Dear Colleagues,

Our genomes are subject to potentially deleterious alterations resulting from endogenous sources, exogenous sources, and medical diagnostic and treatment applications. Genome integrity and cellular homeostasis are maintained through an intricate network of pathways that serve to recognize the DNA damage, activate cell cycle checkpoints and facilitate DNA repair, or to eliminate highly injured cells from the proliferating population. Mutations in genes that encode the key players of the DNA surveillance networks are associated with a wide spectrum of human cancer-prone disorders, as well as human cancers.

Anticancer agents have been extensively studied in the context of triggering programmed cell death (apoptosis). Single-cell observation methods have demonstrated heterogeneity in cancer cells within a given tumor and that apoptosis is not always associated with cancer cell demise. For example, cells exhibiting some features of apoptosis post-treatment can undergo a reversal process (anastasis) and survive. In addition, studies with solid tumors and solid tumor-derived cell lines have demonstrated that exposure to moderate, clinically relevant doses of anticancer agents predominantly triggers cancer cell dormancy (sustained proliferation arrest through, e.g., senescence and/or polyploidy) rather than apoptosis. Dormant cancer cells exhibit an enlarged morphology, remain viable, secrete a myriad of tumor promoting factors, and can give rise to progeny with stem cell-like properties.

The purpose of this Special Issue is to provide a comprehensive update on the growing complexity of cellular responses to DNA-damaging agents. Articles on advances in single-cell detection methodology to study the long-term fate of human cells following anticancer treatment are particularly welcomed.

Potential topics include, but are not limited to:

• DNA repair deficiency syndromes
• DNA repair pathways
• Cell cycle checkpoints
• Biological outputs orchestrated by p53 signaling
• Cancer cell dormancy and disease relapse post-therapy
• Reversible apoptosis (anastasis)
• Reversible polyploidy/multinucleation (atavistic model of cancer)
• Novel therapeutic strategies targeting dormant cancer cells

Prof. Dr. Razmik Mirzayans
Guest Editor

Manuscript Submission Information

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• Human DNA repair-deficiency syndromes
• DNA damage response
• DNA repair
• Cell cycle checkpoints
• Radiotherapy
• Chemotherapy
• p53 signaling
• Senescence
• Apoptosis
• Polyploidy
• Multinucleation
• Stemness
• Anastasis
• Atavistic model of cancer
• Cancer cell dormancy
• Single cell analysis