Fibrotic activity quantified in serum by measurements of type III collagen pro-peptides can be used for prognosis across different solid tumor types

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  • Nicholas Willumsen
  • Christina Jensen
  • George Green
  • Neel I. Nissen
  • Jaclyn Neely
  • David M. Nelson
  • Rasmus S. Pedersen
  • Peder Frederiksen
  • Inna M. Chen
  • Mogens K. Boisen
  • Astrid Z. Johansen
  • Allan Lipton
  • Kim Leitzel
  • Suhail M. Ali
  • Daan P. Hurkmans
  • Ron H.J. Mathijssen
  • Joachim Aerts
  • Mohammed Eslam
  • Jacob George
  • Claus Christiansen
  • Mina J. Bissel
  • Morten A. Karsdal

Due to activation of fibroblast into cancer-associated fibroblasts, there is often an increased deposition of extracellular matrix and fibrillar collagens, e.g. type III collagen, in the tumor microenvironment (TME) that leads to tumor fibrosis (desmoplasia). Tumor fibrosis is closely associated with treatment response and poor prognosis for patients with solid tumors. To assure that the best possible treatment option is provided for patients, there is medical need for identifying patients with high (or low) fibrotic activity in the TME. Measuring unique collagen fragments such as the pro-peptides released into the bloodstream during fibrillar collagen deposition in the TME can provide a non-invasive measure of the fibrotic activity. Based on data from 8 previously published cohorts, this review provides insight into the prognostic value of quantifying tumor fibrosis by measuring the pro-peptide of type III collagen in serum of a total of 1692 patients with different solid tumor types and discusses the importance of tumor fibrosis for understanding prognosis and for potentially guiding future drug development efforts that aim at overcoming the poor outcome associated with a fibrotic TME.

OriginalsprogEngelsk
Artikelnummer204
TidsskriftCellular and Molecular Life Sciences
Vol/bind79
Udgave nummer4
Antal sider11
ISSN1420-682X
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
NW is employed and have stockownership and patents in Nordic Bioscience. CJ is employed at Nordic Bioscience. GG is employed and have stockownership and patents or other related intellectual property in Bristol Myers Squibb. NIN is employed in Nordic Bioscience. JN is employed and have stockownership in Bristol Myers Squibb. DMN is employed and have stockownership and patents or other related intellectual property in Bristol Myers Squibb. PF is employed in Nordic Bioscience. RSP is employed in Nordic Bioscience. IMC declares a consultancy/advisory role at Amgen, to have received research funding from Bristol Myers Squibb, Roche, Genis TILT, Lytix and travels expenses paid by Bristol Myers Squibb, Roche, Bayer. MKB declares no competing interests. AZJ declares no competing interests. DHM declares no competing interests. IMS declares paid honoraria from IO Biotech, MSD, a consultancy/advisory role at Pierre Fabre and Novartis, to have received research funding from Bristol Myers Squibb, Roche, TILT, Lytix and travels expenses paid by MSD. AL declares no competing interests. KL declares no competing interests. SMA declares no competing interests. JTE is a founder and CEO of LOXiGen ApS and was CEO of LOXiPharm IVS. DPH declares no competing interests. RHJM declares a consultancy/advisory role at Servier, to have received research funding from Astellas, Bayer, BI, Cristal tx, Pamgene, Pfizer, Novastis, Roche, Servier, Sanofi and to have patents or other related intellectual property pending at Pamgene. JA declares to have patents or other related intellectual property at Amphera and travels expenses paid by MSD. ME declares paid honoraria from Sanofi and a consultancy/advisory role at Pfizer. JG declares paid honoraria and a consultancy/advisory role at Roche, MSD, Pfizer, Abbvie, AstraZeneca, Novartis, Pharmaxis, Cincera, Novo, Gilead, Norgine, Eisai. CC have stockownership and patents in Nordic Bioscience. MBL declares no competing interests. MK is employed and have stockownership and patents in Nordic Bioscience.

Publisher Copyright:
© 2022, The Author(s).

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