p53 Signaling in Cancer Progression and Therapy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 2703

Special Issue Editor


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Guest Editor
Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland
Interests: p53 protein; regulation of p53 expression; cancer development; translation initiation mechanisms; structure and function of the 5' - terminus of RNAs

Special Issue Information

Dear Colleagues,

The p53 protein is one of gatekeepers in the cell which plays a pivotal role as a transcriptional factor involved in cell cycle regulation and tumorigenesis prevention. Under normal conditions the level of p53 protein is kept low due to interaction with E3 ubiquitin ligase Mdm2. In the presence of stress factors p53 is phosphorylated to prevent the interaction with Mdm2 and as a consequence p53 signaling pathway is activated. It eventually leads to rebuild cell homeostasis. Mutations in TP53 gene cause production of faulty p53 protein which loses its ability to govern the efficient cell response to stress. This, in many cases, results in cancer development. It has been pointed that mutations in TP53 gene are observed in approximately 50-60% of cancers including breast, lung, colon, prostate, liver and bladder. Since effectiveness of p53 signaling pathway is crucial to suppress tumor development mutated p53 protein is one of a major target in anti-cancer therapies. Restoration of ability of p53 to act properly seems to be an attractive alternative approach in treatment of cancer patients.

In this Special Issue we will discuss the multi-functions of p53 protein; its involvement in stress response and tumor suppression. Hopefully, this Special Issue will provide fascinating insight into the p53 signaling pathway and how mutant of p53 is able to change the cell fate. This Special Issue will also be a great opportunity to examine potential therapeutic approaches based on targeting p53 mutants to restore proper acting of p53 signaling network.

Dr. Agata Świa̧tkowska
Guest Editor

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Keywords

  • p53 protein
  • p53 signaling pathway
  • Mdm2-p53 axe
  • TP53 gene
  • p53 hotspot mutations
  • cell cycle
  • apoptosis
  • tumor progression
  • anti-cancer therapy

Published Papers (1 paper)

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Review

18 pages, 1428 KiB  
Review
TP53 Alterations in Myelodysplastic Syndromes and Acute Myeloid Leukemia
by Ramy Rahmé, Thorsten Braun, James J. Manfredi and Pierre Fenaux
Biomedicines 2023, 11(4), 1152; https://doi.org/10.3390/biomedicines11041152 - 11 Apr 2023
Cited by 3 | Viewed by 2384
Abstract
TP53 mutations are less frequent in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) than in solid tumors, except in secondary and therapy-related MDS/AMLs, and in cases with complex monosomal karyotype. As in solid tumors, missense mutations predominate, with the same hotspot mutated [...] Read more.
TP53 mutations are less frequent in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) than in solid tumors, except in secondary and therapy-related MDS/AMLs, and in cases with complex monosomal karyotype. As in solid tumors, missense mutations predominate, with the same hotspot mutated codons (particularly codons 175, 248, 273). As TP53-mutated MDS/AMLs are generally associated with complex chromosomal abnormalities, it is not always clear when TP53 mutations occur in the pathophysiological process. It is also uncertain in these MDS/AML cases, which often have inactivation of both TP53 alleles, if the missense mutation is only deleterious through the absence of a functional p53 protein, or through a potential dominant-negative effect, or finally a gain-of-function effect of mutant p53, as demonstrated in some solid tumors. Understanding when TP53 mutations occur in the disease course and how they are deleterious would help to design new treatments for those patients who generally show poor response to all therapeutic approaches. Full article
(This article belongs to the Special Issue p53 Signaling in Cancer Progression and Therapy)
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