- Zahid Hussain Siddik, Ph.D.
- Professor of Medicine (Pharmacology), Department of Experimental Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
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Special Issue Introduction
The tumor suppressor p53 is a critical transcriptional factor in cancer chemotherapy since it facilitates the response of tumors to a variety of chemotherapeutic drugs. Indeed, a vast majority of these drugs rely heavily on p53 to transactivate and/or transrepress its target genes and induce growth arrest and/or activate the apoptotic cell death pathway. This p53-dependent antitumor response, however, is susceptible to downregulation or inhibition from a variety of mechanisms, with p53 mutations dominating the landscape. However, substantial drug resistance is also observed in refractory tumors harboring wild-type p53, where the mechanisms may include overexpression of negative regulators (such as MDM2 and MDM4) and attenuation in post-translational phosphorylation. A critical understanding of mechanisms involved is essential for the design of novel therapies that will circumvent resistance and restore/enhance antitumor response in the clinic.
The Special Issue of The Role of p53 in Cancer Drug Resistance invites contributions that are focused on p53 and describe novel mechanisms of drug resistance, shed new light or challenge existing mechanisms, and propose new therapies or regimens that restore tumor sensitivity or selectivity.
Keywordsp53 tumor suppressor, cancer therapy, drug resistance, p53 mutation, apoptosis, autophagy, post-translational modification, transactivation, transrepression, cell cycle arrest, MDM2, MDM4
Submission Deadline31 Oct 2020