| Literature DB >> 26106143 |
Wilhelm Engström1, Philippa Darbre2, Staffan Eriksson3, Linda Gulliver4, Tove Hultman5, Michalis V Karamouzis6, James E Klaunig7, Rekha Mehta8, Kim Moorwood9, Thomas Sanderson10, Hideko Sone11, Pankaj Vadgama12, Gerard Wagemaker13, Andrew Ward9, Neetu Singh14, Fahd Al-Mulla15, Rabeah Al-Temaimi15, Amedeo Amedei16, Anna Maria Colacci17, Monica Vaccari17, Chiara Mondello18, A Ivana Scovassi18, Jayadev Raju19, Roslida A Hamid20, Lorenzo Memeo21, Stefano Forte21, Rabindra Roy22, Jordan Woodrick22, Hosni K Salem23, Elizabeth P Ryan24, Dustin G Brown24, William H Bisson25.
Abstract
The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.Entities:
Mesh:
Substances:
Year: 2015 PMID: 26106143 PMCID: PMC4565610 DOI: 10.1093/carcin/bgv030
Source DB: PubMed Journal: Carcinogenesis ISSN: 0143-3334 Impact factor: 4.944