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International Journal of Environment Science and Technology
Center for Environment and Energy Research and Studies (CEERS)
ISSN: 1735-1472
EISSN: 1735-2630
Vol. 12, No. 7, 2015, pp. 2415-2426
Bioline Code: st15227
Full paper language: English
Document type: Research Article
Document available free of charge

International Journal of Environment Science and Technology, Vol. 12, No. 7, 2015, pp. 2415-2426

 en Environmental pollutants leading to carcinogenesis: process of natural selection of human cells due to chronic inflammation and sustained stress environment
Venkatesh, H. N.; Jeru Manoj, M.; Ghosh, D. & Chetan, G. K.

Abstract

Epidemiological studies have shown that 70–90 % of all cancers are caused due to the chemicals present in environment. Exogenous exposure to carcinogens and their interaction with genetic sequences and endogenous factors, like exposures to products of metabolism which lead to acute stress, disruption of hormones and inflammation of tissues, are triggering factors. Due to relatively small risk of cancer following immediate exposure, the precise quantification of the burden of human cancer attributed to environmental exposure remains ambiguous, thereby leading to an assumption that a causal relationship is relatively large. Research suggests that 90–95 % of all cancers have their roots in the environmental effects on the DNA leading to genetic defects, whereas only 5–10 % can be attributed to inherited genetic defects. The hypothesis of the present review is that response of the cells to the environmental stimulants could be an evolutionary process of adaptation of the DNA. Carcinogenesis is considered as a process of adaptation of mammalian cells to sustained stress environment (SSE) by means of epigenetic alteration (EA) of the genome, mutations which arise due to EA and finally, natural selection of originated mutant cells evading apoptosis. Process of adaptation to SSE involves the emergence of senescent epigenetically reprogrammed cells with specific cancerrelated EA in the genome.

Keywords
DNA damage; Environmental risk factors; Epigenetic alterations; Genetic risk factors; Adaptive cell environment

 
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