p53 Pathway in Cancer Progression and Cancer Therapy
A special issue of Biomolecules (ISSN 2218-273X).
Deadline for manuscript submissions: closed (26 January 2018) | Viewed by 11472
Special Issue Editor
Interests: cell cycle checkpoint; DNA damage response; cancer
Special Issue Information
Dear Colleagues,
Mutation or functional inactivation of the tumor suppressor p53 promotes cancer development; therefore, p53 has been at the center of researchers’ interest for nearly four decades. Various stress response pathways converge on p53, which, by triggering transcription of target genes, controls essential cell fate decisions, ranging from a temporal cell cycle arrest to permanent senescence or apoptosis. In addition to these canonical roles, p53 is implicated in a plethora of other functions, including DNA repair, miRNA production, autophagy, energy metabolism, and stem cell differentiation. There is now emerging evidence that deficient p53 response, not only contributes to tumorigenesis, but could be also exploited in targeted cancer therapy. It has been shown that loss of p53 in cancer cells shows synthetic lethality with certain forms of chemotherapy. Discovery that p53 reactivation leads to tumor regression in animal models boosted the development of several small molecule antagonists of MDM2, which allow p53 stabilization and the induction of cell death in p53 proficient tumors. Finally, gain-of-function mutations of p53 promote stemness of cancer stem cells and, therefore, specific targeting of the mutant p53 could prevent tumor progression.
We encourage scientists to submit their original work or review articles focused on the novel roles of p53 in cell physiology and cancer development, or on the exploitation of p53 pathway in cancer therapy. Both translational and basic research papers are welcome.
Dr. Libor Macurek
Guest Editor
Manuscript Submission Information
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Keywords
- p53
- cancer
- tumor suppressor
- DNA damage response
- Cell cycle checkpoint
- small-molecule inhibitor
- cell death
- synthetic lethality