Advances in pharmacology. Volume 96, Environmental carcinogenesis / edited by Max Costa. -- Cambridge, MA : Academic Press, c2023. – (63.3/A244/v.96)

Contents

Contributors
Preface
 1. Mechanisms of chromate carcinogenesis by chromatin alterations
     1. Introduction
     2. Chromatin organization and mechanisms of chromium-mediated disruption
     3. Conclusion
     Conflict of interest
     Funding
     References
     Further reading
2. Chemical mechanisms of DNA damage by carcinogenic chromium(VI)
     1. Introduction
     2. Cellular metabolism of Cr(VI)
     3. DNA damage during Cr(VI) reduction by GSH
     4. DNA damage during reduction of Cr(VI) with cysteine
     5. DNA damage during thiol-driven metabolism of Cr(VI) in cells
     6. DNA damage during Cr(VI) reduction by ascorbate
     7. DNA damage by Cr(VI) in ascorbate-restored cells
     8. Conclusion
     Acknowledgments
     Conflict of interest statement
     References
3. The dark side of NRF2 in arsenic carcinogenesis
     1. Introduction
     2. The "light" vs "dark" side of NRF2
     3. Arsenic metabolism and intracellular targets
     4. Arsenic carcinogenesis
     5. Involvement of non-canonical activation of NRF2 in arsenic promotion of other metabolic diseases
     6. Conclusion
     Conflict of interest
     References
4. Breast carcinogenesis induced by organophosphorous pesticides
     1. Introduction
     2. Studies in rat mammary gland carcinogenesis
     3. Studies on carcinogenesis in MCF-10F cell line
     4. Conclusion
     Acknowledgments
     Conflict of interest
     Data availability statement
     References
5. Tungsten toxicity and carcinogenesis
     1. Introduction
     2. Susceptible human populations to high exposure to tungsten
     3. Tungsten deposition and retention in the body
     4. Tungsten carcinogenesis
     5. Tungsten pulmonary toxicity
     6. Tungsten cardiometabolic toxicity
     7. Tungsten bone toxicity
     8. Tungsten immunotoxicity
     9. Conclusion
     Acknowledgments
     Conflict of interest
     References
6. Arsenic and cancer: Evidence and mechanisms
     1. Introduction
     2. Human studies
     3. Mechanisms of arsenic carcinogenesis
     4. Chemical forms of arsenic and carcinogenesis
     5. Conclusion
     Conflict of interest
     References
     Further reading
7. miRNAs and arsenic-induced carcinogenesis
     1. Introduction
     2. Arsenical species and arsenic metabolism
     3. Arsenic exposure
     4. Arsenic-induced cancers
     5. Considerations for models of arsenic-induced carcinogenesis
     6. miRNAs: A proposed mechanism of arsenic-induced carcinogenesis
     7. miRNAs
     8. miRNAs and arsenic-induced carcinogenesis
     9. Conclusion
     Acknowledgments
     Conflict of interest statement
     References
8. Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis
     1. Introduction
     2. Epigenetics and epitranscriptomics
     3. Epigenetic mechanisms of hexavalent chromium carcinogenesis
     4. Epitranscriptomic mechanisms of hexavalent chromium carcinogenesis
     5. Conclusion
     Acknowledgments
     Conflict of interest statement
     References
9. Polyadenylation of canonical histone H3.1 in carcinogenesis
     1. Introduction
     2. Stem loop binding protein loss and polyadenylation of H3.1 (H3.2?)induce carcinogenesis
     3. Carcinogens that cause the loss of SLBP and polyadenylation of H3.1
     4. Conclusion
     Conflict of interest
     Funding
     References
10. Genetic and environmental reprogramming of the sarcoma epigenome
     1. Introduction
     2. Sarcoma genetics
     3. Epigenetic alterations in sarcoma
     4. Types of epigenetic alterations
     5. Environmental risk factors in sarcoma and associated epigenetic changes
     6. Viruses
     7. Conclusion
     Conflicts of interest
     References
11. Epigenomic reprogramming in iAs-mediated carcinogenesis
     1. Introduction
     2. Epigenetic modifications mediated by arsenic exposure
     3. Transcriptional products and outcomes of iAs-mediated epigenetic alterations
     4. Conclusion
     Acknowledgments
     Conflict of interest statement
     References