Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
4.4
Journals
Cancers
Special Issues
Tumor Suppressor Genes and Oncogenes: Genome-Wide Insights into Cancer Biology
cancers-logo
Submit to Special Issue Submit Abstract to Special Issue Review for Cancers Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Tumor Suppressor Genes and Oncogenes: Genome-Wide Insights into Cancer Biology

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1913

Special Issue Editor

Dr. Meena Kanduri

E-Mail Website
Guest Editor
Department of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Interests: epigenetics; cancer; tumor suppressor; oncogenes

Special Issue Information

Dear Colleagues,

Tumor suppressor genes (TSGs) play an important role in cancer progression. In healthy cells, they regulate essential processes such as cell cycle regulation, DNA damage repair and cellular differentiation. However, when mutated or dysregulated, they give rise to aberrant molecular processes in cancer cells. Therefore, understanding their functions in oncogenesis is crucial for establishing cancer prevention and treatment strategies. In cancers, TSGs are primarily silenced through mutations, deletions, DNA methylation, histone modifications and post-transcriptional regulation, resulting in deregulated cellular checkpoints, DNA repair and apoptosis, thereby promoting cancer development. Studies have also shown that TSGs can function in a cell-type-specific manner, with their activity tightly regulated by the epigenetic landscape, transcriptional networks, and microenvironmental signals unique to each tissue.

At the same time, oncogenes—when activated or amplified—drive uncontrolled cell proliferation, survival, and metastasis, acting as powerful tumor-promoting factors. Thus, the interplay between tumor suppressor genes and oncogenes represents a fundamental axis of cancer biology.

Genome analysis using next-generation sequencing techniques has revolutionized our understanding of cancer biology, allowing researchers not only to study the entire genetic landscape of cancer cells but also pave the way for personalized medicine, where treatments are tailored to the genetic profiles of individual patients’ tumors. Techniques such as whole-genome sequencing, exome sequencing, and RNA sequencing enable the identification of tumor suppressor gene alterations, discovery of novel cancer-associated mutations, and development of targeted therapeutic strategies.

In this Special Issue, we highlight the role of and mechanisms behind the regulation of TSGs in cancer, emphasizing genome-wide studies and the systematic characterization of tumor suppressor gene alterations that are essential for advancing cancer diagnostics, prognosis, and personalized treatment strategies.

Dr. Meena Kanduri
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 250 words) can be sent to the Editorial Office for assessment.

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

  • tumor suppressor genes
  • oncogenes
  • cancer
  • genome analysis
  • cancer mutations
  • DNA methylation
  • histone modification
  • cancer progression
  • oncogenesis

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

23 pages, 2501 KB  
Article
SNAT1 (SLC38A1) Is Not the Main Glutamine Transporter in Melanoma, but Controls Metabolism via Glutamine-Dependent Activation of P62 (SQSTM1)/cMYC-Axis
by Sandra Lörentz, Ines Böhme-Schäfer, Jörg König, Heinrich Sticht and Anja Katrin Bosserhoff
Cancers 2026, 18(7), 1068; https://doi.org/10.3390/cancers18071068 - 25 Mar 2026
Viewed by 655
Abstract
Background: Tumor cells can reprogram their metabolism, constituting a hallmark of cancer that plays a crucial role in tumor progression. As tumor cells exhibit an increased demand for nutrients, e.g., amino acids, they rely on extracellular sources and show deregulation of transport [...] Read more.
Background: Tumor cells can reprogram their metabolism, constituting a hallmark of cancer that plays a crucial role in tumor progression. As tumor cells exhibit an increased demand for nutrients, e.g., amino acids, they rely on extracellular sources and show deregulation of transport proteins. Among these, SNAT1 (SLC38A1) is described as the loader for glutamine that is responsible for the main influx of this amino acid. The aim of this study was to assess the molecular function of SNAT1 in melanoma regarding its role in amino acid transport and regulation of cellular metabolism. Methods: siPool-mediated downregulation of SNAT1 expression in melanoma cell lines was used to investigate the molecular function of this protein. Glutamine transport was assessed by measuring the intracellular and extracellular concentrations of glutamine. Regulation of downstream effectors was evaluated with qRT-PCR and Western Blot. Metabolism was investigated by performing Seahorse flux analysis. Mitochondrial staining was examined via flow cytometry. Protein interaction was assessed with Co-IP, and in silico modeling of protein interaction was performed with AlphaFold3. Results: In this study, we uncovered the new finding that SNAT1 is not primarily implicated in glutamine influx into melanoma cells but in signaling in response to extracellular glutamine. We identified P62 and cMYC as downstream effectors of SNAT1. By activating the P62/cMYC-axis and target genes of cMYC, SNAT1 modulates the metabolism of melanoma cells depending on the glutamine level. SNAT1 and P62 are interaction partners. Conclusions: This finding newly suggests that SNAT1 may function as a sensor or receptor (“transceptor”) for glutamine rather than being a direct and primary glutamine transporter, and could open up new therapeutic options targeting melanoma cells. Full article
(This article belongs to the Special Issue Tumor Suppressor Genes and Oncogenes: Genome-Wide Insights into Cancer Biology)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

32 pages, 2880 KB  
Review
p53 Isoforms as Modifiers of the p53-Dependent Responses: A Hidden Code?
by Laura Bartolomei, Beatrice Pretto, Samuele Brugnara, Alessandra Sontacchi, Vanessa Dassi, Aya Bousrih, Chiara Damaggio, Francesca Flangini, Alessandra Bisio and Yari Ciribilli
Cancers 2026, 18(7), 1057; https://doi.org/10.3390/cancers18071057 - 25 Mar 2026
Viewed by 759
Abstract
The tumor suppressor protein p53, encoded by the TP53 gene, is known as the “Guardian of the Genome”, and alterations in TP53 are common to more than 50% of human cancers. p53 is a critical regulator of cellular responses to several stress conditions, [...] Read more.
The tumor suppressor protein p53, encoded by the TP53 gene, is known as the “Guardian of the Genome”, and alterations in TP53 are common to more than 50% of human cancers. p53 is a critical regulator of cellular responses to several stress conditions, such as DNA damage, oncogene activation, and nutrient starvation. p53 was traditionally described as a single transcription factor; however, now it is recognized as a complex family of isoforms generated through alternative promoter usage, alternative splicing, and alternative initiation of translation. These processes give rise to at least 12 distinct p53 isoforms in humans, including p53α (the canonical full-length isoform), p53β, p53γ, Δ40p53, Δ133p53, and Δ160p53, each with unique structural and functional properties. p53 isoforms differ in the presence or absence of specific and fundamental domains located both at N- and C-terminal ends, determining an altered DNA-binding potential, transcriptional activity, and protein–protein interactions. For instance, Δ133p53 isoforms lack part of the N-terminal domains and can exert dominant-negative effects over full-length p53α or modulate alternative transcriptional programs. Similarly, p53β and p53γ isoforms, which have a unique C-termini, influence cellular senescence. The expression patterns of p53 isoforms are tissue-specific and dynamically regulated under both physiological as well as pathological conditions. Alterations of isoform balance have been involved in tumor progression, metastasis, and therapy resistance. Importantly, specific isoforms can either enhance or limit canonical p53 tumor suppressor functions, thereby contributing to the functional diversity of the p53 network. Overall, the p53 isoform landscape adds a critical layer of complexity to p53 biology. In this review, we summarize the mechanisms underlying the production of p53 isoforms, their functions, and their expression in cancer, with the idea that a better understanding of the differential regulation and functional interplay of p53 isoforms may provide novel biomarkers and therapeutic targets in cancer. Full article
(This article belongs to the Special Issue Tumor Suppressor Genes and Oncogenes: Genome-Wide Insights into Cancer Biology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop