2024-03-19T11:55:51Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1429982021-11-22T12:46:01Zcom_10261_11773com_10261_1col_10261_11774
2017-01-25T12:27:33Z
urn:hdl:10261/142998
Disruptive chemicals, senescence and immortality
Carnero, Amancio
Blanco-Aparicio, Carmen
Yasaei, Hemad
Japan Science and Technology Agency
National Centre for the Replacement, Refinement and Reduction of Animals in Research (UK)
Instituto de Salud Carlos III
Ministerio de Economía y Competitividad (España)
Red Temática de Investigación Cooperativa en Cáncer (España)
European Commission
Ministerio de Ciencia e Innovación (España)
Junta de Andalucía
National Institute of Environmental Health Sciences (US)
Maine Center for Toxicology and Environmental Health
National Institutes of Health (US)
Kuwait Foundation for the Advancement of Sciences
Ministry of Education, Culture, Sports, Science and Technology (Japan)
Department of Science and Technology (India)
U.S. Public Health Service
Università degli Studi di Firenze
Ministry of Education (Malaysia)
Ministero dell'Istruzione, dell'Università e della Ricerca
Mutation
Tumorigenesis
Elderly
Carcinogenesis
Cell aging
Carcinogens
Aging
Carnero, Amancio et al.
© The Author 2015. Carcinogenesis is thought to be a multistep process, with clonal evolution playing a central role in the process. Clonal evolution involves the repeated 'selection and succession' of rare variant cells that acquire a growth advantage over the remaining cell population through the acquisition of 'driver mutations' enabling a selective advantage in a particular micro-environment. Clonal selection is the driving force behind tumorigenesis and possesses three basic requirements: (i) effective competitive proliferation of the variant clone when compared with its neighboring cells, (ii) acquisition of an indefinite capacity for self-renewal, and (iii) establishment of sufficiently high levels of genetic and epigenetic variability to permit the emergence of rare variants. However, several questions regarding the process of clonal evolution remain. Which cellular processes initiate carcinogenesis in the first place? To what extent are environmental carcinogens responsible for the initiation of clonal evolution? What are the roles of genotoxic and non-genotoxic carcinogens in carcinogenesis?
2017-01-25T12:27:33Z
2017-01-25T12:27:33Z
2015-06-19
2017-01-25T12:27:33Z
artículo
Carcinogenesis 36(Suppl 1): S19-S37 (2015)
http://hdl.handle.net/10261/142998
10.1093/carcin/bgv029
http://dx.doi.org/10.13039/501100002241
http://dx.doi.org/10.13039/501100000849
http://dx.doi.org/10.13039/501100004587
http://dx.doi.org/10.13039/501100003329
http://dx.doi.org/10.13039/501100000780
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/100000066
http://dx.doi.org/10.13039/100000002
http://dx.doi.org/10.13039/501100003286
http://dx.doi.org/10.13039/501100001700
http://dx.doi.org/10.13039/100007197
http://dx.doi.org/10.13039/501100004434
http://dx.doi.org/10.13039/501100003407
http://dx.doi.org/10.13039/501100001409
http://dx.doi.org/10.13039/501100011011
26106138
eng
http://doi.org/10.1093/carcin/bgv029
Sí
closedAccess
Oxford University Press