About this Research Topic
In 1979, several groups independently discovered p53 by using sera from animals with SV40- induced tumors to immunoprecipitate large T antigen from SV40, which binds a non-viral protein with an apparent molecular mass of about 53 kDa. The p53 protein is encoded by the TP53 gene and was initially described as a cellular oncogene because when the gene was transfected into certain types of cells, it could immortalize them and cooperate with other oncogenes in cell transformation. However, it was not until the late 1980s that p53 was identified as a tumor suppressor and that evidence of its supposed oncogenic functions had been wrongly obtained from mutant tumor-derived clones. Therefore, the potential of p53 mutant protein to promote cancer was one of the first findings in the field of p53 research. So, we have, on one hand, p53 wild-type protein is one of the most important tumor suppressors. But, on the other hand, p53 mutant proteins contribute to the development of cancer. This stark comparison creates an interesting duality to study and understand in cancer.
p53 is a multifunctional protein, regulating cell cycle, DNA repair, apoptosis, differentiation, metabolism, inflammation, immune response, senescence, and autophagy. However, inactivating mutations in the TP53 gene occur in around 50% of all human tumors and are associated with tumor progression and resistance to cancer therapy. Several reports support the gain of function shown in mutant p53 in tumor development. Therefore, this topic could contribute to join several works that help to suggest or give ideas of how targeting p53 mutants can act as an anticancer treatment strategy.
We welcome Original Research and Review Articles that cover recent and current wild type and mutant p53 research in cancer, these works can describe different aspects of our biochemical, biophysical, molecular, cellular, genetic, physiological, pathological, and translational understandings of wild type and mutant p53 and its importance for cancer prevention and cancer therapy. This collection will cover, but is not limited to, the following sub-topics:
• p53 Biological Activities in tumor Suppression
• p53 and family members
• p53 and isoforms
• Mutant p53 Gain-of-Function in cancer
• Mechanism of Mutant p53 Gain-of-Function
• Mouse models for p53 mutation in cancer
• Targeting oncogenic mutant p53 for cancer therapy
We would like to acknowledge Dr. Fernanda Cisneros-Soberanis as the Research Topic coordinator for this article collection.
p53 is a multifunctional protein, regulating cell cycle, DNA repair, apoptosis, differentiation, metabolism, inflammation, immune response, senescence, and autophagy. However, inactivating mutations in the TP53 gene occur in around 50% of all human tumors and are associated with tumor progression and resistance to cancer therapy. Several reports support the gain of function shown in mutant p53 in tumor development. Therefore, this topic could contribute to join several works that help to suggest or give ideas of how targeting p53 mutants can act as an anticancer treatment strategy.
We welcome Original Research and Review Articles that cover recent and current wild type and mutant p53 research in cancer, these works can describe different aspects of our biochemical, biophysical, molecular, cellular, genetic, physiological, pathological, and translational understandings of wild type and mutant p53 and its importance for cancer prevention and cancer therapy. This collection will cover, but is not limited to, the following sub-topics:
• p53 Biological Activities in tumor Suppression
• p53 and family members
• p53 and isoforms
• Mutant p53 Gain-of-Function in cancer
• Mechanism of Mutant p53 Gain-of-Function
• Mouse models for p53 mutation in cancer
• Targeting oncogenic mutant p53 for cancer therapy
We would like to acknowledge Dr. Fernanda Cisneros-Soberanis as the Research Topic coordinator for this article collection.
Keywords: p53, cancer, mutant p53, isoforms. Gain of function.
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