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Cells
Special Issues
Genetic Disorders in Breast and Ovarian Cancer
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Genetic Disorders in Breast and Ovarian Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: 25 April 2025 | Viewed by 8613

Special Issue Editors

Prof. Dr. Marek Nowak

E-Mail Website
Guest Editor
1. Department of Operative Gynecology and Gynecologic Oncology, Polish Mother’s Memorial Hospital-Research Institute, Rzgowska 281/289, 93-338 Lodz, Poland
2. Department of Operative and Endoscopic Gynecology, Medical University of Lodz, Lodz, Poland
Interests: ovarian cancer; carcinogenesis; immunology of solid tumors; targeted therapy; tumor markers
Dr. Miłosz Wilczyński

E-Mail Website
Guest Editor
Department of Surgical Gynecology, Endoscopic Gynecology and Gynecological Oncology, Polish Mother’s Memorial Hospital-Research Institute, Rzgowska 281/289, 93-338 Lodz, Poland
Interests: the molecular basis of gynecological malignant tumors; ovarian cancer carcinogenesis; non-coding RNAs; miRNAs

Special Issue Information

Dear Colleagues,

We are delighted to announce a new Special Issue on the critical topic of “Genetic Disorders in Breast and Ovarian Cancer”. This Special Issue aims to highlight the complexity of genetic landscapes in ovarian and breast cancers, especially in regard to the development, progression, and management.

Ovarian cancer continues to be a significant public health concern. The majority of ovarian cancer patients are diagnosed with advanced stages of the disease. Therefore, excessive efforts are being undertaken to improve early diagnoses and develop new management options. Recent advancements in genetic research have demonstrated the crucial role of genetic disorders in women’s malignancies. Initiatives such as The Cancer Genome Atlas (TCGA) has improved our understanding of malignant diseases, uncovering novel genetic markers and potential therapeutic targets. The use of poly (ADP-ribose) and polymerase (PARP) inhibitors has revolutionized therapeutic options in patients with BRCA mutations.

We encourage submissions of original papers or reviews that address various aspects of genetic disorders in ovarian and breast cancers, including predisposition, oncogenesis, treatment, etc. We hope that a deeper understanding of the genetic basis of breast and ovarian cancer may improve preventive strategies, personalized therapies, and enhanced patient outcomes. We will consider a broad scope of papers, however, original papers that do not have any molecular or cellular validation will not be considered for publication.

This Special Issue provides researchers with an opportunity to present the results of their studies and showcase their expertise in the field, so we eagerly anticipate your submissions.

Prof. Dr. Marek Nowak
Dr. Miłosz Wilczyński
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. Cells 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 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

  • ovarian cancer
  • breast cancer
  • oncogenesis
  • genetic disorders
  • targeted therapy

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Published Papers (3 papers)

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Review

14 pages, 703 KiB  
Review
MiRNAs as Regulators of Immune Cells in the Tumor Microenvironment of Ovarian Cancer
by Miłosz Wilczyński, Jacek Wilczyński and Marek Nowak
Cells 2024, 13(16), 1343; https://doi.org/10.3390/cells13161343 - 13 Aug 2024
Viewed by 1880
Abstract
Ovarian cancer is one of the leading causes of cancer deaths among women. There is an ongoing need to develop new biomarkers and targeted therapies to improve patient outcomes. One of the most critical research areas in ovarian cancer is identifying tumor microenvironment [...] Read more.
Ovarian cancer is one of the leading causes of cancer deaths among women. There is an ongoing need to develop new biomarkers and targeted therapies to improve patient outcomes. One of the most critical research areas in ovarian cancer is identifying tumor microenvironment (TME) functions. TME consists of tumor-infiltrating immune cells, matrix, endothelial cells, pericytes, fibroblasts, and other stromal cells. Tumor invasion and growth depend on the multifactorial crosstalk between tumor cells and immune cells belonging to the TME. MiRNAs, which belong to non-coding RNAs that post-transcriptionally control the expression of target genes, regulate immune responses within the TME, shaping the landscape of the intrinsic environment of tumor cells. Aberrant expression of miRNAs may lead to the pathological dysfunction of signaling pathways or cancer cell-regulatory factors. Cell-to-cell communication between infiltrating immune cells and the tumor may depend on exosomes containing multiple miRNAs. MiRNAs may exert both immunosuppressive and immunoreactive responses, which may cause cancer cell elimination or survival. In this review, we highlighted recent advances in the field of miRNAs shaping the landscape of immune cells in the TME. Full article
(This article belongs to the Special Issue Genetic Disorders in Breast and Ovarian Cancer)
►▼ Show Figures

Figure 1

Figure 1
<p>miRNAs regulate both TME and tumor, being part of a multilayered and mutual network between cancer and immune cells. Tumor-derived exosomes containing miRNAs modulate the actions of immune cells in the TME. Up- or downregulation of certain miRNAs in immune cells being part of the TME also affects tumor growth and progression. Such phenomena may cause immunotolerance or tumor elimination. Immune cells: natural killer cells—NK cells; myeloid-derived suppressor cells—MDSC; regulatory T cells—Treg; CD8<sup>+</sup> T cells—T cytotoxic; dendritic cells—DC; cancer-associated fibroblasts—CAFs.</p> Full article ">
16 pages, 306 KiB  
Review
Complexity of the Genetic Background of Oncogenesis in Ovarian Cancer—Genetic Instability and Clinical Implications
by Marek Murawski, Adam Jagodziński, Aleksandra Bielawska-Pohl and Aleksandra Klimczak
Cells 2024, 13(4), 345; https://doi.org/10.3390/cells13040345 - 15 Feb 2024
Cited by 4 | Viewed by 3886
Abstract
Ovarian cancer is a leading cause of death among women with gynecological cancers, and is often diagnosed at advanced stages, leading to poor outcomes. This review explores genetic aspects of high-grade serous, endometrioid, and clear-cell ovarian carcinomas, emphasizing personalized treatment approaches. Specific mutations [...] Read more.
Ovarian cancer is a leading cause of death among women with gynecological cancers, and is often diagnosed at advanced stages, leading to poor outcomes. This review explores genetic aspects of high-grade serous, endometrioid, and clear-cell ovarian carcinomas, emphasizing personalized treatment approaches. Specific mutations such as TP53 in high-grade serous and BRAF/KRAS in low-grade serous carcinomas highlight the need for tailored therapies. Varying mutation prevalence across subtypes, including BRCA1/2, PTEN, PIK3CA, CTNNB1, and c-myc amplification, offers potential therapeutic targets. This review underscores TP53’s pivotal role and advocates p53 immunohistochemical staining for mutational analysis. BRCA1/2 mutations’ significance as genetic risk factors and their relevance in PARP inhibitor therapy are discussed, emphasizing the importance of genetic testing. This review also addresses the paradoxical better prognosis linked to KRAS and BRAF mutations in ovarian cancer. ARID1A, PIK3CA, and PTEN alterations in platinum resistance contribute to the genetic landscape. Therapeutic strategies, like restoring WT p53 function and exploring PI3K/AKT/mTOR inhibitors, are considered. The evolving understanding of genetic factors in ovarian carcinomas supports tailored therapeutic approaches based on individual tumor genetic profiles. Ongoing research shows promise for advancing personalized treatments and refining genetic testing in neoplastic diseases, including ovarian cancer. Clinical genetic screening tests can identify women at increased risk, guiding predictive cancer risk-reducing surgery. Full article
(This article belongs to the Special Issue Genetic Disorders in Breast and Ovarian Cancer)
16 pages, 2767 KiB  
Review
Prognostic Role of Prolactin-Induced Protein (PIP) in Breast Cancer
by Natalia Sauer, Igor Matkowski, Grażyna Bodalska, Marek Murawski, Piotr Dzięgiel and Jacek Calik
Cells 2023, 12(18), 2252; https://doi.org/10.3390/cells12182252 - 11 Sep 2023
Viewed by 2419
Abstract
Prolactin-inducible protein (PIP), also referred to as gross cystic disease fluid protein 15 (GCDFP-15), has been a trending topic in recent years due to its potential role as a specific marker in breast cancer. PIP binds to aquaporin-5 (AQP5), CD4, actin, fibrinogen, β-tubulin, [...] Read more.
Prolactin-inducible protein (PIP), also referred to as gross cystic disease fluid protein 15 (GCDFP-15), has been a trending topic in recent years due to its potential role as a specific marker in breast cancer. PIP binds to aquaporin-5 (AQP5), CD4, actin, fibrinogen, β-tubulin, serum albumin, hydroxyapatite, zinc α2-glycoprotein, and the Fc fragment of IgGs, and the expression of PIP has been demonstrated to be modulated by various cytokines, including IL4/13, IL1, and IL6. PIP gene expression has been extensively studied due to its captivating nature. It is influenced by various factors, with androgens, progesterone, glucocorticosteroids, prolactin, and growth hormone enhancing its expression while estrogens suppress it. The regulatory mechanisms involve important proteins such as STAT5A, STAT5B, Runx2, and androgen receptor, which collaborate to enhance PIP gene transcription and protein production. The expression level of PIP in breast cancer is dependent on the tumor stage and subtype. Higher expression is observed in early-stage tumors of the luminal A subtype, while lower expression is associated with luminal B, basal-like, and triple-negative subtypes, which have a poorer prognosis. PIP expression is also correlated with apocrine differentiation, hormone receptor positivity, and longer metastasis-free survival. PIP plays a role in supporting the immune system’s antitumor response during the early stages of breast cancer development. However, as cancer progresses, the protective role of PIP may become less effective or diminished. In this work, we summarized the clinical significance of the PIP molecule in breast cancer and its potential role as a new candidate for cell-based therapies. Full article
(This article belongs to the Special Issue Genetic Disorders in Breast and Ovarian Cancer)
►▼ Show Figures

Figure 1

Figure 1
<p>Crystal structure of the complex formed between zinc 2-glycoprotein (ZAG) and prolactin-inducible protein (PIP) [<a href="#B11-cells-12-02252" class="html-bibr">11</a>].</p> Full article ">Figure 2
<p>PIP expression overview in tissues of the human body, visualization shows RNA-seq data generated by The Cancer Genome Atlas (TCGA) (image credit: Human Protein Atlas <a href="http://www.proteinatlas.org" target="_blank">www.proteinatlas.org</a>. Image available at the following URL: <a href="https://v21.proteinatlas.org/ENSG00000159763-PIP/tissue" target="_blank">https://v21.proteinatlas.org/ENSG00000159763-PIP/tissue</a>, accessed on 9 July 2023).</p> Full article ">Figure 3
<p>The antigen location on the target protein(s) and the features of the target protein. At the top, the position of the antigen (identified by the corresponding HPA identifier) is shown as a green bar. Below the antigens, the maximum percent sequence identity of the protein to all other proteins from other human genes is displayed, using a sliding window of 10 aa residues (HsID 10) or 50 aa residues (HsID 50). The region with the lowest possible identity is always selected for antigen design, with a maximum identity of 60% allowed for designing a single-target antigen. The curve in blue displays the predicted antigenicity, i.e., the tendency for different regions of the protein to generate an immune response, with peak regions being predicted to be more antigenic. The curve shows average values based on a sliding window approach using an in-house propensity scale. If a signal peptide predicted by a majority of the signal peptide predictors SPOCTOPUS, SignalP 4.0, and Phobius (turquoise) is predicted by MDM, it is displayed. Low-complexity regions are shown in yellow and InterPro regions in green. Common (purple) and unique (grey) regions between different splice variants of the gene are also displayed, and at the bottom of the protein view is the protein scale. (Image credit: Human Protein Atlas <a href="http://www.proteinatlas.org" target="_blank">www.proteinatlas.org</a>. Image available at the following URL: <a href="https://v21.proteinatlas.org/ENSG00000159763-PIP#gene_information" target="_blank">https://v21.proteinatlas.org/ENSG00000159763-PIP#gene_information</a>, accessed on 9 July 2023).</p> Full article ">Figure 4
<p>One of the regulatory mechanisms of PIP. The mechanism involves several steps as follows: (1) Prolactin (PRL) binding to prolactin receptor (PRLR); (2) phosphorylation in STAT5; (3) dimerization of STAT5; (4) entering the nucleus by STAT5; (5) binding to the STAT5-responsive element (STAT5 RE) by STAT5, binding by the androgen receptor (AR) to androgen-responsive elements (AREs), enhancing PIP expression of PIP gene.</p> Full article ">Figure 5
<p>One of the regulatory mechanisms of PIP. The mechanism involves several steps as follows: (1) Binding 5α-dihydrotestosterone (DHT) to the androgen receptor (AR) inducing dimerization of the AR; (2) AR entering nucleus facilitated by PIP; (3) binding to enhancer element of the PIP promoter by androgen receptor and Runx2 increasing expression of the PIP gene. ** Stimulation of androgen-dependent genes by PIP.</p> Full article ">Figure 6
<p>One of the regulatory mechanisms of PIP: PIP possesses aspartic-type protease activity, targeting fibronectin and activating β1-integrin. This triggers a cascade involving ILK1, ErbB2, ERK, and Akt signaling pathways. ERK and Akt phosphorylate RSK and MSK kinases, leading to CREB1 activation and increased PIP gene transcription. Positive feedback loops involve PIP degradation of fibronectin, CREB1 transcriptional regulation, and AR-mediated induction of ErbB2.</p> Full article ">
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