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Recent Advances in Breast Cancer Research, 2nd Edition
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Recent Advances in Breast Cancer Research, 2nd Edition

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: 30 December 2024 | Viewed by 9863

Special Issue Editor

Dr. Daniela Grimm

E-Mail Website
Guest Editor
1. Institute of Biomedicine, Aarhus University, Ole Worms Allé 4, 8000 Aarhus, Denmark
2. Department of Microgravity and Translational Regenerative Medicine, Otto von Guericke University Magdeburg, Pfälzerplatz 2, 39106 Magdeburg, Germany
Interests: breast cancer; thyroid cancer; prostate cancer; cell biology; gravitational biology; space medicine; tissue engineering; pharmacology; apoptosis; SOX transcription factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancer is the leading cause of cancer death in females. The incidence has risen dramatically in recent decades. Dismissed as an “unsolved problem of the last century”, breast cancer still represents a health burden with no effective solution identified so far. As estimated by the latest GLOBOCAN (Global Cancer Observatory) survey in 2020, breast cancer (BC) comprises 2.3 million new cases of female BC and 684,996 death incidents worldwide. Local options for treatment are surgery and radiation. Systemic treatments comprise chemotherapy, hormone therapy, immunotherapy, and drug-targeted treatment strategies. Various drugs are available for BC therapy, but adverse effects and the problematic development of drug resistance make it important to search for novel strategies and new drug targets. This SI will provide an updated overview covering all aspects of targeted therapies in breast cancer, from basic science to the clinical trials. In addition, there will be a special focus on potential biomarkers that are predictive for a therapeutic response.

Furthermore, new research fields comprise organoid studies and microgravity (µg) research, which is an unusual method to combat the disease. Numerous studies have indicated that µg has a great impact on cancer cells. By influencing proliferation, survival, and migration, it shifts breast cancer cells toward a less-aggressive phenotype. In addition, through the de novo generation of tumor spheroids, µg research provides a reliable in vitro 3D tumor model for preclinical cancer drug development and for the study various processes of cancer progression.

In this SI, studies using animal or cell culture models to investigate molecular mechanisms of BC will be published. This SI will also cover reports on patients, providing novel mechanistic insights into the underlying pathogenesis or new aspects that may impact clinical therapy.

Dr. Daniela Grimm
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.

Keywords

  • breast cancer
  • drugs
  • OMICS investigations
  • cell signaling
  • biomarker
  • tyrosine kinase inhibitors
  • in vitro studies
  • organoids
  • animal studies

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Related Special Issue

Published Papers (4 papers)

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Research

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24 pages, 17704 KiB  
Article
HER4 Affects Sensitivity to Tamoxifen and Abemaciclib in Luminal Breast Cancer Cells and Restricts Tumor Growth in MCF-7-Based Humanized Tumor Mice
by Veruschka Albert, Christina Bruss, Deniz Tümen, Gerhard Piendl, Florian Weber, Edgar Dahl, Stephan Seitz, Olaf Ortmann, Anja K. Wege and Gero Brockhoff
Int. J. Mol. Sci. 2024, 25(13), 7475; https://doi.org/10.3390/ijms25137475 - 8 Jul 2024
Viewed by 1284
Abstract
The impact of the HER4 receptor on the growth and treatment of estrogen receptor-positive breast cancer is widely uncertain. Using CRISPR/Cas9 technology, we generated stable HER4 knockout variants derived from the HER4-positive MCF-7, T-47D, and ZR-75-1 breast cancer cell lines. We investigated tumor [...] Read more.
The impact of the HER4 receptor on the growth and treatment of estrogen receptor-positive breast cancer is widely uncertain. Using CRISPR/Cas9 technology, we generated stable HER4 knockout variants derived from the HER4-positive MCF-7, T-47D, and ZR-75-1 breast cancer cell lines. We investigated tumor cell proliferation as well as the cellular and molecular mechanisms of tamoxifen, abemaciclib, AMG232, and NRG1 treatments as a function of HER4 in vitro. HER4 differentially affects the cellular response to tamoxifen and abemaciclib treatment. Most conspicuous is the increased sensitivity of MCF-7 in vitro upon HER4 knockout and the inhibition of cell proliferation by NRG1. Additionally, we assessed tumor growth and immunological effects as responses to tamoxifen and abemaciclib therapy in humanized tumor mice (HTM) based on MCF-7 HER4-wildtype and the corresponding HER4-knockout cells. Without any treatment, the enhanced MCF-7 tumor growth in HTM upon HER4 knockout suggests a tumor-suppressive effect of HER4 under preclinical but human-like conditions. This phenomenon is associated with an increased HER2 expression in MCF-7 in vivo. Independent of HER4, abemaciclib and tamoxifen treatment considerably inhibited tumor growth in these mice. However, abemaciclib-treated hormone receptor-positive breast cancer patients with tumor-associated mdm2 gene copy gains or pronounced HER4 expression showed a reduced event-free survival. Evidently, the presence of HER4 affects the efficacy of tamoxifen and abemaciclib treatment in different estrogen receptor-positive breast cancer cells, even to different extents, and is associated with unfavorable outcomes in abemaciclib-treated patients. Full article
(This article belongs to the Special Issue Recent Advances in Breast Cancer Research, 2nd Edition)
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16 pages, 3190 KiB  
Article
Type II Interleukin-4 Receptor Activation in Basal Breast Cancer Cells Promotes Tumor Progression via Metabolic and Epigenetic Modulation
by Demond Williams, Ebony Hargrove-Wiley, Wendy Bindeman, Daniel Valent, Adam X. Miranda, Jacob Beckstead and Barbara Fingleton
Int. J. Mol. Sci. 2024, 25(9), 4647; https://doi.org/10.3390/ijms25094647 - 24 Apr 2024
Cited by 1 | Viewed by 1212
Abstract
Interleukin-4 (IL4) is a Th2 cytokine that can signal through two different receptors, one of which—the type II receptor—is overexpressed by various cancer cells. Previously, we have shown that type II IL4 receptor signaling increases proliferation and metastasis in mouse models of breast [...] Read more.
Interleukin-4 (IL4) is a Th2 cytokine that can signal through two different receptors, one of which—the type II receptor—is overexpressed by various cancer cells. Previously, we have shown that type II IL4 receptor signaling increases proliferation and metastasis in mouse models of breast cancer, as well as increasing glucose and glutamine metabolism. Here, we expand on those findings to determine mechanistically how IL4 signaling links glucose metabolism and histone acetylation to drive proliferation in the context of triple-negative breast cancer (TNBC). We used a combination of cellular, biochemical, and genomics approaches to interrogate TNBC cell lines, which represent a cancer type where high expression of the type II IL4 receptor is linked to reduced survival. Our results indicate that type II IL4 receptor activation leads to increased glucose uptake, Akt and ACLY activation, and histone acetylation in TNBC cell lines. Inhibition of glucose uptake through the deletion of Glut1 ablates IL4-induced proliferation. Additionally, pharmacological inhibition of histone acetyltransferase P300 attenuates IL4-mediated gene expression and proliferation in vitro. Our work elucidates a role for type II IL4 receptor signaling in promoting TNBC progression, and highlights type II IL4 signaling, as well as histone acetylation, as possible targets for therapy. Full article
(This article belongs to the Special Issue Recent Advances in Breast Cancer Research, 2nd Edition)
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14 pages, 2538 KiB  
Article
Combination Treatment with EGFR Inhibitor and Doxorubicin Synergistically Inhibits Proliferation of MCF-7 Cells and MDA-MB-231 Triple-Negative Breast Cancer Cells In Vitro
by Beynon Abrahams, Anthonie Gerber and Donavon Charles Hiss
Int. J. Mol. Sci. 2024, 25(5), 3066; https://doi.org/10.3390/ijms25053066 - 6 Mar 2024
Cited by 1 | Viewed by 2240
Abstract
The role of the epidermal growth factor receptor (EGFR) in tumor progression and survival is often underplayed. Its expression and/or dysregulation is associated with disease advancement and poor patient outcome as well as drug resistance in breast cancer. EGFR is often overexpressed in [...] Read more.
The role of the epidermal growth factor receptor (EGFR) in tumor progression and survival is often underplayed. Its expression and/or dysregulation is associated with disease advancement and poor patient outcome as well as drug resistance in breast cancer. EGFR is often overexpressed in breast cancer and particularly triple-negative breast cancer (TNBC), which currently lacks molecular targets. We examined the synergistic potential of an EGFR inhibitor (EGFRi) in combination with doxorubicin (Dox) in estrogen-positive (ER+) MCF-7 and MDA-MB-231 TNBC cell lines. The exposure of MDA-MB-231 and MCF-7 to EGFRi produced an IC50s of 6.03 µM and 3.96 µM, respectively. Dox induced MDA-MB-231 (IC50 9.67 µM) and MCF-7 (IC50 1.4 µM) cytotoxicity. Combinations of EGFRi-Dox significantly reduced the IC50 in MCF-7 (0.46 µM) and MBA-MB 231 (0.01 µM). Synergistic drug interactions in both cell lines were confirmed using the Bliss independence model. Pro-apoptotic Caspase-3/7 activation occurred in MCF-7 at 0.1–10 µM of EGFRi and Dox single treatments, whilst 1 μM Dox yielded a more potent effect on MDA-MB-231. EGFRi and Dox individually and in combination downregulated the EGFR gene expression in MCF-7 and MDA-MB-231 (p < 0.001). This study demonstrates EGFRi’s potential for eliciting synergistic interactions with Dox, causing enhanced growth inhibition, apoptosis induction, and downregulation of EGFR in both cell lines. Full article
(This article belongs to the Special Issue Recent Advances in Breast Cancer Research, 2nd Edition)
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Review

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26 pages, 1528 KiB  
Review
Omics Technologies Improving Breast Cancer Research and Diagnostics
by Arianna Orsini, Chiara Diquigiovanni and Elena Bonora
Int. J. Mol. Sci. 2023, 24(16), 12690; https://doi.org/10.3390/ijms241612690 - 11 Aug 2023
Cited by 8 | Viewed by 4561
Abstract
Breast cancer (BC) has yielded approximately 2.26 million new cases and has caused nearly 685,000 deaths worldwide in the last two years, making it the most common diagnosed cancer type in the world. BC is an intricate ecosystem formed by both the tumor [...] Read more.
Breast cancer (BC) has yielded approximately 2.26 million new cases and has caused nearly 685,000 deaths worldwide in the last two years, making it the most common diagnosed cancer type in the world. BC is an intricate ecosystem formed by both the tumor microenvironment and malignant cells, and its heterogeneity impacts the response to treatment. Biomedical research has entered the era of massive omics data thanks to the high-throughput sequencing revolution, quick progress and widespread adoption. These technologies—liquid biopsy, transcriptomics, epigenomics, proteomics, metabolomics, pharmaco-omics and artificial intelligence imaging—could help researchers and clinicians to better understand the formation and evolution of BC. This review focuses on the findings of recent multi-omics-based research that has been applied to BC research, with an introduction to every omics technique and their applications for the different BC phenotypes, biomarkers, target therapies, diagnosis, treatment and prognosis, to provide a comprehensive overview of the possibilities of BC research. Full article
(This article belongs to the Special Issue Recent Advances in Breast Cancer Research, 2nd Edition)
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