Cell Cycle Control and Cancer
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Proliferation and Division".
Deadline for manuscript submissions: closed (1 November 2020) | Viewed by 73439
Special Issue Editor
Special Issue Information
Dear Colleagues,
Duplication of the genome followed by cell division is essential for keeping tissue homoeostasis in multicellular organisms. Progression through the cell cycle is tightly regulated by evolutionary conserved cyclin-dependent kinases. In the presence of DNA damage, cells temporarily arrest in the checkpoints to allow DNA repair or they are permanently eliminated by senescence or apoptosis. Replication stress caused by activation of oncogenes is emerging as a major source of DNA damage in precancerous lesions, whereas the checkpoint arrest and apoptosis are now recognized as an intrinsic barrier preventing development of genome instability and cell transformation. Genetic defects in the core cell cycle regulators as well as in DNA repair and surveillance mechanisms are common in human cancers. Most typically, loss of the tumor suppressor p53 allows cell proliferation in the presence of genotoxic stress and promotes genome instability. At the same time, deficient cell cycle control may cause increased vulnerability of cancer cells to various treatments. Inhibitors of the checkpoint kinases CHK1 and WEE1 in combination with various DNA damaging agents efficiently eliminate p53-deficient cancer cells and are now being clinically tested in cancer therapy. Alternative approaches target the negative regulators of p53 (including MDM2 and WIP1) or the mutant p53 itself to allow reactivation of the p53 function, leading to cytotoxicity in cancer cells. Finally, specific CDK4/6 inhibitors significantly improve progression free survival in advanced ER+ breast cancer patients and are now being tested in other clinical settings. Despite the promising results in preclinical testing of the cell cycle targeting drugs, resistance commonly develops during the cancer treatment. Therefore, better understanding of the general molecular mechanisms, identification of new synthetically lethal combinations of the drugs or genetic defects as well as identification of suitable biomarkers are critically needed for exploitation of the cell cycle inhibitors in cancer therapy.
This Special Issue will cover all areas of the cell cycle and checkpoint control in normal and cancer cells. Both original research articles and reviews are welcome.
Dr. Libor Macurek
Guest Editor
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Keywords
- cell cycle
- checkpoint
- senescence
- DNA damage
- replication stress
- P53 pathway
- synthetic lethality
- CHK1 and WEE1 inhibitors
- CDK4 inhibitor
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