Epigenetic mechanisms orchestrate gene expression and passing on of gene modifications to subsequent generations without changing the underlying DNA sequence. Types of epigenetic modulations include, but not limited to, DNA methylation, histone acetylation or methylation, and chromatin remodelling. Recent studies on non-coding RNA functions have added weight to the diversity of epigenetic paradigms. In addition to DNA modulation, chemical modifications also occur on RNA as exemplified by N6-methyladenosine (m6A) methylation. Despite their tremendous heterogeneity, malignancies are well accepted to originate from genetic mutations those play predominant roles in carcinogenesis. In principle, a cancer-driving mutation induces aberrant intracellular signalling that culminates in alterations in expression of genes involved in cell division, migration, and other malignant behaviours. While canonical signal transduction switches on or off these genes through regulation of transcription factors, a cancer-initiating mutation may also change gene expression profile via extensive crosstalk with the epigenetic machineries such as writer and eraser enzyme complexes. This specific issue will focus on the epigenetic mechanisms as potential mediators of gene regulation by cancer-driving pathways, and hopefully provide rationale for epigenetic intervention of malignancies linked with well-defined driver mutations lacking successful targeted therapeutics.
This Research Topic aims to present the most recent advances in epigenetic mechanisms regulated by or displaying interplay with currently established cancer-driving mutations and/or signalling pathways. We thus particularly welcome Original Research and Review articles focusing on epigenetic modifications participating in the regulation of HER2, EGFR, Wnt, Hedgehog and other oncogenic pathways, as well as the function of well-documented oncogenes and tumor suppressors, e.g. Ras, Myc, TP53, and PTEN. The collected studies will potentially shed light on the understanding of regulatory networks of these classical signal pathways consisting of integrated genetic and epigenetic patterns.
Topics of interest include but are not limited to:
- DNA methylation and histone modifications that control or result from classical oncogenic signalling.
- Novel DNA or RNA modifications that occur in cancer with known predisposition or driver mutations.
- Regulation/ function of non-coding RNAs as a new layer in epigenetic modulation of oncogenic signalling.
- Translational studies on targeting epigenetic machineries in cancers harbouring documented genetic mutations or in metastatic cancers being resistant to available therapies.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
Epigenetic mechanisms orchestrate gene expression and passing on of gene modifications to subsequent generations without changing the underlying DNA sequence. Types of epigenetic modulations include, but not limited to, DNA methylation, histone acetylation or methylation, and chromatin remodelling. Recent studies on non-coding RNA functions have added weight to the diversity of epigenetic paradigms. In addition to DNA modulation, chemical modifications also occur on RNA as exemplified by N6-methyladenosine (m6A) methylation. Despite their tremendous heterogeneity, malignancies are well accepted to originate from genetic mutations those play predominant roles in carcinogenesis. In principle, a cancer-driving mutation induces aberrant intracellular signalling that culminates in alterations in expression of genes involved in cell division, migration, and other malignant behaviours. While canonical signal transduction switches on or off these genes through regulation of transcription factors, a cancer-initiating mutation may also change gene expression profile via extensive crosstalk with the epigenetic machineries such as writer and eraser enzyme complexes. This specific issue will focus on the epigenetic mechanisms as potential mediators of gene regulation by cancer-driving pathways, and hopefully provide rationale for epigenetic intervention of malignancies linked with well-defined driver mutations lacking successful targeted therapeutics.
This Research Topic aims to present the most recent advances in epigenetic mechanisms regulated by or displaying interplay with currently established cancer-driving mutations and/or signalling pathways. We thus particularly welcome Original Research and Review articles focusing on epigenetic modifications participating in the regulation of HER2, EGFR, Wnt, Hedgehog and other oncogenic pathways, as well as the function of well-documented oncogenes and tumor suppressors, e.g. Ras, Myc, TP53, and PTEN. The collected studies will potentially shed light on the understanding of regulatory networks of these classical signal pathways consisting of integrated genetic and epigenetic patterns.
Topics of interest include but are not limited to:
- DNA methylation and histone modifications that control or result from classical oncogenic signalling.
- Novel DNA or RNA modifications that occur in cancer with known predisposition or driver mutations.
- Regulation/ function of non-coding RNAs as a new layer in epigenetic modulation of oncogenic signalling.
- Translational studies on targeting epigenetic machineries in cancers harbouring documented genetic mutations or in metastatic cancers being resistant to available therapies.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
