circ0014614 copies in ET patients treated with interferon for 8 months

Countries

China

Contacts

Primary ContactDan Xu

522111156@qq.com+86-20-61641615

Backup ContactXiaofan Chen