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