Signaling pathways and bone marrow microenvironment in myelodysplastic neoplasms
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ceneri, Eleonora | - |
dc.contributor.author | De Stefano, Alessia | - |
dc.contributor.author | Casalin, Irene | - |
dc.contributor.author | Finelli, Carlo | - |
dc.contributor.author | Curti, Antonio | - |
dc.contributor.author | Paolini, Stefania | - |
dc.contributor.author | Parisi, Sarah | - |
dc.contributor.author | Ardizzoia, Federica | - |
dc.contributor.author | Cristiano, Gianluca | - |
dc.contributor.author | Boultwood, Jaqueline | - |
dc.contributor.author | Mccubrey, James A. | - |
dc.contributor.author | Suh, Pann-Ghill | - |
dc.contributor.author | Ramazzotti, Giulia | - |
dc.contributor.author | Fiume, Roberta | - |
dc.contributor.author | Ratti, Stefano | - |
dc.contributor.author | Manzoli, Lucia | - |
dc.contributor.author | Cocco, Lucio | - |
dc.contributor.author | Follo, Matilde Y. | - |
dc.date.accessioned | 2025-03-05T00:30:11Z | - |
dc.date.available | 2025-03-05T00:30:11Z | - |
dc.date.issued | 2025-01 | - |
dc.identifier.issn | 2212-4926 | - |
dc.identifier.issn | 2212-4934 | - |
dc.identifier.uri | http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/1248 | - |
dc.description.abstract | Key signaling pathways within the Bone Marrow Microenvironment (BMM), such as Notch, Phosphoinositide-Specific Phospholipase C (PI-PLCs), Transforming Growth Factor β (TGF-β), and Nuclear Factor Kappa B (NF-κB), play a vital role in the progression of Myelodysplastic Neoplasms (MDS). Among the various BMM cell types, Mesenchymal Stromal Cells (MSCs) are particularly central to these pathways. While these signaling routes can independently affect both MSCs and Hematopoietic Stem Cells (HSCs), they most importantly alter the dynamics of their interactions, leading to abnormal changes in survival, differentiation, and quiescence. Notch and PI-PLC signaling facilitate intercellular communication, TGF-β promotes quiescence and suppresses hematopoiesis, and NF-κB-driven inflammatory responses foster an environment detrimental to normal hematopoiesis. This review highlights the role of these pathways within the MDS microenvironment, driving the development and progression of the disease and paving the way for new possible therapeutic strategies. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Elsevier BV | - |
dc.title | Signaling pathways and bone marrow microenvironment in myelodysplastic neoplasms | - |
dc.type | Article | - |
dc.publisher.location | 영국 | - |
dc.identifier.doi | 10.1016/j.jbior.2024.101071 | - |
dc.identifier.scopusid | 2-s2.0-85211236221 | - |
dc.identifier.wosid | 001428211600001 | - |
dc.identifier.bibliographicCitation | Advances in Biological Regulation, v.95 | - |
dc.citation.title | Advances in Biological Regulation | - |
dc.citation.volume | 95 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | esci | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | PHOSPHOLIPASE-C BETA1 | - |
dc.subject.keywordPlus | MDS | - |
dc.subject.keywordAuthor | Myelodysplastic neoplasms | - |
dc.subject.keywordAuthor | Bone marrow microenvironment | - |
dc.subject.keywordAuthor | Notch signaling | - |
dc.subject.keywordAuthor | Phosphoinositide signaling | - |
dc.subject.keywordAuthor | TGF-beta signaling | - |
dc.subject.keywordAuthor | NF-kappa B signaling | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
61, Cheomdan-ro, Dong-gu, Daegu, Republic of Korea , 41062 053-980-8114
COPYRIGHT Korea Brain Research Institute. ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.