While much research focuses on oncogenic proteins and signaling pathways in aggressive cancers, fewer studies investigate how normal cells transform into malignant types. Cancer may arise from an interplay of genetic and environmental factors. In particular, there is a strong association between environmental and/or occupational exposure to heavy metals and cancer incidence and aggressiveness.

Exposure to heavy metals such as arsenic, cadmium, chromium, and nickel have been implicated in carcinogenesis through complex genetic and epigenetic mechanisms. These metals disrupt cellular homeostasis, inducing oxidative stress, DNA damage, and alterations in gene expression. Furthermore, they modify the epigenetic landscape by influencing DNA methylation, histone modifications, and non-coding RNA activity, thereby promoting tumor initiation and progression. Identifying the genes, proteins, or pathways responsible for metal induced carcinogenesis could lead to novel targets that have therapeutic potential.

This manuscript collection will feature a diverse range of article types, including original research, comprehensive reviews, mini-reviews, case studies, and perspectives, aimed at addressing the intricate interplay between metals and carcinogenic pathways, fostering advancements in research and translational opportunities in this field. We will accept manuscripts covering, but not limited to:

- Epigenetic Changes as Drivers of metal-induced carcinogenesis
- Metal-Induced Oxidative Stress and DNA Damage Pathways
- Disrupted Molecular Signaling Pathways in Metal Induced Carcinogenesis
- Biomarkers and Therapeutic Targets in Metal-Induced Cancers

Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases, which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo), are out of scope for this section and will not be accepted as part of this Research Topic.

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Metal-Induced Carcinogenesis: Exploring Genetic and Epigenetic Mechanisms Underpinning Cancer Development