Role of TP53 Gene in Preventing Cancer and Promoting Adaptation
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 4433
Special Issue Editor
Interests: cancer evolution; DNA repair genes; antagonistic pleiotropy and human disease; genetic linkage disequilibrium and multifactorial diseases
Special Issue Information
Dear Colleagues,
The TP53 gene is a major player in cancer formation, and is considered the most important tumor suppressor gene. The P53 protein is involved in DNA repairment, senescence, cell-cycle control, autophagy, and apoptosis. Beyond cancer, there is evidence that TP53 is associated with fertility, aging and longevity. Genetic variants of TP53 may also have adaptive consequences.
It has recently been proven that multiple cancer genes, TP53 included, are under selection in healthy human tissues. It is still unknown why these cancer genes’ mutations do not transform these tissues into cancerous ones. Other studies have shown that elephants and whales have multiple TP53 copies, probably preventing cancer and being the reason for the very low cancer incidence in these species. Additionally, special TP53 amino acid residues or TP53 mutations seem to be adaptive for animals living in hypoxic and cold environments or having been exposed to starvation, respectively.
This Special Issue is focused on the mechanisms that involve TP53 to protect species against cancer and on promoting their adaptation, at any biological level: cells, tissues, organs, individuals, and populations. We invite all scientists working on the p53 pathway to participate in this Special Issue. Original research articles or reviews on all TP53 aspects, such as functional genetics/genomics, pathway investigation, the tumor microenvironment, mechanisms of carcinogenesis, and molecular evolution, are welcome.
Dr. Konstantinos Voskarides
Guest Editor
Manuscript Submission Information
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Keywords
- p53
- pathway analysis
- cancer evolution
- somatic mutation
- tumor suppressor
- tumor microenvironment
- neoplasia
- apoptosis
- adaptation
- stress
