Novel Insights into Molecular Mechanisms of Endometrial Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 3721

Special Issue Editors


E-Mail Website
Guest Editor
Department of Gynecological, Obstetrical and Urological Sciences, \"Sapienza\" University of Rome, Rome, Italy
Interests: gynecology oncology; surgical gynecology; target therapy; gynecology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Gynecologic Oncology, IRCCS National Cancer Institute, Milan, Italy
Interests: HPV; cervical cancer; genital lesions; vaccines; conization; gynecology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website1 Website2
Guest Editor
Department of Medical and Surgical Sciences and Translational Medicine, Sapienza University, Rome, Italy
Interests: ovarian cancer; gynecologic oncology; gynaecological surgery; laparoscopic surgery; surgical and invasive medical procedures; oncology; cancer treatment; obstetrics and gynecology; endometrial cancer; cervical cancer; vulvar cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endometrial diseases are the most common gynecological pathologies in Western countries. Molecular profiling has shown stimulating results for diagnostic, therapeutic, and prognostic pathways. The molecular classification, in fact, offers the possibility to improve the risk stratification and management of endometrial disease, especially for endometrial cancer (EC). The Cancer Genome Atlas (TCGA) Research Network revolutionized the approach to EC classification with the introduction of four molecular groups: polymerase epsilon (POLE) ultramutated, microsatellite instability hypermutated, copy-number (CN) low, and CN high. Moreover, a new model called ProMisE (Proactive Molecular Risk Classifier for Endometrial Cancer) has been introduced as a new approach for risk stratification, which is simpler and less expensive than that proposed by the TCGA. This model has been applied in the recent ESMO-ESGO-ESTRO 2020 Guidelines for the management of EC patients according to the tumor aggressiveness and the likelihood of recurrence.

Nevertheless, given the young age of patients affected by other endometrial diseases, the treatment required should be conservative. Unfortunately, few data are available for the use of molecular analysis for such diseases; therefore, this is a field of great interest for research, especially for predicting treatment response and reducing the risk of unfavorable outcomes of precancerous lesions.

This Special Issue is dedicated to focusing on novel insights into molecular mechanisms of endometrial diseases.

Dr. Violante Di Donato
Dr. Giorgio Bogani
Dr. Andrea Giannini
Guest Editors

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. Biomolecules 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 2700 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

  • endometrial disease
  • molecular profiling
  • target therapy
  • personalized treatment

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Other

4 pages, 226 KiB  
Editorial
Novel Insights into Molecular Mechanisms of Endometrial Diseases
by Tullio Golia D’Augè, Ilaria Cuccu, Giusi Santangelo, Ludovico Muzii, Andrea Giannini, Giorgio Bogani and Violante Di Donato
Biomolecules 2023, 13(3), 499; https://doi.org/10.3390/biom13030499 - 09 Mar 2023
Cited by 43 | Viewed by 1528
Abstract
Endometrial diseases are the most common gynecological pathologies in Western Countries [...] Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Endometrial Diseases)

Research

Jump to: Editorial, Other

13 pages, 1503 KiB  
Article
Differential Expression of Insulin Growth Factor 1 (IGF-1) Isoforms in Different Types of Endometriosis: Preliminary Results of a Single-Center Study
by Nikolaos Blontzos, Despoina Mavrogianni, Konstantinos Ntzeros, Nikolaos Kathopoulis, Athanasios Moustogiannis, Anastassios Philippou, Michael Koutsilieris and Athanasios Protopapas
Biomolecules 2024, 14(1), 7; https://doi.org/10.3390/biom14010007 - 20 Dec 2023
Viewed by 824
Abstract
Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in [...] Read more.
Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in the eutopic endometrium of the same endometriosis patients and to compare their expression with that in the eutopic endometrium of women without endometriosis. A total of 39 patients were included: 28 with endometriosis, of whom 15 had endometriomas only, 7 had DIE nodules only, and 6 had both DIE and endometriomas, and 11 without endometriosis served as controls. We noticed a similar pattern of expression between IGF-1Ea and IGF-1Ec, which differed from that of the IGF-1Eb isoform, possibly implying differential biological actions of different isoforms in DIE subtypes. We observed a tendency of lower expression of IGF-1Ea and IGF-1Ec in endometriomas without DIE compared to endometriomas with concurrent DIE or in DIE nodules. In conclusion, differential expression of IGF-1 isoforms may indicate that DIE with its associated ovarian lesions and simple ovarian endometriosis should be considered as two forms of the disease developing under different molecular pathways. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Endometrial Diseases)
Show Figures

Figure 1

Other

Jump to: Editorial, Research

24 pages, 1614 KiB  
Systematic Review
Reproductive and Oncologic Outcomes in Young Women with Stage IA and Grade 2 Endometrial Carcinoma Undergoing Fertility-Sparing Treatment: A Systematic Review
by Andrea Etrusco, Antonio Simone Laganà, Vito Chiantera, Mislav Mikuš, Hafiz Muhammad Arsalan, Antonio d’Amati, Amerigo Vitagliano, Ettore Cicinelli, Alessandro Favilli and Antonio D’Amato
Biomolecules 2024, 14(3), 306; https://doi.org/10.3390/biom14030306 - 05 Mar 2024
Cited by 1 | Viewed by 972
Abstract
Background: Endometrial cancer (EC) is the most common gynecological malignancy in both Europe and the USA. Approximately 3–5% of cases occur in women of reproductive age. Fertility-sparing treatment (FST) options are available, but very limited evidence regarding grade 2 (G2) ECs exists in [...] Read more.
Background: Endometrial cancer (EC) is the most common gynecological malignancy in both Europe and the USA. Approximately 3–5% of cases occur in women of reproductive age. Fertility-sparing treatment (FST) options are available, but very limited evidence regarding grade 2 (G2) ECs exists in the current literature. This systematic review aimed to comprehensively evaluate reproductive and oncologic outcomes among young women diagnosed with stage IA or G2EC disease who underwent FST. Methods: A comprehensive search of the literature was carried out on the following databases: MEDLINE, EMBASE, Global Health, The Cochrane Library (Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, Cochrane Methodology Register), the Health Technology Assessment Database, and Web of Science. Only original studies that reported the oncologic and reproductive outcomes of patients with stage IA and G2EC tumors who underwent FST were considered eligible for inclusion in this systematic review (CRD42023484892). Studies describing only the FST for endometrial hyperplasia or G1 EC were excluded. Results: Twenty-two papers that met the abovementioned inclusion criteria were included in the present systematic review. Preliminary analysis suggested encouraging oncologic and reproductive outcomes after FST. Conclusions: The FST approach may represent a feasible and safe option for women of childbearing age diagnosed with G2EC. Despite these promising findings, cautious interpretation is warranted due to inherent limitations, including heterogeneity in study designs and potential biases. Further research with standardized methodologies and larger sample sizes is imperative for obtaining more robust conclusions. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Endometrial Diseases)
Show Figures

Figure 1

Back to TopTop