Unifying Different Cancer Theories in a Unique TumourModel: Chronic Inflammation and Deaminases as Meeting Points
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AuthorHernández Camarero, Pablo; López Ruiz, Elena; Marchal Corrales, Juan Antonio; Perán, Macarena
Deaminases dysregulationAIDAPOBECADARCancer phenotype plasticityCancer stem cellsTumour development model
Hernández-Camarero, P... [et al.]. Unifying Different Cancer Theories in a Unique Tumour Model: Chronic Inflammation and Deaminases as Meeting Points. Int. J. Mol. Sci. 2022, 23, 8720. [https://doi.org/10.3390/ijms23158720]
SponsorshipFPU grant from the Ministry of Education, Culture and Sport; University of Jaen, Accion I apoyo a la investigacion BIO-349; Excellence Research Unit "Modeling Nature" (MNat); Junta de Andalucia European Commission SOMM17/6109/UGR; Consejeria de Salud y Familias de la Junta de Andalucia (FEDER funds) PEMP-0205-2020; Ministry of Economy and Competitiveness (FEDER funds) PIE16/00045; Ministry of Science, Innovation and Universities RTI2018-101309-B-C22; Chair "Doctors Galera-Requena in cancer stem cell research" CMC-CTS963
The increase in cancer incidences shows that there is a need to better understand tumour heterogeneity to achieve efficient treatments. Interestingly, there are several common features among almost all types of cancers, with chronic inflammation induction and deaminase dysfunctions singled out. Deaminases are a family of enzymes with nucleotide-editing capacity, which are classified into two main groups: DNA-based and RNA-based. Remarkably, a close relationship between inflammation and the dysregulation of these molecules has been widely documented, which may explain the characteristic intratumor heterogeneity, both at DNA and transcriptional levels. Indeed, heterogeneity in cancer makes it difficult to establish a unique tumour progression model. Currently, there are three main cancer models—stochastic, hierarchic, and dynamic—although there is no consensus on which one better resembles cancer biology because they are usually overly simplified. Here, to accurately explain tumour progression, we propose interactions among chronic inflammation, deaminases dysregulation, intratumor genetic heterogeneity, cancer phenotypic plasticity, and even the previously proposed appearance of cancer stem-like cell populations in the edges of advanced solid tumour masses (instead of being the cells of origin of primary malignancies). The new tumour development model proposed in this study does not contradict previously accepted models and it may open up a window to interesting therapeutic approaches.