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Cancers
Special Issues
Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis
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Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 September 2022) | Viewed by 24973

Special Issue Editor

Prof. Dr. Takashi Kojima

E-Mail Website
Guest Editor
Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan
Interests: tight junctions; p63; pathophysiology; cell biology; molecular pathology; oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endometrial cancer is the most common malignancy among diseases affecting women, and the incidence is rising in high-income countries. Therefore, further elucidation of the pathophysiology of endometrial cancer is needed to develop new treatments. Endometrial carcinoma is classified into two clinicopathological types (Type I and Type II). Type I endometrial carcinoma is the most common subtype, accounting for >80% of endometrial tumors. The relation between diabetes and endometrial cancer is controversial, and diabetes may contribute to endometrial cancer progression. Endometriosis causes chronic pelvic pain, dysmenorrhea, and infertility in women. Endometrioid endometrial adenocarcinoma arising from endometriosis is rare in premenopausal women. 

However, recent advances in understanding the genetic and epigenetic alterations including cell–cell interaction that underlie endometrioid–endometrial Carcinoma and Endometriosis provide novel approaches to their treatment. The Special Issue on “Therapy for Human Endometrioid–Endometrial Carcinoma and Endometriosis” will comprise a selection of original research papers and reviews focusing on the molecular mechanisms and the pathophysiology of human endometrioid–endometrial carcinoma and endometriosis for the development of novel therapeutic approaches.

Prof. Dr. Takashi Kojima
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

  • endometrioid–endometrial carcinoma
  • endometriosis
  • endometrial hyperplasia
  • endometrial stromal cells
  • EMT
  • malignancy
  • cell–cell interaction
  • obesity

Published Papers (10 papers)

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Research

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10 pages, 981 KiB  
Article
Endometrial Cancer with and without Endometriosis: Clinicopathological Differences
by Takahiro Minamikawa, Nozomi Yachida, Kotaro Takahashi, Kyota Saito, Tomoyuki Sekizuka, Hidehiko Akashi, Miho Suzuki, Yutaro Mori, Kaoru Yamawaki, Kazuaki Suda, Ryo Tamura, Sosuke Adachi and Kosuke Yoshihara
Cancers 2023, 15(23), 5635; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15235635 - 29 Nov 2023
Viewed by 732
Abstract
Endometriosis is known to be associated with an increased risk of endometrioid and clear cell ovarian cancer. However, the association between endometriosis and endometrial cancer is controversial. Therefore, we retrospectively analyzed the medical records of women with endometrial cancer who had undergone surgery [...] Read more.
Endometriosis is known to be associated with an increased risk of endometrioid and clear cell ovarian cancer. However, the association between endometriosis and endometrial cancer is controversial. Therefore, we retrospectively analyzed the medical records of women with endometrial cancer who had undergone surgery at our institution to evaluate the clinicopathological relationship between endometrial cancer and endometriosis. The study included 720 women pathologically diagnosed with endometrial cancer at our hospital between 2000 and 2020. The participants were allocated to two groups of patients with endometrial cancer: patients with endometriosis (n = 101) and patients without endometriosis (n = 619). Endometrial cancer patients with endometriosis were significantly younger (median age 54.0 vs. 58.0; p = 0.002). In addition, endometrial cancer patients with endometriosis had fewer pregnancies and deliveries (median pregnancy 1.58 vs. 1.99; p = 0.019, median delivery 1.25 vs. 1.56; p = 0.012). The percentage of patients classified as stage IA was significantly higher in those with endometrial cancer with endometriosis (68.3% vs. 56.4%; p = 0.029). In the analysis of synchronous ovarian cancer, the percentage of dual primary cancer was higher in patients with endometriosis (14.9% vs. 1.6%; p < 0.001). The association of young-onset early-stage endometrial cancer with endometriosis is an important finding that cannot be ignored clinically. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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9 pages, 275 KiB  
Article
Molecular Signature of Endometrial Cancer with Coexistent Adenomyosis: A Multicentric Exploratory Analysis
by Diego Raimondo, Antonio Raffone, Agnese Virgilio, Stefano Ferla, Manuela Maletta, Daniele Neola, Antonio Travaglino, Roberto Paradisi, Alicia Hernández, Emanuela Spagnolo, Virginia García-Pineda, Jacopo Lenzi, Maurizio Guida, Paolo Casadio and Renato Seracchioli
Cancers 2023, 15(21), 5208; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15215208 - 30 Oct 2023
Viewed by 982
Abstract
Adenomyosis has been associated with better survival outcomes in women with endometrial cancer. However, although the endometrial cancer patients’ risk stratification has been revolutionized by molecular findings, the impact of the molecular signature on the favorable prognosis of endometrial cancer patients with coexistent [...] Read more.
Adenomyosis has been associated with better survival outcomes in women with endometrial cancer. However, although the endometrial cancer patients’ risk stratification has been revolutionized by molecular findings, the impact of the molecular signature on the favorable prognosis of endometrial cancer patients with coexistent adenomyosis is unknown. The aim of our study was to compare the prevalence of molecular groups at poor and intermediate prognosis between endometrial cancer patients with and without coexistent adenomyosis. A multicentric, observational, retrospective, cohort study was performed to assess the differences in the prevalence of p53-abnormal expression (p53-abn) and mismatch repair protein-deficient expression (MMR-d) signatures between endometrial cancer patients with and without coexistent adenomyosis. A total of 147 endometrial cancer patients were included in the study: 38 in the adenomyosis group and 109 in the no adenomyosis group. A total of 37 patients showed the MMR-d signature (12 in the adenomyosis group and 25 in the no adenomyosis group), while 12 showed the p53-abn signature (3 in the adenomyosis group and 9 in the no adenomyosis group). No significant difference was found in the prevalence of p53-abn (p = 1.000) and MMR-d (p = 0.2880) signatures between endometrial cancer patients with and without coexistent adenomyosis. In conclusion, the molecular signature does not appear to explain the better prognosis associated with coexistent adenomyosis in endometrial cancer patients. Further investigation of these findings is necessary through future larger studies. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
21 pages, 5134 KiB  
Article
A Label-Free Proteomic Approach for the Identification of Biomarkers in the Exosome of Endometrial Cancer Serum
by Eduardo Sommella, Valeria Capaci, Michelangelo Aloisio, Emanuela Salviati, Pietro Campiglia, Giuseppe Molinario, Danilo Licastro, Giovanni Di Lorenzo, Federico Romano, Giuseppe Ricci, Lorenzo Monasta and Blendi Ura
Cancers 2022, 14(24), 6262; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14246262 - 19 Dec 2022
Cited by 7 | Viewed by 2238
Abstract
Endometrial cancers (ECs) are mostly adenocarcinomas arising from the inner part of the uterus. The identification of serum biomarkers, either soluble or carried in the exosome, may be useful in making an early diagnosis. We used label-free quantification mass spectrometry (LFQ-MS)-based proteomics to [...] Read more.
Endometrial cancers (ECs) are mostly adenocarcinomas arising from the inner part of the uterus. The identification of serum biomarkers, either soluble or carried in the exosome, may be useful in making an early diagnosis. We used label-free quantification mass spectrometry (LFQ-MS)-based proteomics to investigate the proteome of exosomes in the albumin-depleted serum from 12 patients with EC, as compared to 12 healthy controls. After quantification and statistical analysis, we found significant changes in the abundance (p < 0.05) of 33 proteins in EC vs. control samples, with a fold change of ≥1.5 or ≤0.6. Validation using Western blotting analysis in 36 patients with EC as compared to 36 healthy individuals confirmed the upregulation of APOA1, HBB, CA1, HBD, LPA, SAA4, PF4V1, and APOE. A multivariate logistic regression model based on the abundance of these proteins was able to separate the controls from the EC patients with excellent sensitivity levels, particularly for stage 1 ECs. The results show that using LFQ-MS to explore the specific proteome of serum exosomes allows for the identification of biomarkers in EC. These observations suggest that PF4V1, CA1, HBD, and APOE represent biomarkers that are able to reach the clinical stage, after a validation phase. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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13 pages, 3959 KiB  
Article
Inhibition of LIFR Blocks Adiposity-Driven Endometrioid Endometrial Cancer Growth
by Logan Blankenship, Uday P. Pratap, Xue Yang, Zexuan Liu, Kristin A. Altwegg, Bindu Santhamma, Kumaraguruparan Ramasamy, Swapna Konda, Yidong Chen, Zhao Lai, Siyuan Zheng, Gangadhara R. Sareddy, Philip T. Valente, Edward R. Kost, Hareesh B. Nair, Rajeshwar R. Tekmal, Ratna K. Vadlamudi and Suryavathi Viswanadhapalli
Cancers 2022, 14(21), 5400; https://doi.org/10.3390/cancers14215400 - 02 Nov 2022
Cited by 2 | Viewed by 1740
Abstract
Endometrial cancer (EC) is the fourth most common cancer in women, and half of the endometrioid EC (EEC) cases are attributable to obesity. However, the underlying mechanism(s) of obesity-driven EEC remain(s) unclear. In this study, we examined whether LIF signaling plays a role [...] Read more.
Endometrial cancer (EC) is the fourth most common cancer in women, and half of the endometrioid EC (EEC) cases are attributable to obesity. However, the underlying mechanism(s) of obesity-driven EEC remain(s) unclear. In this study, we examined whether LIF signaling plays a role in the obesity-driven progression of EEC. RNA-seq analysis of EEC cells stimulated by adipose conditioned medium (ADP-CM) showed upregulation of LIF/LIFR-mediated signaling pathways including JAK/STAT and interleukin pathways. Immunohistochemistry analysis of normal and EEC tissues collected from obese patients revealed that LIF expression is upregulated in EEC tissues compared to the normal endometrium. Treatment of both primary and established EEC cells with ADP-CM increased the expression of LIF and its receptor LIFR and enhanced proliferation of EEC cells. Treatment of EEC cells with the LIFR inhibitor EC359 abolished ADP-CM induced colony formation andcell viability and decreased growth of EEC organoids. Mechanistic studies using Western blotting, RT-qPCR and reporter assays confirmed that ADP-CM activated LIF/LIFR downstream signaling, which can be effectively attenuated by the addition of EC359. In xenograft assays, co-implantation of adipocytes significantly enhanced EEC xenograft tumor growth. Further, treatment with EC359 significantly attenuated adipocyte-induced EEC progression in vivo. Collectively, our data support the premise that LIF/LIFR signaling plays an important role in obesity-driven EEC progression and the LIFR inhibitor EC359 has the potential to suppress adipocyte-driven tumor progression. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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16 pages, 334 KiB  
Article
Correlation of Leptin, Proinflammatory Cytokines and Oxidative Stress with Tumor Size and Disease Stage of Endometrioid (Type I) Endometrial Cancer and Review of the Underlying Mechanisms
by Clelia Madeddu, Elisabetta Sanna, Giulia Gramignano, Luciana Tanca, Maria Cristina Cherchi, Brunella Mola, Marco Petrillo and Antonio Macciò
Cancers 2022, 14(2), 268; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14020268 - 06 Jan 2022
Cited by 17 | Viewed by 2058
Abstract
Endometrioid endometrial cancer is associated with increased BMI and obesity through multiple pathogenetic mechanisms involving hyperestrogenism, hyperinsulinemia, altered adipokine secretion, inflammation, and oxidative stress. In the present study, we aimed to investigate the correlation between BMI, leptin, the proinflammatory cytokines IL-6 and TNFα, [...] Read more.
Endometrioid endometrial cancer is associated with increased BMI and obesity through multiple pathogenetic mechanisms involving hyperestrogenism, hyperinsulinemia, altered adipokine secretion, inflammation, and oxidative stress. In the present study, we aimed to investigate the correlation between BMI, leptin, the proinflammatory cytokines IL-6 and TNFα, reactive oxygen species (ROS), and the traditional prognostic factors T, G, N and M status among type I endometrioid and type II endometrial cancer patients. We enrolled 305 consecutive endometrial cancer patients prospectively. We found that BMI, leptin, and IL-6 significantly correlated with T status, N status, and M status among endometrioid type I endometrial cancer patients. Among type II endometrial cancer patients, BMI and leptin did not correlate with any of the prognostic parameters, whereas there was a positive correlation between IL-6 and the presence of distant metastases. In the multivariate regression analysis, BMI, leptin, and IL-6 were independent predictive variables of T, N, and M status in endometrioid type I endometrial cancer patients. Our study demonstrates that weight gain, adiposity-related adipokines, inflammation, and oxidative stress correlate with the prognostic factors of endometrioid endometrial cancer. Knowledge of the role of obesity-related biological pathways and mediators in the pathogenesis and prognosis of endometrioid endometrial malignancies may offer new perspectives on combined therapeutic strategies that have not been explored to date, both in the advanced disease and in the adjuvant setting. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)

Review

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15 pages, 1888 KiB  
Review
Atypical Macropinocytosis Contributes to Malignant Progression: A Review of Recent Evidence in Endometrioid Endometrial Cancer Cells
by Takayuki Kohno and Takashi Kojima
Cancers 2022, 14(20), 5056; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14205056 - 15 Oct 2022
Cited by 2 | Viewed by 1973
Abstract
Macropinocytosis is an essential mechanism for the non-specific uptake of extracellular fluids and solutes. In recent years, additional functions have been identified in macropinocytosis, such as the intracellular introduction pathway of drugs, bacterial and viral infection pathways, and nutritional supplement pathway of cancer [...] Read more.
Macropinocytosis is an essential mechanism for the non-specific uptake of extracellular fluids and solutes. In recent years, additional functions have been identified in macropinocytosis, such as the intracellular introduction pathway of drugs, bacterial and viral infection pathways, and nutritional supplement pathway of cancer cells. However, little is known about the changes in cell function after macropinocytosis. Recently, it has been reported that macropinocytosis is essential for endometrial cancer cells to initiate malignant progression in a dormant state. Macropinocytosis is formed by a temporary split of adjacent bicellular junctions of epithelial sheets, rather than from the apical surface or basal membrane, as a result of the transient reduction of tight junction homeostasis. This novel type of macropinocytosis has been suggested to be associated with the malignant pathology of endometriosis and endometrioid endometrial carcinoma. This review outlines the induction of malignant progression of endometrial cancer cells by macropinocytosis based on a new mechanism and the potential preventive mechanism of its malignant progression. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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19 pages, 1057 KiB  
Review
Metformin as a Potential Treatment Option for Endometriosis
by Żaneta Kimber-Trojnar, Dominik Franciszek Dłuski, Magdalena Wierzchowska-Opoka, Monika Ruszała and Bożena Leszczyńska-Gorzelak
Cancers 2022, 14(3), 577; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14030577 - 24 Jan 2022
Cited by 14 | Viewed by 5778
Abstract
Endometriosis is a common disease in women of reproductive age, and its pathogenesis seems to be largely affected by hormone imbalance, inflammation, oxidative stress, and autophagy dysregulation. These pathophysiological disturbances interact with one another through mechanisms that are still awaiting elucidation. The aim [...] Read more.
Endometriosis is a common disease in women of reproductive age, and its pathogenesis seems to be largely affected by hormone imbalance, inflammation, oxidative stress, and autophagy dysregulation. These pathophysiological disturbances interact with one another through mechanisms that are still awaiting elucidation. The aim of this article is to present current knowledge regarding the possibilities of using metformin in the pharmacological treatment of endometriosis. Metformin is an insulin sensitizer widely used for the treatment of type 2 diabetes mellitus. The pleiotropic effects of metformin are mainly exerted through the activation of AMP-activated protein kinase, which is the key cellular energy homeostasis regulator that inhibits mTOR, a major autophagy suppressor. Metformin regresses endometriotic implants by increasing the activity of superoxide dismutase. It is also an inhibitor of metalloproteinase-2, decreasing the levels of the vascular endothelial growth factor and matrix metalloproteinase-9 in animal studies. In endometriosis, metformin might modify the stroma–epithelium communication via Wnt2/β-catenin. With its unique therapeutic mechanisms and no serious side effects, metformin seems to be a helpful anti-inflammatory and anti-proliferative agent in the treatment of endometriosis. It could be a missing link for the successful treatment of this chronic disease. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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14 pages, 4933 KiB  
Review
The Roles of Tricellular Tight Junction Protein Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Endometriosis and Endometrioid-Endometrial Carcinoma
by Hiroshi Shimada, Takayuki Kohno, Takumi Konno, Tadahi Okada, Kimihito Saito, Yuma Shindo, Shin Kikuchi, Mitsuhiro Tsujiwaki, Marie Ogawa, Motoki Matsuura, Tsuyoshi Saito and Takashi Kojima
Cancers 2021, 13(24), 6341; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13246341 - 17 Dec 2021
Cited by 8 | Viewed by 3391
Abstract
Tight junction proteins play roles beyond permeability barriers functions and control cell proliferation and differentiation. The relation between tight junctions and the signal transduction pathways affects cell growth, invasion and migration. Abnormality of tight junction proteins closely contributes to epithelial mesenchymal transition (EMT) [...] Read more.
Tight junction proteins play roles beyond permeability barriers functions and control cell proliferation and differentiation. The relation between tight junctions and the signal transduction pathways affects cell growth, invasion and migration. Abnormality of tight junction proteins closely contributes to epithelial mesenchymal transition (EMT) and malignancy of various cancers. Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) forms tricellular contacts that has a barrier function. Downregulation of angulin-1/LSR correlates with the malignancy in various cancers, including endometrioid-endometrial carcinoma (EEC). These alterations have been shown to link to not only multiple signaling pathways such as Hippo/YAP, HDAC, AMPK, but also cell metabolism in ECC cell line Sawano. Moreover, loss of angulin-1/LSR upregulates claudin-1, and loss of apoptosis stimulating p53 protein 2 (ASPP2) downregulates angulin-1/LSR. Angulin-1/LSR and ASPP2 concentrate at both midbody and centrosome in cytokinesis. In EEC tissues, angulin-1/LSR and ASPP2 are reduced and claudin-2 is overexpressed during malignancy, while in the tissues of endometriosis changes in localization of angulin-1/LSR and claudin-2 are seen. This review highlights how downregulation of angulin-1/LSR promotes development of endometriosis and EEC and discusses about the roles of angulin-1/LSR and its related proteins, including claudins and ASPP2. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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14 pages, 852 KiB  
Systematic Review
Endometrial Cancer Arising in Adenomyosis (EC-AIA): A Systematic Review
by Antonio Raffone, Diego Raimondo, Manuela Maletta, Antonio Travaglino, Federica Renzulli, Daniele Neola, Umberto De Laurentiis, Francesco De Laurentiis, Mohamed Mabrouk, Manuel Maria Ianieri, Renato Seracchioli, Paolo Casadio and Antonio Mollo
Cancers 2023, 15(4), 1142; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15041142 - 10 Feb 2023
Cited by 2 | Viewed by 1870
Abstract
Endometrial cancer arising in adenomyosis (EC-AIA) is a rare uterine disease characterized by the malignant transformation of the ectopic endometrium within the adenomyotic foci. Clinicopathological and survival data are mostly limited to case reports and a few cohort studies. We aimed to assess [...] Read more.
Endometrial cancer arising in adenomyosis (EC-AIA) is a rare uterine disease characterized by the malignant transformation of the ectopic endometrium within the adenomyotic foci. Clinicopathological and survival data are mostly limited to case reports and a few cohort studies. We aimed to assess the clinicopathological features and survival outcomes of women with EC-AIA through a systematic review of the literature. Six electronic databases were searched, from 2002 to 2022, for all peer-reviewed studies that reported EC-AIA cases. Thirty-seven EC-AIA patients from 27 case reports and four case series were included in our study. In our analysis, EC-AIA appeared as a rare disease that mainly occurs in menopausal women, shares symptoms with endometrial cancer, and is challenging to diagnose preoperatively. Differently from EC, it shows a higher prevalence of the non-endometrioid histotype, advanced FIGO stages, and p53-signature, which might be responsible for its worse prognosis. Future studies are necessary, to confirm our findings and further investigate this rare condition. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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10 pages, 805 KiB  
Systematic Review
Clinical Characteristics of Patients with Endometrial Cancer and Adenomyosis
by Paolo Casadio, Antonio Raffone, Manuela Maletta, Antonio Travaglino, Diego Raimondo, Ivano Raimondo, Angela Santoro, Roberto Paradisi, Gian Franco Zannoni, Antonio Mollo and Renato Seracchioli
Cancers 2021, 13(19), 4918; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13194918 - 30 Sep 2021
Cited by 5 | Viewed by 3095
Abstract
A better endometrial cancer (EC) prognosis in patients with coexistent adenomyosis has been reported. Unfortunately, it is still unclear if this better prognosis is related to a more favorable clinical profile of adenomyosis patients. We aimed to evaluate differences in the clinical profiles [...] Read more.
A better endometrial cancer (EC) prognosis in patients with coexistent adenomyosis has been reported. Unfortunately, it is still unclear if this better prognosis is related to a more favorable clinical profile of adenomyosis patients. We aimed to evaluate differences in the clinical profiles of EC patients with and without adenomyosis. A systematic review and meta-analysis was performed by searching seven electronics databases for all studies that allowed extraction of data about clinical characteristics in EC patients with and without adenomyosis. Clinical characteristics assessed were: age, Body Mass Index (BMI), premenopausal status, and nulliparity. Mean difference in mean ± standard deviation (SD) or odds ratio (OR) for clinical characteristics between EC patients with and without adenomyosis were calculated for each included study and as a pooled estimate, and graphically reported on forest plots with a 95% confidence interval (CI). The Z test was used for assessing the overall effect by considering a p value < 0.05 as significant. Overall, eight studies with 5681 patients were included in the qualitative analysis, and seven studies with 4366 patients in the quantitative analysis. Pooled mean difference in mean ± SD between EC women with and without adenomyosis was −1.19 (95% CI: −3.18 to 0.80; p = 0.24) for age, and 0.23 (95% CI: −0.62 to 1.07; p = 0.60) for BMI. When compared to EC women without adenomyosis, EC women with adenomyosis showed a pooled OR of 1.53 (95% CI: 0.92 to 2.54; p = 0.10) for premenopausal status, and of 0.60 (95% CI: 0.41 to 0.87; p = 0.007) for nulliparity. In conclusion, there are not significant differences in clinical characteristics between EC patients with and without adenomyosis, with the exception for nulliparity. Clinical features seem to not underlie the better EC prognosis of patients with adenomyosis compared to patients without adenomyosis. Full article
(This article belongs to the Special Issue Therapy for Human Endometrioid - Endometrial Carcinoma and Endometriosis)
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