Document Type
Article
Publication Date
2-17-2020
Abstract
The goal of our study was to measure the kinetics of human colorectal cancer (CRC) development in order to identify aberrant mechanisms in tissue dynamics and processes that contribute to colon tumorigenesis. The kinetics of tumor development were investigated using age-at-tumor diagnosis (adenomas and CRCs) of familial adenomatous coli (FAP) patients and sporadic CRC patients. Plots of age-at-tumor diagnosis data as a function of age showed a distinct sigmoidal-shaped curve that is characteristic of an autocatalytic reaction. Consequently, we performed logistics function analysis and found an excellent fit (p < 0.05) of the logistic equation to the curves for age-at-tumor diagnoses. These findings indicate that the tissue mechanism that becomes altered in CRC development and growth involves an autocatalytic reaction. We conjecture that colonic epithelium normally functions as a polymer of cells which dynamically maintains itself in a steady state through an autocatalytic polymerization mechanism. Further, in FAP and sporadic CRC patients, mutation in the adenomatous polyposis coli (APC) gene increases autocatalytic tissue polymerization and induces tumor tissues to autocatalyze their own progressive growth, which drives tumor development in the colon.
Recommended Citation
Boman, Bruce M; Guetter, Arthur; Boman, Ryan M; and Runquist, Olaf A, "Autocatalytic Tissue Polymerization Reaction Mechanism in Colorectal Cancer Development and Growth." (2020). Department of Pharmacology and Experimental Therapeutics Faculty Papers. Paper 114.
https://jdc.jefferson.edu/petfp/114
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
32079164
Language
English
Comments
This article has been peer-reviewed. It is the author's final published version in Cancers, Volume 12, Issue 2, 2020. E460.
The published version is available at https://doi.org/10.3390/cancers12020460. Copyright Boman et al.