Serum Procollagen‐iii‐peptide as a Marker for Primary Myelofibrosis: Effect of Anthracyclin

Parmentier, Céline; Schlumberger, M; Caillou, Bernard; Boaziz, C.

doi:10.1111/j.1600-0609.1987.tb01460.x

Cited by 1 publication

(2 citation statements)

References 3 publications

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“…Prior to collagen fiber formation, the procollagens are converted to collagens. During this process, the propeptide regions of the procollagen molecules are cleaved off in the extracellular space and released into the circulation [81][82][83][84][85][86]158,159,[260][261][262][263][264][265][266][267][268][269][270][271]. Since the propeptides are released in equimolar amounts to the collagen molecules formed, the measurement of circulating levels of these propeptides is thought to reflect collagen synthesis (Figure 1).…”

Section: The Aminoterminal Propeptide Of Type III Procollagen (Piiinp)mentioning

confidence: 99%

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Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms

Hasselbalch,

Junker,

Skov

et al. 2023

Cancers

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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.

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Section: The Aminoterminal Propeptide Of Type III Procollagen (Piiinp)mentioning

confidence: 99%

“…S-PIIINP values were elevated in PMF, S-PIIINP values decreased during treatment with anthracycline, which was given due to accelerated phase disease [268]. S-PIIINP is a valuable biomarker in PMF.…”

Section: S-piiinp Is a Useful Indicator Of Disease Activity In Mpnsmentioning

confidence: 99%

Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms

Hasselbalch,

Junker,

Skov

et al. 2023

Cancers

View full text Add to dashboard Cite

show abstract

Serum Procollagen‐iii‐peptide as a Marker for Primary Myelofibrosis: Effect of Anthracyclin

Cited by 1 publication

References 3 publications

Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms

Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms

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