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Development of New Cancer Treatment by Identifying and Targeting Pathogenic...
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Development of New Cancer Treatment by Identifying and Targeting Pathogenic Abnormalities of Genes

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 August 2021) | Viewed by 7062

Special Issue Editor

Dr. Hiroyuki Tsuchiya

E-Mail Website
Guest Editor
Faculty of Medicine, Tottori University, Yonago, Tottori 683-8504, Japan
Interests: genetic medicine; pathology; gene expression regulation; signal pathway
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A number of diseases still require the development of new drugs or the improvement of therapeutic efficacy of current drugs. In order to meet the clinical needs, a number of studies have so far been devoted to clarifying previously unrecognized mechanisms of diseases.

Abnormalities of genes bring about changes in cellular functions, and thereby lead to the development of specific pathologies, in particular cancers. Therefore, the identification of such abnormalities provides a great advantage to the invention of new cancer treatment strategies.

Currently, abnormalities associated with cancers can be approached by small molecule drugs, monoclonal antibodies or gene therapy. However, it has been clarified that tumorigenic abnormalities of genes include not only mutations, but also aberrant alternative splicing, and uncontrolled gene expression by epigenetic factors and non-coding genes, most of which are not sufficiently understood yet.

This Special Issue calls for original articles, short reports, reviews, and perspectives covering novel tumorigenic abnormalities of coding and non-coding genes, and epigenetic factors that advance our current understanding of cancers. Besides, studies investigating novel small molecules, antibodies, and gene therapy targeting tumorigenic abnormalities are also welcome.

We look forward to your contributions.

Dr. Hiroyuki Tsuchiya
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. Genes is an international peer-reviewed open access monthly 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 2600 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

  • Tumorigenic abnormalities of gene
  • Uncontrolled gene expression
  • Aberrant alternative splicing
  • Epigenetic factors
  • Noncoding genes
  • Mutations
  • Small molecule drugs
  • Gene therapy
  • Novel treatment

Published Papers (2 papers)

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Review

18 pages, 1319 KiB  
Review
Epithelial–Mesenchymal Transition Signaling and Prostate Cancer Stem Cells: Emerging Biomarkers and Opportunities for Precision Therapeutics
by Luiz Paulo Chaves, Camila Morais Melo, Fabiano Pinto Saggioro, Rodolfo Borges dos Reis and Jeremy Andrew Squire
Genes 2021, 12(12), 1900; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12121900 - 27 Nov 2021
Cited by 25 | Viewed by 4268
Abstract
Prostate cancers may reactivate a latent embryonic program called the epithelial–mesenchymal transition (EMT) during the development of metastatic disease. Through EMT, tumors can develop a mesenchymal phenotype similar to cancer stem cell traits that contributes to metastasis and variation in therapeutic responses. Some [...] Read more.
Prostate cancers may reactivate a latent embryonic program called the epithelial–mesenchymal transition (EMT) during the development of metastatic disease. Through EMT, tumors can develop a mesenchymal phenotype similar to cancer stem cell traits that contributes to metastasis and variation in therapeutic responses. Some of the recurrent somatic mutations of prostate cancer affect EMT driver genes and effector transcription factors that induce the chromatin- and androgen-dependent epigenetic alterations that characterize castrate-resistant prostate cancer (CRPC). EMT regulators in prostate cancer comprise transcription factors (SNAI1/2, ZEB1, TWIST1, and ETS), tumor suppressor genes (RB1, PTEN, and TP53), and post-transcriptional regulators (miRNAs) that under the selective pressures of antiandrogen therapy can develop an androgen-independent metastatic phenotype. In prostate cancer mouse models of EMT, Slug expression, as well as WNT/β-Catenin and notch signaling pathways, have been shown to increase stemness potential. Recent single-cell transcriptomic studies also suggest that the stemness phenotype of advanced prostate cancer may be related to EMT. Other evidence correlates EMT and stemness with immune evasion, for example, activation of the polycomb repressor complex I, promoting EMT and stemness and cytokine secretion through RB1, TP53, and PRC1. These findings are helping clinical trials in CRPC that seek to understand how drugs and biomarkers related to the acquisition of EMT can improve drug response. Full article
(This article belongs to the Special Issue Development of New Cancer Treatment by Identifying and Targeting Pathogenic Abnormalities of Genes)
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22 pages, 724 KiB  
Review
Development of New Cancer Treatment by Identifying and Focusing the Genetic Mutations or Altered Expression in Gynecologic Cancers
by Yun-Hsin Tang, Chiao-Yun Lin and Chyong-Huey Lai
Genes 2021, 12(10), 1593; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12101593 - 09 Oct 2021
Cited by 2 | Viewed by 2307
Abstract
With the advent of next-generation sequencing (NGS), The Cancer Genome Atlas (TCGA) research network has given gynecologic cancers molecular classifications, which impacts clinical practice more and more. New cancer treatments that identify and target pathogenic abnormalities of genes have been in rapid development. [...] Read more.
With the advent of next-generation sequencing (NGS), The Cancer Genome Atlas (TCGA) research network has given gynecologic cancers molecular classifications, which impacts clinical practice more and more. New cancer treatments that identify and target pathogenic abnormalities of genes have been in rapid development. The most prominent progress in gynecologic cancers is the clinical efficacy of poly(ADP-ribose) polymerase (PARP) inhibitors, which have shown breakthrough benefits in reducing hazard ratios (HRs) (HRs between 0.2 and 0.4) of progression or death from BRCA1/2 mutated ovarian cancer. Immune checkpoint inhibition is also promising in cancers that harbor mismatch repair deficiency (dMMR)/microsatellite instability (MSI). In this review, we focus on the druggable genetic alterations in gynecologic cancers by summarizing literature findings and completed and ongoing clinical trials. Full article
(This article belongs to the Special Issue Development of New Cancer Treatment by Identifying and Targeting Pathogenic Abnormalities of Genes)
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