Cancer Cell Response to Radiation Therapy
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 11381
Special Issue Editors
Interests: cell biology; immunology; cancer research; cancer biology; radiation biology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Radiotherapy is an effective method in the treatment of various tumor entities. The aim of radiotherapy is to inhibit the ongoing proliferation of tumor cells. The main biological goal of radiotherapy is the induction of DNA damage in tumor cells. Depending on the radiation dose, oxygenation, ability to repair DNA damage, the cell cycle and the microenvironment of the tumor, different cellular responses can occur. Cells with at least partially functional DNA damage response induce cell cycle arrest and activate DNA damage repair by homologous recombination (HR) or non-homologous end compound (NHEJ). If this is successful, the cells re-enter the cell cycle. If this is not successful, the cells can enter a permanent cell cycle block and induce senescence. In the case of more severe damage, the primary mechanism of radiation-induced cell death in solid tumours is mitotic catastrophe, a pathway that leads to cell death after a disrupted mitosis process. Another form of cell death is apoptosis, which occurs mainly after radiotherapy of haematological malignancies. The expansion of knowledge about the signalling pathways involved and the factors that influence the type of cell death will become increasingly important in the future, as a large number of targeted drugs against the response to DNA damage are currently being studied in clinical trials. These new drugs, known as DNA damage response inhibitors (DDRi), were developed as combination drugs for immune-oncology, but will have a strong influence on the effect of radiotherapy and open up the possibility of new treatment strategies.
We are looking forward to your contributions to this Special Issue.
Prof. Dr. Luitpold Valentin R. Distel
Dr. Markus Hecht
Guest Editors
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Keywords
- radiation
- DNA damage response
- homologous recombination
- non-homologous end joining
- cell death
- mitotic catastrophe
- senescence
- targeted therapy
