Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms
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Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms. / Hasselbalch, Hans Carl; Junker, Peter; Skov, Vibe; Kjær, Lasse; Knudsen, Trine A.; Larsen, Morten Kranker; Holmström, Morten Orebo; Andersen, Mads Hald; Jensen, Christina; Karsdal, Morten A.; Willumsen, Nicholas.
In: Cancers, Vol. 15, No. 17, 4323, 2023.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms
AU - Hasselbalch, Hans Carl
AU - Junker, Peter
AU - Skov, Vibe
AU - Kjær, Lasse
AU - Knudsen, Trine A.
AU - Larsen, Morten Kranker
AU - Holmström, Morten Orebo
AU - Andersen, Mads Hald
AU - Jensen, Christina
AU - Karsdal, Morten A.
AU - Willumsen, Nicholas
N1 - Publisher Copyright: © 2023 by the authors.
PY - 2023
Y1 - 2023
N2 - Philadelphia chromosome-negative chronic myeloproliferative neoplasms (MPNs) arise due to acquired somatic driver mutations in stem cells and develop over 10–30 years from the earliest cancer stages (essential thrombocythemia, polycythemia vera) towards the advanced myelofibrosis stage with bone marrow failure. The JAK2V617F mutation is the most prevalent driver mutation. Chronic inflammation is considered to be a major pathogenetic player, both as a trigger of MPN development and as a driver of disease progression. Chronic inflammation in MPNs is characterized by persistent connective tissue remodeling, which leads to organ dysfunction and ultimately, organ failure, due to excessive accumulation of extracellular matrix (ECM). Considering that MPNs are acquired clonal stem cell diseases developing in an inflammatory microenvironment in which the hematopoietic cell populations are progressively replaced by stromal proliferation—“a wound that never heals”—we herein aim to provide a comprehensive review of previous promising research in the field of circulating ECM fragments in the diagnosis, treatment and monitoring of MPNs. We address the rationales and highlight new perspectives for the use of circulating ECM protein fragments as biologically plausible, noninvasive disease markers in the management of MPNs.
AB - Philadelphia chromosome-negative chronic myeloproliferative neoplasms (MPNs) arise due to acquired somatic driver mutations in stem cells and develop over 10–30 years from the earliest cancer stages (essential thrombocythemia, polycythemia vera) towards the advanced myelofibrosis stage with bone marrow failure. The JAK2V617F mutation is the most prevalent driver mutation. Chronic inflammation is considered to be a major pathogenetic player, both as a trigger of MPN development and as a driver of disease progression. Chronic inflammation in MPNs is characterized by persistent connective tissue remodeling, which leads to organ dysfunction and ultimately, organ failure, due to excessive accumulation of extracellular matrix (ECM). Considering that MPNs are acquired clonal stem cell diseases developing in an inflammatory microenvironment in which the hematopoietic cell populations are progressively replaced by stromal proliferation—“a wound that never heals”—we herein aim to provide a comprehensive review of previous promising research in the field of circulating ECM fragments in the diagnosis, treatment and monitoring of MPNs. We address the rationales and highlight new perspectives for the use of circulating ECM protein fragments as biologically plausible, noninvasive disease markers in the management of MPNs.
KW - circulating extracellular matrix (ECM) proteins
KW - hyaluronan
KW - laminin
KW - MPN
KW - MPNs
KW - myeloproliferative neoplasms
KW - neoepitopes
KW - procollagen type I C-terminal propeptide (PICP)
KW - protein fingerprints
KW - serum procollagen III N-terminal propeptide (PIIINP)
KW - type IV collagen
U2 - 10.3390/cancers15174323
DO - 10.3390/cancers15174323
M3 - Review
C2 - 37686599
AN - SCOPUS:85170245883
VL - 15
JO - Cancers
JF - Cancers
SN - 2072-6694
IS - 17
M1 - 4323
ER -
ID: 370578377