The Role of MDM2 in Tumor Biology and Cancer Therapy
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell and Gene Therapy".
Deadline for manuscript submissions: 30 June 2024 | Viewed by 64
Special Issue Editors
Interests: oncogene; tumor supressor; drug discovery and development; targeted therapy; cancer prevention
Special Issues, Collections and Topics in MDPI journals
Interests: drug discovery; molecular targets; pharmacology; chemical; biology; membrane transporters; flow cytometry
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The MDM2 (Mouse Double Minute 2) oncogene is one of the most-investigated oncogenes, and its p53-dependent and p53-independent activities have been well demonstrated. Recent research has made several breakthrough discoveries. For instance, the in-depth analysis of MDM2-p53 interaction has led to the discovery of novel modulators of this classical pathway and continued efforts to develop and optimize small molecule inhibitors targeting the MDM2-p53 interaction. The exploration of MDM2 in tumor metabolism has shown the role of MDM2 in regulating several metabolic pathways, which could provide insights into novel therapeutic strategies. Beyond its role in the regulation of p53, there has been an increased focus on the non-canonical functions of MDM2, indicating its involvement in DNA repair, chromatin remodeling, and other cellular processes that contribute to tumorigenesis. Studies exploring the interactions between MDM2 and the tumor microenvironment have shown that MDM2 influences immune responses, angiogenesis, and the extracellular matrix within the tumor microenvironment. There are increasing investigations into the crosstalk between MDM2 and epigenetic regulators such as chromatin-modifying enzymes and other epigenetic modifiers. Advances in structural biology and computational modeling have contributed to a deeper understanding of the MDM2-p53 interaction. The role of MDM2 in cancer stem cells has been implicated in tumor initiation, progression, and treatment resistance. Finally, MDM2 as a therapeutic target has been demonstrated in different cancer types, including less well-studied or rare cancers. Investigating mechanisms of resistance to MDM2 inhibitors is crucial for optimizing treatment strategies. Additionally, combining MDM2 inhibitors with immunotherapy approaches is an area of interest. This Special Issue will cover the latest advances made in the last few years.
Prof. Dr. Ruiwen Zhang
Dr. John Buolamwini
Guest Editors
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 short 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. Cells 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 2700 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
- MDM2
- p53
- targeted therapy
- imunotherapy
- drug resistance
