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Unboxing the molecular modalities of mutagens in cancer

The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational eve...

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Autores principales: Kumari, Smita, Sharma, Sudhanshu, Advani, Dia, Khosla, Akanksha, Kumar, Pravir, Ambasta, Rashmi K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492102/
https://www.ncbi.nlm.nih.gov/pubmed/34611806
http://dx.doi.org/10.1007/s11356-021-16726-w
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author Kumari, Smita
Sharma, Sudhanshu
Advani, Dia
Khosla, Akanksha
Kumar, Pravir
Ambasta, Rashmi K.
author_facet Kumari, Smita
Sharma, Sudhanshu
Advani, Dia
Khosla, Akanksha
Kumar, Pravir
Ambasta, Rashmi K.
author_sort Kumari, Smita
collection PubMed
description The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies. GRAPHICAL ABSTRACT: [Image: see text]
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spelling pubmed-84921022021-10-06 Unboxing the molecular modalities of mutagens in cancer Kumari, Smita Sharma, Sudhanshu Advani, Dia Khosla, Akanksha Kumar, Pravir Ambasta, Rashmi K. Environ Sci Pollut Res Int Mutagenic Factors in the Environment Impacting Human and Animal Health The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies. GRAPHICAL ABSTRACT: [Image: see text] Springer Berlin Heidelberg 2021-10-05 2022 /pmc/articles/PMC8492102/ /pubmed/34611806 http://dx.doi.org/10.1007/s11356-021-16726-w Text en © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Mutagenic Factors in the Environment Impacting Human and Animal Health
Kumari, Smita
Sharma, Sudhanshu
Advani, Dia
Khosla, Akanksha
Kumar, Pravir
Ambasta, Rashmi K.
Unboxing the molecular modalities of mutagens in cancer
title Unboxing the molecular modalities of mutagens in cancer
title_full Unboxing the molecular modalities of mutagens in cancer
title_fullStr Unboxing the molecular modalities of mutagens in cancer
title_full_unstemmed Unboxing the molecular modalities of mutagens in cancer
title_short Unboxing the molecular modalities of mutagens in cancer
title_sort unboxing the molecular modalities of mutagens in cancer
topic Mutagenic Factors in the Environment Impacting Human and Animal Health
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492102/
https://www.ncbi.nlm.nih.gov/pubmed/34611806
http://dx.doi.org/10.1007/s11356-021-16726-w
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