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Advances and Mechanisms in Breast Cancer
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Advances and Mechanisms in Breast Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 9584

Special Issue Editor

Dr. Ioannis Boutas

E-Mail Website
Guest Editor
Breast Unit, REA Maternity Hospital, Athens, Greece
Interests: breast cancer; hormone receptors; triple negative; Her-2neu; pregnancy-associated breast cancer; gene mutations

Special Issue Information

Dear Colleagues,

Breast cancer is one of the most prevalent neoplastic diseases in women and the leading cause of cancer-related deaths in women. Breast cancer treatment is based on a multidisciplinary approach involving various specialists, such as breast surgeons, plastic surgeons and radiation and medical oncologists, leading to a reduction in breast cancer mortality. Novel treatment approaches are being developed and research is being focused on the molecular aspects of breast cancer.

There are numerous research areas that must be addressed with regard to this devastating disease. Thus, this Special Issue offers a timely opportunity to publish studies that aim to explore the molecular aspects of breast cancer. Both original research and review articles are all welcome, especially articles describing the genes and molecular pathways that may serve as novel targets for experimental therapeutics and future clinical trials. It is expected that this Special Issue will become a useful resource for all investigators and clinicians interested in breast cancer research, and will inspire new research directions in the years to come.

Since IJMS is a journal of molecular science, purely clinical studies are suitable. However, clinical or pure model submissions reflecting biomolecular experiments are welcome.

Dr. Ioannis Boutas
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

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Published Papers (6 papers)

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Research

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19 pages, 3810 KiB  
Article
Targeting ITGβ3 to Overcome Trastuzumab Resistance through Epithelial–Mesenchymal Transition Regulation in HER2-Positive Breast Cancer
by Asiye Busra Boz Er and Idris Er
Int. J. Mol. Sci. 2024, 25(16), 8640; https://doi.org/10.3390/ijms25168640 - 8 Aug 2024
Cited by 1 | Viewed by 834
Abstract
HER2-positive breast cancer, representing 15–20% of all breast cancer cases, often develops resistance to the HER2-targeted therapy trastuzumab. Unfortunately, effective treatments for advanced HER2-positive breast cancer remain scarce. This study aims to investigate the roles of ITGβ3, and Hedgehog signaling in trastuzumab resistance [...] Read more.
HER2-positive breast cancer, representing 15–20% of all breast cancer cases, often develops resistance to the HER2-targeted therapy trastuzumab. Unfortunately, effective treatments for advanced HER2-positive breast cancer remain scarce. This study aims to investigate the roles of ITGβ3, and Hedgehog signaling in trastuzumab resistance and explore the potential of combining trastuzumab with cilengitide as a therapeutic strategy. Quantitative gene expression analysis was performed to assess the transcription of EMT (epithelial–mesenchymal transition) markers Slug, Snail, Twist2, and Zeb1 in trastuzumab-resistant HER2-positive breast cancer cells. The effects of ITGβ3 and Hedgehog signaling were investigated. Additionally, the combination therapy of trastuzumab and cilengitide was evaluated. Acquired trastuzumab resistance induced the transcription of Slug, Snail, Twist2, and Zeb1, indicating increased EMT. This increased EMT was mediated by ITGB3 and Hedgehog signaling. ITGβ3 regulated both the Hedgehog pathway and EMT, with the latter being independent of the Hedgehog pathway. The combination of trastuzumab and cilengitide showed a synergistic effect, reducing both EMT and Hedgehog pathway activity. Targeting ITGβ3 with cilengitide, combined with trastuzumab, effectively suppresses the Hedgehog pathway and EMT, offering a potential strategy to overcome trastuzumab resistance and improve outcomes for HER2-positive breast cancer patients. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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14 pages, 2979 KiB  
Article
Tumor-Intrinsic Enhancer of Zeste Homolog 2 Controls Immune Cell Infiltration, Tumor Growth, and Lung Metastasis in a Triple-Negative Breast Cancer Model
by Lenore Monterroza, Maria M. Parrilla, Sarah G. Samaranayake, Dormarie E. Rivera-Rodriguez, Sung Bo Yoon, Ramireddy Bommireddy, Justin Hosten, Luisa Cervantes Barragan, Adam Marcus, Brian S. Dobosh, Periasamy Selvaraj and Rabindra Tirouvanziam
Int. J. Mol. Sci. 2024, 25(10), 5392; https://doi.org/10.3390/ijms25105392 - 15 May 2024
Cited by 1 | Viewed by 1481
Abstract
Triple-negative breast cancer (TNBC) is an aggressive and highly metastatic type of tumor. TNBC is often enriched in tumor-infiltrating neutrophils (TINs), which support cancer growth in part by counteracting tumor-infiltrating lymphocytes (TILs). Prior studies identified the enhancer of zeste homolog 2 (EZH2) as [...] Read more.
Triple-negative breast cancer (TNBC) is an aggressive and highly metastatic type of tumor. TNBC is often enriched in tumor-infiltrating neutrophils (TINs), which support cancer growth in part by counteracting tumor-infiltrating lymphocytes (TILs). Prior studies identified the enhancer of zeste homolog 2 (EZH2) as a pro-tumor methyltransferase in primary and metastatic TNBCs. We hypothesized that EZH2 inhibition in TNBC cells per se would exert antitumor activity by altering the tumor immune microenvironment. To test this hypothesis, we used CRISPR to generate EZH2 gene knockout (KO) and overexpressing (OE) lines from parent (wild-type—WT) 4T1 cells, an established murine TNBC model, resulting in EZH2 protein KO and OE, respectively. In vitro, EZH2 KO and OE cells showed early, transient changes in replicative capacity and invasiveness, and marked changes in surface marker profile and cytokine/chemokine secretion compared to WT cells. In vivo, EZH2 KO cells showed significantly reduced primary tumor growth and a 10-fold decrease in lung metastasis compared to WT cells, while EZH2 OE cells were unchanged. Compared to WT tumors, TIN:TIL ratios were greatly reduced in EZH2 KO tumors but unchanged in EZH2 OE tumors. Thus, EZH2 is key to 4T1 aggressiveness as its tumor-intrinsic knockout alters their in vitro secretome and in vivo primary tumor growth, TIN/TIL poise, and metastasis. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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15 pages, 5891 KiB  
Article
Resistance to Combined Anthracycline–Taxane Chemotherapy Is Associated with Altered Metabolism and Inflammation in Breast Carcinomas
by Otília Menyhárt, János Tibor Fekete and Balázs Győrffy
Int. J. Mol. Sci. 2024, 25(2), 1063; https://doi.org/10.3390/ijms25021063 - 15 Jan 2024
Viewed by 1733
Abstract
Approximately 30% of early-stage breast cancer (BC) patients experience recurrence after systemic chemotherapy; thus, understanding therapy resistance is crucial in developing more successful treatments. Here, we investigated the mechanisms underlying resistance to combined anthracycline–taxane treatment by comparing gene expression patterns with subsequent therapeutic [...] Read more.
Approximately 30% of early-stage breast cancer (BC) patients experience recurrence after systemic chemotherapy; thus, understanding therapy resistance is crucial in developing more successful treatments. Here, we investigated the mechanisms underlying resistance to combined anthracycline–taxane treatment by comparing gene expression patterns with subsequent therapeutic responses. We established a cohort of 634 anthracycline–taxane-treated patients with pathological complete response (PCR) and a separate cohort of 187 patients with relapse-free survival (RFS) data, each having transcriptome-level expression data of 10,017 unique genes. Patients were categorized as responders and non-responders based on their PCR and RFS status, and the expression for each gene was compared between the two groups using a Mann–Whitney U-test. Statistical significance was set at p < 0.05, with fold change (FC) > 1.44. Altogether, 224 overexpressed genes were identified in the tumor samples derived from the patients without PCR; among these, the gene sets associated with xenobiotic metabolism (e.g., CYP3A4, CYP2A6) exhibited significant enrichment. The genes ORAI3 and BCAM differentiated non-responders from responders with the highest AUC values (AUC > 0.75, p < 0.0001). We identified 51 upregulated genes in the tumor samples derived from the patients with relapse within 60 months, participating primarily in inflammation and innate immune responses (e.g., LYN, LY96, ANXA1). Furthermore, the amino acid transporter SLC7A5, distinguishing non-responders from responders, had significantly higher expression in tumors and metastases than in normal tissues (Kruskal–Wallis p = 8.2 × 10−20). The identified biomarkers underscore the significance of tumor metabolism and microenvironment in treatment resistance and can serve as a foundation for preclinical validation studies. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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15 pages, 5369 KiB  
Article
The Role of Transcription Factors in the Loss of Inter-Chromosomal Co-Expression for Breast Cancer Subtypes
by Rodrigo Trujillo-Ortíz, Jesús Espinal-Enríquez and Enrique Hernández-Lemus
Int. J. Mol. Sci. 2023, 24(24), 17564; https://doi.org/10.3390/ijms242417564 - 16 Dec 2023
Cited by 1 | Viewed by 1163
Abstract
Breast cancer encompasses a diverse array of subtypes, each exhibiting distinct clinical characteristics and treatment responses. Unraveling the underlying regulatory mechanisms that govern gene expression patterns in these subtypes is essential for advancing our understanding of breast cancer biology. Gene co-expression networks (GCNs) [...] Read more.
Breast cancer encompasses a diverse array of subtypes, each exhibiting distinct clinical characteristics and treatment responses. Unraveling the underlying regulatory mechanisms that govern gene expression patterns in these subtypes is essential for advancing our understanding of breast cancer biology. Gene co-expression networks (GCNs) help us identify groups of genes that work in coordination. Previous research has revealed a marked reduction in the interaction of genes located on different chromosomes within GCNs for breast cancer, as well as for lung, kidney, and hematopoietic cancers. However, the reasons behind why genes on the same chromosome often co-express remain unclear. In this study, we investigate the role of transcription factors in shaping gene co-expression networks within the four main breast cancer subtypes: Luminal A, Luminal B, HER2+, and Basal, along with normal breast tissue. We identify communities within each GCN and calculate the transcription factors that may regulate these communities, comparing the results across different phenotypes. Our findings indicate that, in general, regulatory behavior is to a large extent similar among breast cancer molecular subtypes and even in healthy networks. This suggests that transcription factor motif usage does not fully determine long-range co-expression patterns. Specific transcription factor motifs, such as CCGGAAG, appear frequently across all phenotypes, even involving multiple highly connected transcription factors. Additionally, certain transcription factors exhibit unique actions in specific subtypes but with limited influence. Our research demonstrates that the loss of inter-chromosomal co-expression is not solely attributable to transcription factor regulation. Although the exact mechanism responsible for this phenomenon remains elusive, this work contributes to a better understanding of gene expression regulatory programs in breast cancer. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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Review

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23 pages, 3640 KiB  
Review
The “Forgotten” Subtypes of Breast Carcinoma: A Systematic Review of Selected Histological Variants Not Included or Not Recognized as Distinct Entities in the Current World Health Organization Classification of Breast Tumors
by Nektarios I. Koufopoulos, Ioannis Boutas, Abraham Pouliakis, Menelaos G. Samaras, Christakis Kotanidis, Adamantia Kontogeorgi, Dionysios T. Dimas, Argyro-Ioanna Ieronimaki, Danai Leventakou, Aris Spathis, Magda Zanelli, Andrea Palicelli, Maurizio Zizzo, Dimitrios Goutas, Ioannis S. Pateras and Ioannis G. Panayiotides
Int. J. Mol. Sci. 2024, 25(15), 8382; https://doi.org/10.3390/ijms25158382 - 1 Aug 2024
Cited by 1 | Viewed by 1189
Abstract
Breast carcinoma is the most common cancer in women. Nineteen different subtypes of breast carcinomas are recognized in the current WHO classification of breast tumors. Except for these subtypes, there are a number of carcinomas with special morphologic and immunohistochemical features that are [...] Read more.
Breast carcinoma is the most common cancer in women. Nineteen different subtypes of breast carcinomas are recognized in the current WHO classification of breast tumors. Except for these subtypes, there are a number of carcinomas with special morphologic and immunohistochemical features that are not included in the 5th WHO classification, while others are considered special morphologic patterns of invasive breast carcinoma of no special type. In this manuscript, we systematically review the literature on four different subtypes of invasive breast carcinoma, namely lymphoepithelioma-like breast carcinoma, breast carcinoma with osteoclast-like giant cells, signet-ring breast carcinoma, and metaplastic breast carcinoma with melanocytic differentiation. We describe their clinicopathological characteristics, focusing on the differential diagnosis, treatment, and prognosis. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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13 pages, 1027 KiB  
Review
Reverse Onco-Cardiology: What Is the Evidence for Breast Cancer? A Systematic Review of the Literature
by Ioannis Boutas, Adamantia Kontogeorgi, Sophia N. Kalantaridou, Constantine Dimitrakakis, Panagiotis Patsios, Maria Kalantzi and Theodoros Xanthos
Int. J. Mol. Sci. 2023, 24(22), 16500; https://doi.org/10.3390/ijms242216500 - 19 Nov 2023
Cited by 1 | Viewed by 2572
Abstract
Breast cancer and cardiovascular diseases (CVD) represent significant global health challenges, with CVD being the leading cause of mortality and breast cancer, showing a complex pattern of incidence and mortality. We explore the intricate interplay between these two seemingly distinct medical conditions, shedding [...] Read more.
Breast cancer and cardiovascular diseases (CVD) represent significant global health challenges, with CVD being the leading cause of mortality and breast cancer, showing a complex pattern of incidence and mortality. We explore the intricate interplay between these two seemingly distinct medical conditions, shedding light on their shared risk factors and potential pathophysiological connections. A specific connection between hypertension (HTN), atrial fibrillation (AF), myocardial infarction (MI), and breast cancer was evaluated. HTN is explored in detail, emphasizing the role of aging, menopause, insulin resistance, and obesity as common factors linking HTN and breast cancer. Moreover, an attempt is made to identify the potential impact of antihypertensive medications and highlight the increased risk of breast cancer among those women, with a focus on potential mechanisms. A summary of key findings underscores the need for a multisystem approach to understanding the relationship between CVD and breast cancer is also explored with a highlight for all the gaps in current research, such as the lack of clinical observational data on MI and breast cancer in humans and the need for studies specifically designed for breast cancer. This paper concludes that there should be a focus on potential clinical applications of further investigation in this field, including personalized prevention and screening strategies for women at risk. Overall, the authors attempt to provide a comprehensive overview of the intricate connections between breast cancer and cardiovascular diseases, emphasizing the importance of further research in this evolving field of cardio-oncology. Full article
(This article belongs to the Special Issue Advances and Mechanisms in Breast Cancer)
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