Intratumor Heterogeneity and Therapy Resistance of Solid Tumors: Treacherous Apoptosis, Reversible Senescence, Genome Chaos, and More

Dear Colleagues,

Single-cell biology has revealed that acquired resistance of cancer cells to therapeutic agents is multifactorial, with several unrelated mechanisms employed simultaneously by different subsets of cancer cells within the same tumor (intratumor heterogeneity). These include therapy-induced dormancy (durable proliferation arrest through polyploidy, multinucleation, and other manifestations of genome chaos), oncogenic caspase-3 activation (treacherous apoptosis), anastasis (a cell recovery phenomenon that rescues cancer cells from the brink of apoptotic and other modes of cell death), and cell fusion. The wild-type p53 and its downstream effector p21^WAF1 also contribute to intratumor heterogeneity by activating transient cell cycle checkpoints to promote DNA repair, downregulating apoptotic cell death, and triggering a reversible proliferation arrest through premature senescence.

The purpose of this Special Issue is to provide a comprehensive update on the growing complexity of molecular and cellular responses to anticancer agents. Reviews and original research articles that utilize single cell biology to study the long-term fate of solid tumors/tumor-derived cell lines following treatment with anticancer agents are particularly welcomed.

Prof. Dr. Razmik Mirzayans
Guest Editor

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• intratumor heterogeneity
• p53 signaling
• cell fusion
• reversible senescence
• anastasis
• oncogenic caspse-3
• chromothripsis (genome chaos)
• polyploid giant cancer cells (PGCCS)
• atavistic basis of therapy resistance
• cancer cell dormancy