Disruptive chemicals, senescence and immortality

Amancio Carnero, Carmen Blanco-Aparicio, Hiroshi Kondoh, Matilde E. Lleonart, Juan Fernando Martinez-Leal, Chiara Mondello, A. Ivana Scovassi, William H. Bisson, Amedeo Amedei, Rabindra Roy, Jordan Woodrick, Annamaria Colacci, Monica Vaccari, Jayadev Raju, Fahd Al-Mulla, Rabeah Al-Temaimi, Hosni K. Salem, Lorenzo Memeo, Stefano Forte, Neetu SinghRoslida A. Hamid, Elizabeth P. Ryan, Dustin G. Brown, John Pierce Wise, Sandra S. Wise, Hemad Yasaei

Research output: Contribution to journalReview articlepeer-review

18 Citations (Scopus)


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?

Original languageEnglish
Pages (from-to)S19-S37
Publication statusPublished - 1 Jan 2015


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