Mechanisms and Models of Comorbidities in Cancer Progression and Treatments

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (1 September 2023) | Viewed by 1787

Special Issue Editors


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Guest Editor
Center for Mathematical Modeling-Human Health and Disease (COMMAND), Roskilde University, 4000 Roskilde, Denmark
Interests: cancer progression and treatment; inflammation; immune response; comorbidity; digital twins; computational disease modelling; mathematical modelling of diseases

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Guest Editor
Department of Mathematics, University of California Irvine, Irvine, CA 92617, USA
Interests: mathematical models of evolutionary processes; cancer evolution; resistance evolution; infection dynamics

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Guest Editor
1. Center for Mathematical Modeling-Human Health and Disease (COMMAND), Roskilde University, 4000 Roskilde, Denmark
2. Mathematics and Physics (IMFUFA), Department of Science and Environment, Roskilde University, 4000 Roskilde, Denmark
Interests: mathematical modeling of hematopoiesis during health and disease and the coupling to the immune system; vortex dynamics

Special Issue Information

Dear Colleagues,

Recently, there have been an increasing focus on the role of inflammation in cancer progression and treatment. Most cancer is accompanied by an immune response and inflammation is known to be a trigger of and an accelerator for most cancer progression. Such inflammation may be imposed by environmental and lifestyle factors (stress, pollution, or smoking), bacterial or virus infections (HPV, COVID-19), or secondary diseases, such as bowel diseases (Morbus Crohn, arthritis). Thus, cancers, inflammation, and comorbidities constitute a severe disease complication triangle (DCT), which is considered vital.

The approach to study the couplings of the DCT is manyfold, however, a combined effort between clinicians, engineers, applied mathematicians, and many more disciplines are considered necessary to obtain a significant better understanding of the DCT problem.

In this Special Issue, we welcome new ideas, approaches, and methods for studying DCT preferable but not exclusively on physiological mechanisms using in silico methods.

Prof. Dr. Johnny T. Ottesen
Prof. Dr. Dominik Wodarz
Dr. Morten Andersen
Guest Editor

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Keywords

  • cancer progression and treatment
  • inflammation
  • immune response
  • comorbidity
  • digital twins
  • computational disease modelling
  • mathematical modelling of diseases

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Published Papers (1 paper)

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Research

18 pages, 2849 KiB  
Article
Aging, Inflammation, and Comorbidity in Cancers—A General In Silico Study Exemplified by Myeloproliferative Malignancies
by Johnny T. Ottesen and Morten Andersen
Cancers 2023, 15(19), 4806; https://doi.org/10.3390/cancers15194806 - 29 Sep 2023
Cited by 2 | Viewed by 1401
Abstract
(1) Background: We consider dormant, pre-cancerous states prevented from developing into cancer by the immune system. Inflammatory morbidity may compromise the immune system and cause the pre-cancer to escape into an actual cancerous development. The immune deficiency described is general, but the results [...] Read more.
(1) Background: We consider dormant, pre-cancerous states prevented from developing into cancer by the immune system. Inflammatory morbidity may compromise the immune system and cause the pre-cancer to escape into an actual cancerous development. The immune deficiency described is general, but the results may vary across specific cancers due to different variances (2) Methods: We formulate a general conceptual model to perform rigorous in silico consequence analysis. Relevant existing data for myeloproliferative malignancies from the literature are used to calibrate the in silico computations. (3) Results and conclusions: The hypothesis suggests a common physiological origin for many clinical and epidemiological observations in relation to cancers in general. Examples are the observed age-dependent prevalence for hematopoietic cancers, a general mechanism-based explanation for why the risk of cancer increases with age, and how somatic mutations in general, and specifically seen in screenings of citizens, sometimes are non-increased or even decrease when followed over time. The conceptual model is used to characterize different groups of citizens and patients, describing different treatment responses and development scenarios. Full article
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