The p53 Pathway in Cancer Research
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (24 May 2024) | Viewed by 478
Special Issue Editor
2. Laboratory of Biophysics and p53 Protein Biology, Department of Biochemistry, Medical University of Warsaw, Warsaw, Poland
Interests: p53; p73; driver mutations; drug discovery; drug repurposing; cancer metabolism; oncology and hematology; longevity
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
It is a pleasure to announce the launch of the Special Issue “The p53 Pathway in Cancer Research”.
The p53 tumor suppressor is evolutionarily conserved, and evolved from unicellular choanoflagellates. The last common ancestor of the choanoflagellates and humans, likely urchoanozoan, lived around 800 million years ago and may be one of the earliest multicellular organisms with a p53-like protein.
TP53 belongs to the p53 protein family, which includes TP63 and TP73; all three are characterized by high conservation in structure and function. p53 is a transcription factor and has transcription-dependent and independent activities. p53 requires a functional DNA binding domain to drive the transcription of target genes. The amino acid sequence and structure of the DNA binding domains of the p53 protein family have been preserved over broad evolutionary time frames and highlight the central role of this domain in their cellular functions.
p53 partakes in DNA damage and stress response, cell cycle regulation, senescence, cell death, immunity, fertility, and energy metabolism or longevity. In cancers, the mutated p53 protein contributes to stemness, metastasis, and drug resistance and supports the tumor microenvironment. Mutations in the TP53 gene, which revoke the tumor suppressor activities of its encoded protein, are present in around 50% of all cancer cases. Thus, TP53 mutations are the most common single gene alterations in cancers and have become classified as driver events in many types of tumors.
Despite significant advances in understanding the role of p53 in tumor suppression, cancer progression and cancer drug resistance, TP53 mutated cancers remain a great, unmet medical challenge.
This Special Issue focuses on how and to what avail the p53 protein family members drive the p53 pathway in cancers.
Dr. Joanna Zawacka
Guest Editor
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
Keywords
- p53
- p73
- p63
- isoforms, drivers
- tumor microenvironment
- cell death
- metabolism
- drug response and resistance
- immunosurveillance
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