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Cancers
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Translational Research in Gynecologic Cancer
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Translational Research in Gynecologic Cancer

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

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 3909

Special Issue Editor

Prof. Dr. Noriomi Matsumura

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Kindai University Faculty of Medicine, Osakasayama, Osaka 589-8511, Japan
Interests: gynecologic oncology; ovarian cancer; omics analysis; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Research and treatment in the field of gynecological cancers have dramatically changed with the advent of various molecular-targeted drugs and immune checkpoint inhibitors. The development of these novel therapies was largely due to technological advances in genomic and transcriptomic analysis of cancers and the accumulation of their multi-omics data. Furthermore, single-cell analysis of gynecological cancers is expected to lead to the development of novel therapies based on the analysis of intratumor heterogeneity and stromal cells. This Special Issue aims to collect original papers and innovative review articles detailing translational research on cancer of the uterus, ovary, fallopian tubes, vagina, and vulva.

Please note that reviews and meta-analyses of clinical studies, analyses of epidemiological data, and analyses of public omics data that do not involve the development of novel bioinformatics techniques fall out of scope of this Special Issue.

Prof. Dr. Noriomi Matsumura
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. 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

  • gynecologic cancer
  • translational research
  • omics
  • molecular target
  • immune therapy

Published Papers (2 papers)

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Research

16 pages, 991 KiB  
Article
Concordance between Three Homologous Recombination Deficiency (HRD) Assays in Patients with High-Grade Epithelial Ovarian Cancer
by Elena Fountzilas, Kyriaki Papadopoulou, Thomas Chatzikonstantinou, Georgios Karakatsoulis, Pantelis Constantoulakis, Aikaterini Tsantikidi, Georgios Tsaousis, Sofia Karageorgopoulou, Anna Koumarianou, Davide Mauri, Anastasios Ntavatzikos, Zacharenia Saridaki, Georgios Petrakis, Florentia Fostira, George Fountzilas and Michalis Liontos
Cancers 2023, 15(23), 5525; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15235525 - 22 Nov 2023
Viewed by 1184
Abstract
Our aim was to evaluate the concordance between the Myriad MyChoice and two alternative homologous recombination deficiency (HRD) assays (AmoyDx HRD Focus NGS Panel and OncoScan™) in patients with epithelial ovarian cancer (EOC). Tissue samples from 50 patients with newly diagnosed EOC and [...] Read more.
Our aim was to evaluate the concordance between the Myriad MyChoice and two alternative homologous recombination deficiency (HRD) assays (AmoyDx HRD Focus NGS Panel and OncoScan™) in patients with epithelial ovarian cancer (EOC). Tissue samples from 50 patients with newly diagnosed EOC and known Myriad MyChoice HRD status were included. DNA aliquots from tumor samples, previously evaluated with Myriad MyChoice and centrally reassessed, were distributed to laboratories to assess their HRD status using the two platforms, after being blinded for the Myriad MyChoice CDx HRD status. The primary endpoint was the concordance between Myriad MyChoice and each alternative assay. Tumor samples were evaluated with an AmoyDx® HRD Focus Panel (n = 50) and with OncoScan™ (n = 43). Both platforms provided results for all tumors. Analysis showed that correlation was high for the Myriad MyChoice GI score and AmoyDx® HRD Focus Panel (r = 0.79) or OncoScan™ (r = 0.87) (continuous variable). The overall percent agreement (OPA) between Myriad MyChoice GI status (categorical variable) and each alternative assay was 83.3% (68.6–93.3%) with AmoyDx and 77.5% (61.5–89.2%) with OncoScan™. The OPA in HRD status between Myriad MyChoice and AmoyDx was 88.6% (75.4–96.2). False-positive rates were 31.6% (6/19) for AmoyDx GI status and 31.9% (7/22) for OncoScan™, while false-negative rates were 0% (0/28, AmoyDx) and 11.1% (2/18, OncoScan™) compared with the Myriad MyChoice GI status. While substantial concordance between Myriad MyChoice and alternative assays was demonstrated, prospective validation of the analytical performance and clinical relevance of these assays is warranted. Full article
(This article belongs to the Special Issue Translational Research in Gynecologic Cancer)
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19 pages, 3009 KiB  
Article
The Histone Methyltransferase SETD8 Regulates the Expression of Tumor Suppressor Genes via H4K20 Methylation and the p53 Signaling Pathway in Endometrial Cancer Cells
by Asako Kukita, Kenbun Sone, Syuzo Kaneko, Eiryo Kawakami, Shinya Oki, Machiko Kojima, Miku Wada, Yusuke Toyohara, Yu Takahashi, Futaba Inoue, Saki Tanimoto, Ayumi Taguchi, Tomohiko Fukuda, Yuichiro Miyamoto, Michihiro Tanikawa, Mayuyo Mori-Uchino, Tetsushi Tsuruga, Takayuki Iriyama, Yoko Matsumoto, Kazunori Nagasaka, Osamu Wada-Hiraike, Katsutoshi Oda, Ryuji Hamamoto and Yutaka Osugaadd Show full author list remove Hide full author list
Cancers 2022, 14(21), 5367; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14215367 - 31 Oct 2022
Cited by 5 | Viewed by 2180
Abstract
The histone methyltransferase SET domain-containing protein 8 (SETD8), which methylates histone H4 lysine 20 (H4K20) and non-histone proteins such as p53, plays key roles in human carcinogenesis. Our aim was to determine the involvement of SETD8 in endometrial cancer and its therapeutic potential [...] Read more.
The histone methyltransferase SET domain-containing protein 8 (SETD8), which methylates histone H4 lysine 20 (H4K20) and non-histone proteins such as p53, plays key roles in human carcinogenesis. Our aim was to determine the involvement of SETD8 in endometrial cancer and its therapeutic potential and identify the downstream genes regulated by SETD8 via H4K20 methylation and the p53 signaling pathway. We examined the expression profile of SETD8 and evaluated whether SETD8 plays a critical role in the proliferation of endometrial cancer cells using small interfering RNAs (siRNAs). We identified the prognostically important genes regulated by SETD8 via H4K20 methylation and p53 signaling using chromatin immunoprecipitation sequencing, RNA sequencing, and machine learning. We confirmed that SETD8 expression was elevated in endometrial cancer tissues. Our in vitro results suggest that the suppression of SETD8 using siRNA or a selective inhibitor attenuated cell proliferation and promoted the apoptosis of endometrial cancer cells. In these cells, SETD8 regulates genes via H4K20 methylation and the p53 signaling pathway. We also identified the prognostically important genes related to apoptosis, such as those encoding KIAA1324 and TP73, in endometrial cancer. SETD8 is an important gene for carcinogenesis and progression of endometrial cancer via H4K20 methylation. Full article
(This article belongs to the Special Issue Translational Research in Gynecologic Cancer)
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