Tumor-Promoting Functions of DNA Damage and Stress Response Signaling
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 13326
Special Issue Editors
Interests: DNA damage signaling; stress-induced signaling; tumor heterogeneity; stemness; senescence; epigenetic reprogramming; tumor microenvironment; autophagy; apoptosis
Special Issue Information
Dear Colleagues,
Therapies with broad targeting anticancer activity have significant favorable effects. Nevertheless, the presence of resistant cancer cells or acquisition of resistance in response to drug treatment represent major barriers to a full cure. Activation of DNA damage response (DDR) remains the main route for efficient cancer treatment in response to chemo- and radiotherapy. It is well documented, however, that under certain conditions, DDR can promote tumorigenesis. The mechanisms of this phenomenon are not completely understood but generally attributed to an increased mutation rate that is believed to either activate oncogenes or disable tumor suppressors, thus favoring tumorigenesis. Increasing evidence, however, suggests that chemo- and radiotherapy exert numerous tumor-promoting effects that cannot be exclusively explained by genetic alterations in cancer cells.
This Special Issue will highlight the emerging role of DNA damage and stress responses as important drivers of cancer evolution at the level of epigenetic reprogramming, modulation of senescence, induction of cancer cell plasticity, regulation of immune responses and tumor microenvironment, as well as other non-genetic changes. These novel basic and translational aspects could advance our understanding of targeting DNA damage and stress responses, ultimately improving our current anticancer therapeutic regimes.
Dr. Dmitry V. Bulavin
Dr. Alexander Emelyanov
Guest Editors
Manuscript Submission Information
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Keywords
- DNA damage signaling
- stress-induced signaling
- tumor heterogeneity
- stemness
- senescence
- epigenetic reprogramming
- tumor microenvironment
- autophagy
- apoptosis
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