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Pathophysiology
Special Issues
MYC in Regeneration and Tumorigenesis
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MYC in Regeneration and Tumorigenesis

A special issue of Pathophysiology (ISSN 1873-149X).

Deadline for manuscript submissions: closed (15 July 2024) | Viewed by 9425

Special Issue Editor

Dr. Roderik Kortlever

E-Mail Website
Guest Editor
Francis Crick Institute, London NW1 1AT, UK
Interests: Myc; oncogenes; tumor microenvironment; lung cancer; inflammation; immunotherapy

Special Issue Information

Dear Colleagues,

Myc is a master regulator of a myriad of cellular functions.  As a transcription factor, Myc controls the growth, death and motility of a cell; organizes the cell's metabolism; promotes inter and intracellular signalling; and drives angiogenesis, among others. Its expression and activity is tightly controlled and precisely timed according to the need of a growing tissue, either during development or regeneration after damage or wounding. Myc is a non-redundant and necessary conduit for driving cellular growth and death in both an intrinsic and extrinsic fashion; it is pivotal in programming cellular and microenvironmental organisation. Consequently, when deregulated, the proto-oncogene Myc is associated with promoting the growth and spread of most—if not all—cancers, and its pleiotropic array of traits mirror many cancer hallmarks. Over three decades of Myc research have fortified an understanding that this makes it ideally suited as an anti-cancer target. The challenge lies in targeting Myc itself, or, second best, the programs that Myc executes to establish growth. The last few years have seen exciting progress towards achieving either goal, but it remains highly important to continue deepening our understanding of the biology driven by Myc.

For this Special Issue, we invite you to submit original research or review articles on the topic of ‘Myc in Regeneration and Tumorigenesis’.

Dr. Roderik Kortlever
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 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. Pathophysiology is an international peer-reviewed open access quarterly 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 1400 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

  • Myc 
  • oncogene 
  • regeneration 
  • cancer 
  • transcription factor 
  • tumorigenesis

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 papers)

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Research

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18 pages, 3461 KiB  
Article
Shift of N-MYC Oncogene Expression in AML Patients Carrying the FLT3-ITD Mutation
by Konstantin Bogdanov, Ekaterina Kudryavtseva, Yulia Fomicheva, Irina Churkina, Elza Lomaia, Larisa Girshova, Yuri Osipov and Andrey Zaritskey
Pathophysiology 2023, 30(3), 296-313; https://doi.org/10.3390/pathophysiology30030024 - 1 Aug 2023
Viewed by 1420
Abstract
Mutations in the FLT3 gene not only lead to abnormalities in its structure and function, but also affect the expression of other genes involved in leukemogenesis. This study evaluated the expression of genes that are more characteristic of neuroblastoma but less studied in [...] Read more.
Mutations in the FLT3 gene not only lead to abnormalities in its structure and function, but also affect the expression of other genes involved in leukemogenesis. This study evaluated the expression of genes that are more characteristic of neuroblastoma but less studied in leukemia. N-MYC oncogene expression was found to be more than 3-fold higher in primary AML patients carrying the FLT3-ITD mutation compared to carriers of other mutations as well as patients with normal karyotype (p = 0.03946). In contrast to the expression of several genes (C-MYC, SPT16, AURKA, AURKB) directly correlated to the allelic load of FLT3-ITD, the expression of the N-MYC oncogene is extremely weakly related or independent of it (p = 0.0405). Monitoring of N-MYC expression in some patients with high FLT3-ITD allelic load receiving therapy showed that a decrease in FLT3-ITD allelic load is not always accompanied by a decrease in N-MYC expression. On the contrary, N-MYC expression may remain elevated during the first three months after therapy, which is additional evidence of the emergence of resistance to therapy and progression of AML. Full article
(This article belongs to the Special Issue MYC in Regeneration and Tumorigenesis)
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Review

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20 pages, 2048 KiB  
Review
Unraveling MYC’s Role in Orchestrating Tumor Intrinsic and Tumor Microenvironment Interactions Driving Tumorigenesis and Drug Resistance
by Zinab O. Doha and Rosalie C. Sears
Pathophysiology 2023, 30(3), 400-419; https://doi.org/10.3390/pathophysiology30030031 - 11 Sep 2023
Cited by 4 | Viewed by 2462
Abstract
The transcription factor MYC plays a pivotal role in regulating various cellular processes and has been implicated in tumorigenesis across multiple cancer types. MYC has emerged as a master regulator governing tumor intrinsic and tumor microenvironment interactions, supporting tumor progression and driving drug [...] Read more.
The transcription factor MYC plays a pivotal role in regulating various cellular processes and has been implicated in tumorigenesis across multiple cancer types. MYC has emerged as a master regulator governing tumor intrinsic and tumor microenvironment interactions, supporting tumor progression and driving drug resistance. This review paper aims to provide an overview and discussion of the intricate mechanisms through which MYC influences tumorigenesis and therapeutic resistance in cancer. We delve into the signaling pathways and molecular networks orchestrated by MYC in the context of tumor intrinsic characteristics, such as proliferation, replication stress and DNA repair. Furthermore, we explore the impact of MYC on the tumor microenvironment, including immune evasion, angiogenesis and cancer-associated fibroblast remodeling. Understanding MYC’s multifaceted role in driving drug resistance and tumor progression is crucial for developing targeted therapies and combination treatments that may effectively combat this devastating disease. Through an analysis of the current literature, this review’s goal is to shed light on the complexities of MYC-driven oncogenesis and its potential as a promising therapeutic target. Full article
(This article belongs to the Special Issue MYC in Regeneration and Tumorigenesis)
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11 pages, 932 KiB  
Review
Long Non-Coding RNAs as “MYC Facilitators”
by Daniel García-Caballero, Jonathan R. Hart and Peter K. Vogt
Pathophysiology 2023, 30(3), 389-399; https://doi.org/10.3390/pathophysiology30030030 - 1 Sep 2023
Viewed by 1455
Abstract
In this article, we discuss a class of MYC-interacting lncRNAs (long non-coding RNAs) that share the following criteria: They are direct transcriptional targets of MYC. Their expression is coordinated with the expression of MYC. They are required for sustained MYC-driven cell proliferation, and [...] Read more.
In this article, we discuss a class of MYC-interacting lncRNAs (long non-coding RNAs) that share the following criteria: They are direct transcriptional targets of MYC. Their expression is coordinated with the expression of MYC. They are required for sustained MYC-driven cell proliferation, and they are not essential for cell survival. We refer to these lncRNAs as “MYC facilitators” and discuss two representative members of this class of lncRNAs, SNHG17 (small nuclear RNA host gene) and LNROP (long non-coding regulator of POU2F2). We also present a general hypothesis on the role of lncRNAs in MYC-mediated transcriptional regulation. Full article
(This article belongs to the Special Issue MYC in Regeneration and Tumorigenesis)
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20 pages, 1255 KiB  
Review
Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration
by Barbara Illi and Sergio Nasi
Pathophysiology 2023, 30(3), 346-365; https://doi.org/10.3390/pathophysiology30030027 - 2 Aug 2023
Cited by 5 | Viewed by 2839
Abstract
Myc is one of the most well-known oncogenes driving tumorigenesis in a wide variety of tissues. From the brain to blood, its deregulation derails physiological pathways that grant the correct functioning of the cell. Its action is carried out at the gene expression [...] Read more.
Myc is one of the most well-known oncogenes driving tumorigenesis in a wide variety of tissues. From the brain to blood, its deregulation derails physiological pathways that grant the correct functioning of the cell. Its action is carried out at the gene expression level, where Myc governs basically every aspect of transcription. Indeed, in addition to its role as a canonical, chromatin-bound transcription factor, Myc rules RNA polymerase II (RNAPII) transcriptional pause–release, elongation and termination and mRNA capping. For this reason, it is evident that minimal perturbations of Myc function mirror malignant cell behavior and, consistently, a large body of literature mainly focuses on Myc malfunctioning. In healthy cells, Myc controls molecular mechanisms involved in pivotal functions, such as cell cycle (and proliferation thereof), apoptosis, metabolism and cell size, angiogenesis, differentiation and stem cell self-renewal. In this latter regard, Myc has been found to also regulate tissue regeneration, a hot topic in the research fields of aging and regenerative medicine. Indeed, Myc appears to have a role in wound healing, in peripheral nerves and in liver, pancreas and even heart recovery. Herein, we discuss the state of the art of Myc’s role in tissue regeneration, giving an overview of its potent action beyond cancer. Full article
(This article belongs to the Special Issue MYC in Regeneration and Tumorigenesis)
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