About this Research Topic
Cancer remains a significant global health challenge, with conventional therapies often facing limitations in efficacy and adverse effects. To decipher the sheer complexity and the multi-faceted nature of cancer, systems biology (cancer attractors), comparative oncology, Single cell biology, evolution, ecology, quantum, entropy or thermodynamics, and other areas have been developed and applied.
In this Research Topic, we are inviting contributions from authors with expertise in cancer molecular genetics, cytogenetics, and cell biology. Recent insights in cancer cell biology have demonstrated that both carcinogenesis and tumorigenesis, as well as recurrence, lead to genomic dysfunctionality in cancer stem cells (CSCs) and progenitor cell lineages due to stress and oxygen excess. To restore the functionality and stability of the genome, dysfunctional cells with irreparable DNA double-strand breaks (DSBs) and aberrant tetraploid/aneuploid cell cycles are repaired through cell-to-cell fusion and epigenetic modifications, leading to the formation of polyploid/multinucleated giant cancer cells (PGCCs/MNGCs) and hyperpolyploidy. The functional genome of PGCC progeny regains differentiation and stemness potential, thereby restoring functional genome architecture and countering stress-induced genome dysfunctionality.
All these processes are orchestrated by various players and intracellular pathways that can be leveraged in the fight against cancer. We anticipate new findings and explanations documenting the loss and regain of genome stability at the molecular level, thereby enlightening readers with diverse aspects of cancer genomics and comparative genomics. This Research Topic welcomes high-quality Original Research and Review articles highlighting the evolution in our understanding of cancer genomes and postulating where we can progress from here.
In this Research Topic, we are inviting contributions from authors with expertise in cancer molecular genetics, cytogenetics, and cell biology. Recent insights in cancer cell biology have demonstrated that both carcinogenesis and tumorigenesis, as well as recurrence, lead to genomic dysfunctionality in cancer stem cells (CSCs) and progenitor cell lineages due to stress and oxygen excess. To restore the functionality and stability of the genome, dysfunctional cells with irreparable DNA double-strand breaks (DSBs) and aberrant tetraploid/aneuploid cell cycles are repaired through cell-to-cell fusion and epigenetic modifications, leading to the formation of polyploid/multinucleated giant cancer cells (PGCCs/MNGCs) and hyperpolyploidy. The functional genome of PGCC progeny regains differentiation and stemness potential, thereby restoring functional genome architecture and countering stress-induced genome dysfunctionality.
All these processes are orchestrated by various players and intracellular pathways that can be leveraged in the fight against cancer. We anticipate new findings and explanations documenting the loss and regain of genome stability at the molecular level, thereby enlightening readers with diverse aspects of cancer genomics and comparative genomics. This Research Topic welcomes high-quality Original Research and Review articles highlighting the evolution in our understanding of cancer genomes and postulating where we can progress from here.
Keywords: Cancer evolution, Comparative genomics, Tumor heterogeneity, Cancer ecology, Tumor ecosystem, Oncology dynamics, Tumor microenvironment, Comparative oncology, Single-cell oncology, Quantum and Chaos oncology, Omics and Evolution oncology
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
