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Tumour Suppressor Function 2.0
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Tumour Suppressor Function 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Role of Xenobiotics".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 7413

Special Issue Editor

Dr. Charles Bailey

E-Mail Website
Guest Editor
Group Leader, Cancer & Gene Regulation Laboratory Centenary Institute, The University of Sydney, Camperdown, NSW 2050, Australia
Interests: gene regulation; transcription factor biology; cancer biology; cancer genetics; chromatin organisation; disease models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumour suppressor genes act as a vanguard against the development and progression of cancer. Tumour suppressor genes are recurrently mutated in human cancers, removing important blockades on uncontrolled cellular growth such as cell cycle checkpoints, apoptosis, and DNA repair. The tumour suppressor function has been revealed from the analysis of specific genes or genetic pathways in human cancers and validated with complementary in vitro cell models and in vivo tumour xenograft studies. More recently, detailed analysis of the molecular genetic landscapes of human cancers using genomic, transcriptomic, and epigenetic techniques has revealed unexpected tumour suppressor gene functions, often in a tissue- or subset-specific fashion. Moreover, CRISPR/Cas9-based genetic screens often highlight entire pathways or signalling cascades that augment the tumour suppressor gene function.

Submission to this Special Issue, “Tumour Suppressor Function”, may include focussed molecular genetic studies in specific human cancers, the application of innovative techniques or approaches to reveal new tumour suppressor gene roles, genetic or chemical screens exploiting vulnerabilities in tumour suppressor gene-mutant cancers, or reviews offering new insights into tumour suppressor gene function in cancer.

Dr. Charles G Bailey
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • tumour suppressor gene
  • human cancers
  • cell cycle checkpoints
  • apoptosis
  • DNA repair
  • metastasis
  • epigenetic regulation
  • CRISPR/Cas9
  • genetic screen
  • chemical screen

Related Special Issue

Published Papers (2 papers)

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Research

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15 pages, 20305 KiB  
Article
Quantitative Analysis of the Potency of Equimolar Two-Drug Combinations and Combi-Molecules Involving Kinase Inhibitors In Vitro: The Concept of Balanced Targeting
by Suman Rao, Benoît Thibault, Lisa Peyrard, Anne-Laure Larroque-Lombard, Martin Rupp, Cédric Thauvin and Bertrand J. Jean-Claude
Int. J. Mol. Sci. 2021, 22(17), 9569; https://doi.org/10.3390/ijms22179569 - 3 Sep 2021
Cited by 2 | Viewed by 2081
Abstract
The median-effect principle proposed by Chou and Talalay is the most effective approach to parameterize interactions between several agents in combination. However, this method cannot be used to evaluate the effectiveness of equimolar drug combinations, which are comparative references for dual-targeting molecular design. [...] Read more.
The median-effect principle proposed by Chou and Talalay is the most effective approach to parameterize interactions between several agents in combination. However, this method cannot be used to evaluate the effectiveness of equimolar drug combinations, which are comparative references for dual-targeting molecular design. Here, using data acquired through the development of “combi-molecules” blocking two kinases (e.g., EGFR-c-Src and EGFR-c-Met), we established potency indices for equimolar and dual-targeted inhibitors. If the fold difference (κ) between the IC50 of the two individual kinase inhibitors was >6, the IC50 of their equimolar combination resembled that of the more potent inhibitor. Hence, the “combi-targeting” of the two kinases was considered “imbalanced” and the combination ineffective. However, if κ ≤ 6, the IC50 of the combination fell below that of each individual drug and the combi-targeting was considered “balanced” and the combination effective. We also showed that combi-molecules should be compared with equimolar combinations only under balanced conditions and propose a new parameter Ω for validating their effectiveness. A multi-targeted drug is effective if Ω < 1, where Ω is defined as the IC50 of the drug divided by that of the corresponding equimolar combination. Our study provides a methodology to determine the in vitro potency of equimolar two-drug combinations as well as combi-/hybrid molecules inhibiting two different kinase targets. Full article
(This article belongs to the Special Issue Tumour Suppressor Function 2.0)
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Review

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15 pages, 597 KiB  
Review
Loss of Von Hippel–Lindau (VHL) Tumor Suppressor Gene Function: VHL–HIF Pathway and Advances in Treatments for Metastatic Renal Cell Carcinoma (RCC)
by Hyunho Kim, Byoung Yong Shim, Seung-Ju Lee, Ji Youl Lee, Hyo-Jin Lee and In-Ho Kim
Int. J. Mol. Sci. 2021, 22(18), 9795; https://doi.org/10.3390/ijms22189795 - 10 Sep 2021
Cited by 41 | Viewed by 4827
Abstract
Renal cell carcinoma (RCC) is a malignancy of the kidney originating from the tubular epithelium. Inactivation of the von Hippel–Lindau tumor-suppressor gene (VHL) is found in most clear cell renal cell carcinomas (ccRCCs). The VHL–HIF–VEGF/VEGFR pathway, which involves the von [...] Read more.
Renal cell carcinoma (RCC) is a malignancy of the kidney originating from the tubular epithelium. Inactivation of the von Hippel–Lindau tumor-suppressor gene (VHL) is found in most clear cell renal cell carcinomas (ccRCCs). The VHL–HIF–VEGF/VEGFR pathway, which involves the von Hippel–Lindau tumor suppressor protein (VHL), hypoxia-inducible factor (HIF), vascular endothelial growth factor (VEGF), and its receptor (VEGFR), is a well-studied therapeutic target for metastatic ccRCC. Therefore, over the past decade, anti-angiogenic agents targeting VEGFR have served as the standard treatment for metastatic RCC. Recently, based on the immunomodulatory effect of anti-VEGFR therapy, anti-angiogenic agents and immune checkpoint inhibitor combination strategies have also emerged as therapeutic strategies. These advances were made possible by the improved understanding of the VHL–HIF pathway. In this review, we summarize the historical evolution of ccRCC treatments, with a focus on the involvement of the VHL–HIF pathway. Full article
(This article belongs to the Special Issue Tumour Suppressor Function 2.0)
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