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Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Causes, Screening and Diagnosis".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 11318

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Special Issue Editors

Prof. Dr. Emmanouil Karteris

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Guest Editor

Division of Biomedical Sciences, Brunel University, London, UK
Interests: mTOR signaling; ovarian cancer; cancer biomarkers; liquid biopsies
Special Issues, Collections and Topics in MDPI journals

Dr. Ioannis Kyrou

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Co-Guest Editor

1. Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, School of Food and Nutritional Sciences, Agricultural University of Athens, 11855 Athens, Greece
2. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK
3. Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK
4. Centre for Sport, Exercise and Life Sciences, Research Institute for Health & Wellbeing, Coventry University, Coventry CV1 5FB, UK
5. Aston Medical School, College of Health and Life Sciences, Aston University, Birmingham B4 7ET, UK
6. College of Health, Psychology and Social Care, University of Derby, Derby DE22 1GB, UK
Interests: women's health; endocrinology, gynecological cancers; PCOS; metabolism, nutrition, diabetes; endocrine disrupting chemicals (EDCs); links between obesity and cancer
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Harpal S. Randeva

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Co-Guest Editor

1. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK
2. Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK
Interests: women’s health; endocrinology; gynaecological cancers; PCOS; metabolism; nutrition; diabetes; endocrine-disrupting chemicals (EDCs); links between obesity and cancer
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Eva Kassi

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Co-Guest Editor

1. Department of Biochemistry, Medical School of Athens, National and Kapodistrian University of Athens, 11527 Athens, Greece
2. Unit of Endocrinology, First Department of Propaedeutic Internal Medicine, Laiko Hospital, National & Kapodistrian University of Athens, 11527 Athens, Greece
Interests: women’s health; cardiovascular endocrinology; atherosclerosis; non-alcoholic fatty liver disease; endocrinology of adrenals; oestrogen receptor signalling; glucocorticoid receptor signalling; clock system in benign diseases and malignancies; ICI (immune checkpoint inhibitor)-related endocrinopathies; neuroendocrine tumours; vitamin D; calcium and phosphate metabolic disorders; gynaecological cancers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a new Special Issue entitled “Women's Health and Gynaecological Cancers: from nutrition and environmental factors to novel diagnostics and therapies”.

We are producing this Special Issue given that gynaecological cancers, such as breast, ovarian, cervical and uterine cancers, are an important cause of cancer-related mortality globally. With an annual incidence of approximately 2.8 million worldwide, this group of malignancies constitutes a major public health problem and poses a significant disease burden in women. This Special Issue will focus on the latest therapeutic and diagnostic advancements in this field, including chemo-radiotherapy, immunotherapy, PARP inhibitors and current therapeutic advancements, including personalised medicine. We would also like to invite manuscripts relating to novel diagnostics, particularly using liquid biopsies (e.g., circulating tumour DNA, circulating tumour cells, miRNA and extracellular vesicles, to name a few). Finally, we also welcome papers on potential links between gynaecological cancers and obesity, nutrition and environmental factors.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

Breast cancer
Ovarian cancer
Cervical cancer
Endometrial cancer
Vaginal cancer
Nutrition and gynaecological cancers
Obesity and gynaecological cancers
Environmental factors and gynaecological cancers
Personalised medicine and gynaecological cancers
Biomarkers and gynaecological cancers
Liquid biopsies and gynaecological cancers

If you have an alternative topic that is not mentioned above but appears to align with the overall theme of this Special Issue, we welcome your suggestions. We look forward to receiving your contributions.

Prof. Dr. Emmanouil Karteris
Dr. Ioannis Kyrou
Prof. Dr. Harpal S. Randeva
Prof. Dr. Eva Kassi
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 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

breast cancer
ovarian cancer
cervical cancer
endometrial cancer
nutrition
obesity
environmental factors
women's health
gynaecological cancers

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Published Papers (6 papers)

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Research

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17 pages, 1406 KiB

Open AccessArticle

Histologic Characterization of Tumor-Adjacent Mammary Adipose Tissue in Normal-Weight and Overweight/Obese Patients with Triple-Negative Breast Cancer

by Marietta Wolf, Christoph Brochhausen, Vignesh Ramakrishnan, Sabine Iberl, Jonas Roth, Stephan Seitz, Ralph Burkhardt and Sonja C. Stadler

Cancers 2024, 16(20), 3515; https://doi.org/10.3390/cancers16203515 - 17 Oct 2024

Cited by 1 | Viewed by 1393

Abstract

Background: Obesity is a risk factor of several types of cancer, including breast cancer. In this study, we aimed to histologically characterize the adipose tissue of the tumor microenvironment (TME) of triple-negative breast cancer (TNBC) in overweight/obese versus normal-weight patients. Methods: TNBC tissue sections from normal-weight (BMI_<25) and overweight/obese patients (BMI_≥25) were stained with antibodies against CD68, CD163, CD31, CD34, and vimentin. At the invasive tumor front, positive cells were counted in tumor adjacent adipose tissue (AT) and within cancer tissue (CT). Further, the size of the tumor-adjacent and distant mammary adipocytes was determined in perilipin stained sections. Expression of ANGPTL4, CD36 and FABP4, proteins involved in fatty acid metabolism, was analyzed in marginal tumor cells using an immune reactive score. Results: Overweight/obese TNBC patients had significantly larger adipocytes, higher numbers of CD163+ macrophages (BMI_<25: 2.80 vs. BMI_≥25: 10.45; p = 0.011) and lower numbers of CD31+ (BMI_<25: 4.20 vs. BMI_≥25: 2.40; p = 0.018) and CD34+ (BMI_<25: 14.60 vs. BMI_≥25: 5.20; p = 0.045) cells as markers of angiogenesis in the AT as well as a higher frequency of cancer-associated-fibroblast-like cells in the AT and CT (BMI_<25: 7.60 vs. BMI_≥25: 25.39 in total; p = 0.001). Moreover, expression of CD36 (BMI_<25: 2.15 vs. BMI_≥25: 2.60; p = 0.041) and ANGPTL4 (BMI_<25: 6.00 vs. BMI_≥25: 9.80; p = 0.026) was elevated in the TNBC cells of overweight/obese patients. Conclusions: Our data suggest BMI-related changes in the TME of overweight/obese TNBC patients, including hypertrophied adipocytes, reduced vascularization, more M2-like macrophages and CAF-like cells, and an increase in the expression of fatty acid metabolizing proteins in marginal tumor cells, all contributing to a more tumor-promoting, immunosuppressive environment. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

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13 pages, 2367 KiB

Open AccessArticle

Silmitasertib (CX-4945) Disrupts ERα/HSP90 Interaction and Drives Proteolysis through the Disruption of CK2β Function in Breast Cancer Cells

by Hogyoung Kim, Emma Elkins, Rahib Islam, Bo Cao, Nour Abbes, Kaela Battles, Sihyoung Kim, Sichan Kim and Christopher Williams

Cancers 2024, 16(14), 2501; https://doi.org/10.3390/cancers16142501 - 10 Jul 2024

Viewed by 1303

Abstract

Aberrant estrogen receptor (ERα) signaling mediates detrimental effects of tamoxifen including drug resistance and endometrial hyperplasia. ERα36, an alternative isoform of ERα, contributes to these effects. We have demonstrated that CK2 modulates ERα expression and function in breast cancer (BCa). Here, we assess if CX-4945 (CX), a clinical stage CK2 inhibitor, can disrupt ERα66 and ERα36 signaling in BCa. Using live cell imaging, we assessed the antiproliferative effects of CX in tamoxifen-sensitive and tamoxifen-resistant BCa cells in monolayer and/or spheroid cultures. CX-induced alterations in ERα66 and ERα36 mRNA and protein expression were assessed by RT-PCR and immunoblot. Co-immunoprecipitation was performed to determine the differential interaction of ERα isoforms with HSP90 and CK2 upon CX exposure. CX caused concentration-dependent decreases in proliferation in tamoxifen-sensitive MCF-7 and tamoxifen-resistant MCF-7 Tam1 cells and significantly repressed spheroid growth in 3D models. Additionally, CX caused dramatic decreases in endogenous or exogenously expressed ERα66 and ERα36 protein. Silencing of CK2β, the regulatory subunit of CK2, resulted in destabilization and decreased proliferation, similar to CX. Co-immunoprecipitation demonstrated that ERα66/36 show CK2 dependance for interaction with molecular chaperone HSP90. Our findings show that CK2 functions regulate the protein stability of ERα66 and ERα36 through a mechanism that is dependent on CK2β subunit and HSP90 chaperone function. CX may be a component of a novel therapeutic strategy that targets both tamoxifen-sensitive and tamoxifen-resistant BCa, providing an additional tool to treat ERα-positive BCa. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

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19 pages, 6685 KiB

Open AccessArticle

In Silico and In Vitro Mapping of Receptor-Type Protein Tyrosine Phosphatase Receptor Type D in Health and Disease: Implications for Asprosin Signalling in Endometrial Cancer and Neuroblastoma

by Sophie Orton, Rebecca Karkia, Denis Mustafov, Seley Gharanei, Maria Braoudaki, Alice Filipe, Suzana Panfilov, Sayeh Saravi, Nabeel Khan, Ioannis Kyrou, Emmanouil Karteris, Jayanta Chatterjee and Harpal S. Randeva

Cancers 2024, 16(3), 582; https://doi.org/10.3390/cancers16030582 - 30 Jan 2024

Cited by 1 | Viewed by 2225

Abstract

Background: Protein Tyrosine Phosphatase Receptor Type D (PTPRD) is involved in the regulation of cell growth, differentiation, and oncogenic transformation, as well as in brain development. PTPRD also mediates the effects of asprosin, which is a glucogenic hormone/adipokine derived following the cleavage of the C-terminal of fibrillin 1. Since the asprosin circulating levels are elevated in certain cancers, research is now focused on the potential role of this adipokine and its receptors in cancer. As such, in this study, we investigated the expression of PTPRD in endometrial cancer (EC) and the placenta, as well as in glioblastoma (GBM). Methods: An array of in silico tools, in vitro models, tissue microarrays (TMAs), and liquid biopsies were employed to determine the gene and protein expression of PTPRD in healthy tissues/organs and in patients with EC and GBM. Results: PTPRD exhibits high expression in the occipital lobe, parietal lobe, globus pallidus, ventral thalamus, and white matter, whereas in the human placenta, it is primarily localised around the tertiary villi. PTPRD is significantly upregulated at the mRNA and protein levels in patients with EC and GBM compared to healthy controls. In patients with EC, PTPRD is significantly downregulated with obesity, whilst it is also expressed in the peripheral leukocytes. The EC TMAs revealed abundant PTPRD expression in both low- and high-grade tumours. Asprosin treatment upregulated the expression of PTPRD only in syncytialised placental cells. Conclusions: Our data indicate that PTPRD may have potential as a biomarker for malignancies such as EC and GBM, further implicating asprosin as a potential metabolic regulator in these cancers. Future studies are needed to explore the potential molecular mechanisms/signalling pathways that link PTPRD and asprosin in cancer. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

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Review

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12 pages, 563 KiB

Open AccessReview

Unveiling Prostate-Specific Membrane Antigen’s Potential in Breast Cancer Management

by Lucia Motta, Marialuisa Puglisi, Giuliana Pavone, Gianmarco Motta, Federica Martorana, Michelangelo Bambaci, Demetrio Aricò and Paolo Vigneri

Cancers 2025, 17(3), 456; https://doi.org/10.3390/cancers17030456 - 28 Jan 2025

Viewed by 690

Abstract

Background: In recent years, the role of prostate-specific membrane antigen (PSMA) in the imaging and treatment of prostate cancer (PCa) has been extensively investigated. However, despite its name, PSMA is not exclusively specific to PCa. It has been found to be expressed in the neo-vasculature of various solid tumors, including breast cancer (BC), in which it is associated with tumor angiogenesis. Methods: This review aims to assess the potential of PSMA-based radiopharmaceuticals for BC diagnosis and treatment. It explores the current landscape by analyzing preclinical and clinical studies, as well as ongoing clinical trials, to provide insights into the PSMA-targeted approaches in BC management. Results: Early studies suggest PSMA-based imaging could improve BC lesion detection, especially in TNBC. The available data remains too preliminary to conclusively assess whether PSMA-based imaging or therapy will offer a significant advantage in BC. However, some preclinical findings suggest that this approach may hold promise as a novel strategy for managing this widespread malignancy. Conclusions: PSMA-based strategies show potential for BC diagnosis and treatment, but further research is needed. Ongoing and future clinical trials are expected to provide deeper insights into the potential utility of this approach. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

16 pages, 29464 KiB

Open AccessReview

Molecular Subtypes of Vulvar Squamous Cell Carcinoma: The Significance of HPV-Independent/p53 Wild Type

by Lars-Christian Horn, Christine E. Brambs, Blake Gilks, Lien Hoang, Naveena Singh, Grit Gesine Ruth Hiller, Kathrin Hering, Jessica N. McAlpine, Amy Jamieson, Mona Alfaraidi, Bahriye Aktas, Nadja Dornhöfer and Anne Kathrin Höhn

Cancers 2024, 16(24), 4216; https://doi.org/10.3390/cancers16244216 - 18 Dec 2024

Viewed by 699

Abstract

Vulvar carcinoma is a rare disease, meeting the criteria for a “rare cancer”, but its incidence is increasing, especially in women <60 years of age. Squamous cell carcinoma (VSCC) accounts for the overwhelming majority of vulvar carcinomas and is the focus of this review. As with many cancers, the increased understanding of molecular events during tumorigenesis has led to the emergence of the molecular subclassification of VSCC, which is subclassified into tumors that arise secondary to high-risk human papillomavirus infection (HPV-associated, or HPVa) and those that arise independently of HPV (HPVi), most commonly in the setting of a chronic inflammatory condition of the vulvar skin. This latter group of HPVi VSCC arises in most cases secondary to mutations in TP53, but recently, attention has focused on the uncommon TP53 wild-type HPVi VSCC. These three molecular subtypes of VSCC (HPVa, HPVi p53 abnormal, and HPVi p53 wild type), as well as their precursor lesions, cannot be diagnosed based on a routine histopathological examination or immunostaining for p53 and p16 as surrogate markers for TP53 mutation and high-risk HPV infection, respectively, are required. The molecular subtyping of VSCC shows high reproducibility and provides important prognostic information. HPVa VSCC has the most favorable prognosis, while HPVi VSCC with TP53 mutations (p53abn) has the worst prognosis, and HPVi VSCC with wild-type TP53 (p53wt) has an intermediate prognosis. In this review, we discuss the evidence supporting this molecular subclassification and its implications for the diagnosis and treatment of VSCC and its precursors. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

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22 pages, 1410 KiB

Open AccessEditor’s ChoiceReview

Triple-Negative Breast Cancer and Emerging Therapeutic Strategies: ATR and CHK1/2 as Promising Targets

by Amalia Sofianidi, Ecaterina E. Dumbrava, Konstantinos N. Syrigos and Azadeh Nasrazadani

Cancers 2024, 16(6), 1139; https://doi.org/10.3390/cancers16061139 - 13 Mar 2024

Cited by 6 | Viewed by 4278

Abstract

Worldwide, breast cancer is the most frequently diagnosed malignancy in women, with triple-negative breast cancer (TNBC) being the most aggressive molecular subtype. Due to the dearth of effective therapeutic options for TNBC, novel agents targeting key mechanisms and pathways in cancer cells are continuously explored; these include ATR inhibitors, which target the ATR kinase involved in the DNA damage response (DDR) pathway, and CHK1/2 inhibitors, which target the Checkpoint Kinase 1/2 (CHK1/2) involved in cell cycle arrest and DNA repair. ATR and CHK1/2 inhibitors show potential as prospective treatments for TNBC by focusing on the DDR and interfering with cell cycle regulation in cancer cells. Preliminary preclinical and clinical findings suggest that when combined with chemotherapy, ATR and CHK1/2 inhibitors demonstrate significant anti-proliferative efficacy against TNBC. In this article, we introduce ATR and CHK1/2 inhibitors as promising therapeutic approaches for the management of TNBC. Preclinical and clinical studies performed evaluating ATR and CHK1/2 inhibitors for the treatment of TNBC and associated challenges encountered in this context to date are reviewed. Full article

(This article belongs to the Special Issue Women’s Health and Gynaecological Cancers: From Nutrition and Environmental Factors to Novel Diagnostics and Therapies)

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