@misc{10481/76757,
year = {2022},
month = {8},
url = {http://hdl.handle.net/10481/76757},
abstract = {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.},
organization = {FPU grant from the Ministry of Education, Culture and Sport},
organization = {University of Jaen, Accion I apoyo a la investigacion	BIO-349},
organization = {Excellence Research Unit "Modeling Nature" (MNat)},
organization = {Junta de Andalucia		
European Commission	SOMM17/6109/UGR},
organization = {Consejeria de Salud y Familias de la Junta de Andalucia (FEDER funds)	PEMP-0205-2020},
organization = {Ministry of Economy and Competitiveness (FEDER funds)	PIE16/00045},
organization = {Ministry of Science, Innovation and Universities	RTI2018-101309-B-C22},
organization = {Chair "Doctors Galera-Requena in cancer stem cell research"	CMC-CTS963},
publisher = {MDPI},
keywords = {Deaminases dysregulation},
keywords = {AID},
keywords = {APOBEC},
keywords = {ADAR},
keywords = {Cancer phenotype plasticity},
keywords = {Cancer stem cells},
keywords = {Tumour development model},
title = {Unifying Different Cancer Theories in a Unique TumourModel: Chronic Inflammation and Deaminases as Meeting Points},
doi = {10.3390/ijms23158720},
author = {Hernández Camarero, Pablo and López Ruiz, Elena and Marchal Corrales, Juan Antonio and Perán, Macarena},
}