ArticlePloS one2017
Mathematical modelling as a proof of concept for MPNs as a human inflammation model for cancer development.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- Mathematical modeling ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
- Dynamically adjusted cell fate decisions and resilience to mutant invasion during steady-state hematopoiesis revealed by an experimentally parameterized mathematical model.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Computational modeling reveals key factors driving treatment-free remission in chronic myeloid leukemia patients.NPJ systems biology and applications · 2024Article
- Investigation of Serum Albumin as a Dynamic Treatment-Specific Surrogate for Outcomes in Patients With Myelofibrosis Treated With Ruxolitinib.JCO precision oncology · 2024Article
- Inherited polygenic effects on common hematological traits influence clonal selection on JAK2Nature genetics · 2024Article
- Mathematical modelling of stem and progenitor cell dynamics during ruxolitinib treatment of patients with myeloproliferative neoplasms.Frontiers in immunology · 2024Article
- Stem cell graft dose and composition could impact on the expansion of donor-derived clones after allogeneic hematopoietic stem cell transplantation - a virtual clinical trial.Frontiers in immunology · 2024Article
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
- HSC Niche Dynamics in Regeneration, Pre-malignancy, and Cancer: Insights From Mathematical Modeling.Stem cells (Dayton, Ohio) · 2023Article
- Serum levels of IL-4, IL-13 and IL-33 in patients with age-related macular degeneration and myeloproliferative neoplasms.Scientific reports · 2023Article
- The multidisciplinary approach to eosinophilia.Frontiers in oncology · 2023Review
- Mutations, inflammation and phenotype of myeloproliferative neoplasms.Frontiers in oncology · 2023Review
- Recombinant Interferon-β in the Treatment of Polycythemia Vera and Related Neoplasms: Rationales and Perspectives.Cancers · 2022Article
- Age-related macular degeneration and myeloproliferative neoplasms - A common pathway.Acta ophthalmologica · 2022Article
- PD-1/PD-L1, MDSC Pathways, and Checkpoint Inhibitor Therapy inInternational journal of molecular sciences · 2022Review
- Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation.International journal of molecular sciences · 2022Review
- Patients with MPNs and retinal drusen show signs of complement system dysregulation and a high degree of chronic low-grade inflammation.EClinicalMedicine · 2022Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chronic Philadelphia-negative myeloproliferative neoplasms (MPNs) are acquired stem cell neoplasms which ultimately may transform to acute myelogenous leukemia. Most recently, chronic inflammation has been described as an important factor for the development and progression of MPNs in the biological continuum from early cancer stage to the advanced myelofibrosis stage, the MPNs being described as "A Human Inflammation Model for Cancer Development". This novel concept has been built upon clinical, experimental, genomic, immunological and not least epidemiological studies. Only a few studies have described the development of MPNs by mathematical models, and none have addressed the role of inflammation for clonal evolution and disease progression. Herein, we aim at using mathematical modelling to substantiate the concept of chronic inflammation as an important trigger and driver of MPNs.The basics of the model describe the proliferation from stem cells to mature cells including mutations of healthy stem cells to become malignant stem cells. We include a simple inflammatory coupling coping with cell death and affecting the basic model beneath. First, we describe the system without feedbacks or regulatory interactions. Next, we introduce inflammatory feedback into the system. Finally, we include other feedbacks and regulatory interactions forming the inflammatory-MPN model. Using mathematical modeling, we add further proof to the concept that chronic inflammation may be both a trigger of clonal evolution and an important driving force for MPN disease progression. Our findings support intervention at the earliest stage of cancer development to target the malignant clone and dampen concomitant inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.