Drug Resistance and Cell Death in Cancer
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (15 April 2021) | Viewed by 43013
Special Issue Editors
Interests: cell death; drug resistance; apoptosis; necroptosis; death receptor; Caspase-8; FLIP
Interests: p53; p63; transcription factors; genomics; computational biology; data integration
Special Issue Information
Dear Colleagues,
Drug resistance limits the efficacy of all chemotherapies and targeted-therapies used to treat cancer, and ultimately arises because of a failure of these therapies to eliminate (“kill”) all of the cancerous cells. In recent years, our knowledge of the mechanisms underpinning programmed cell death, “apoptosis”, has significantly increased, and novel therapeutics that leverage this knowledge to directly engage apoptosis in tumor cells have now reached the clinic and achieved their first FDA approvals. Apoptosis is affected by changes in the cellular metabolism and response to DNA damage amongst other critical homeostatic processes that are frequently dysfunctional in cancer. Thus, the apoptotic response of cancer cells to therapy is highly dependent on the genetic and molecular drivers of a particular tumor. The interplay between the immune system and cancer cells is critical for the elimination of cancer cells, not only by immune-oncology agents, but also by chemotherapy and targeted therapies. Furthermore, novel forms of programmed cell death, such as necroptosis and ferroptosis, are being increasingly well characterized; however, their roles in drug resistance are relatively unknown. In this Special Edition, we review several critical aspects of drug resistance and cell death.
Prof. Daniel Longley
Dr. Simon McDade
Dr. Emma Kerr
Guest Editors
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Keywords
- drug resistance
- cell death
- apoptosis
- necroptosis
- ferroptosis
- metabolism
- p53
- chemotherapy
- targeted therapy
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