Still a burning question: the interplay between inflammation and fibrosis in myeloproliferative neoplasms

Hélène F.E. Gleitz; Adam Benabid; Rebekka K. Schneider

doi:10.1097/MOH.0000000000000669

Still a burning question: the interplay between inflammation and fibrosis in myeloproliferative neoplasms

Hélène F.E. Gleitz, Adam Benabid, Rebekka K. Schneider^*

^*Corresponding author for this work

Developmental Biology

Research output: Contribution to journal › Article › Academic › peer-review

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Abstract

PURPOSE OF REVIEW: Bone marrow fibrosis is the progressive replacement of blood-forming cells by reticulin fibres, caused by the acquisition of somatic mutations in hematopoietic stem cells. The molecular and cellular mechanisms that drive the progression of bone marrow fibrosis remain unknown, yet chronic inflammation appears to be a conserved feature in most patients suffering from myeloproliferative neoplasms. RECENT FINDINGS: Here, we review recent literature pertaining to the role of inflammation in driving bone marrow fibrosis, and its effect on the various hematopoietic and nonhematopoietic cell populations. SUMMARY: Recent evidence suggests that the pathogenesis of MPN is primarily driven by the hematopoietic stem and progenitor cells, together with their mutated progeny, which in turn results in chronic inflammation that disrupts the bone marrow niche and perpetuates a disease-permissive environment. Emerging data suggests that specifically targeting stromal inflammation in combination with JAK inhibition may be the way forward to better treat MPNs, and bone marrow fibrosis specifically.

Original language	English
Pages (from-to)	364-371
Number of pages	8
Journal	Current Opinion in Hematology
Volume	28
Issue number	5
DOIs	https://doi.org/10.1097/MOH.0000000000000669
Publication status	Published - 1 Sept 2021

Bibliographical note

Financial support and sponsorship
H.F.E.G. was supported a Marie Curie-Sklodowska grant
(707404, LEaDing Fellow). R.K.S. is an Oncode Institute
investigator and was supported by grants from the MPN
Foundation (2017 MPNRF/LLS Award), a KWF Kankerbestrijding young investigator grant (11031/2017–1,
Bas Mulder Award; Dutch Cancer Foundation), an ERC
grant (deFIBER; ERC-StG 757339), a grant of the Deutsche Forschungsgemeinschaft (DFG) (German Research
Foundation) (SCHN1188/6-1) within the clinical
research unit CRU344. R.K.S. is a member of the
E:MED Consortia Fibromap funded by the German Ministry of Education and Science (BMBF).

Publisher Copyright:
Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc.

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abstract = "PURPOSE OF REVIEW: Bone marrow fibrosis is the progressive replacement of blood-forming cells by reticulin fibres, caused by the acquisition of somatic mutations in hematopoietic stem cells. The molecular and cellular mechanisms that drive the progression of bone marrow fibrosis remain unknown, yet chronic inflammation appears to be a conserved feature in most patients suffering from myeloproliferative neoplasms. RECENT FINDINGS: Here, we review recent literature pertaining to the role of inflammation in driving bone marrow fibrosis, and its effect on the various hematopoietic and nonhematopoietic cell populations. SUMMARY: Recent evidence suggests that the pathogenesis of MPN is primarily driven by the hematopoietic stem and progenitor cells, together with their mutated progeny, which in turn results in chronic inflammation that disrupts the bone marrow niche and perpetuates a disease-permissive environment. Emerging data suggests that specifically targeting stromal inflammation in combination with JAK inhibition may be the way forward to better treat MPNs, and bone marrow fibrosis specifically.",

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note = "Financial support and sponsorship H.F.E.G. was supported a Marie Curie-Sklodowska grant (707404, LEaDing Fellow). R.K.S. is an Oncode Institute investigator and was supported by grants from the MPN Foundation (2017 MPNRF/LLS Award), a KWF Kankerbestrijding young investigator grant (11031/2017–1, Bas Mulder Award; Dutch Cancer Foundation), an ERC grant (deFIBER; ERC-StG 757339), a grant of the Deutsche Forschungsgemeinschaft (DFG) (German Research Foundation) (SCHN1188/6-1) within the clinical research unit CRU344. R.K.S. is a member of the E:MED Consortia Fibromap funded by the German Ministry of Education and Science (BMBF). Publisher Copyright: Copyright {\textcopyright} 2021 The Author(s). Published by Wolters Kluwer Health, Inc.",

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Still a burning question: the interplay between inflammation and fibrosis in myeloproliferative neoplasms

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