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Molecular Mechanisms and Targeted Therapies of Breast Cancer
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Molecular Mechanisms and Targeted Therapies of Breast Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 812

Special Issue Editors

Prof. Dr. Piotr Dzięgiel

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Guest Editor
Division of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, 50-367 Wroclaw, Poland
Interests: cancer biology; cell proliferation; cancer biomarkers; tumor microenvironment; immunohistochemistry; histology
Special Issues, Collections and Topics in MDPI journals
Dr. Karolina Jabłońska

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Guest Editor
Division of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, 50-368 Wroclaw, Poland
Interests: lung cancer
Dr. Katarzyna Nowińska

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Guest Editor
Division of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, 50-368 Wroclaw, Poland
Interests: cancer-associated fibroblasts; tumor microenvironment; cell proliferation; cancer immunotherapy; histology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancer is the most common malignancy in women and is a serious public health challenge. Current research focuses on searching for new markers that will allow us to understand the molecular mechanisms of individual breast cancer cell subtypes. The molecular profile of breast cancer cells allows for the development of personalized therapy. Although targeted therapies are more effective and specific than classic therapeutic pathways, they are also associated with the development of molecular resistance. The combination of classic clinical and histopathological tests with omics allows the development of new therapeutic strategies combining classic chemotherapy and immunotherapy with other innovative forms of treatment.

This special issue is open to submission of research articles on molecular aspects of the biology of breast cancer, including diagnostic, prognostic, and predictive biomarkers. The aim of this special issue is to collect the latest knowledge on the signaling pathways involved in the proliferation, and metastasis of breast cancer cells, intercellular communication, and the role of the tumor microenvironment. In addition, we expect work in the areas of genomics, transcriptomics, and epigenetics in the aspect of molecularly targeted therapies. We invite original research and review papers describing the latest achievements and perspectives in this field.

Prof. Dr. Piotr Dzięgiel
Dr. Karolina Jabłońska
Dr. Katarzyna Nowińska
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. 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
  • cancer progression
  • cancer metastasis
  • tumor microenvironment
  • molecular mechanisms
  • molecular markers
  • epigenetics
  • genomics
  • transcriptomics
  • EMT
  • targeted therapies
  • signaling pathways
  • exosomes
  • EMT
  • hormonal regulation
  • drugs
  • apoptosis

Published Papers (2 papers)

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Research

17 pages, 3587 KiB  
Article
Migratory Tumor Cells Cooperate with Cancer Associated Fibroblasts in Hormone Receptor-Positive and HER2-Negative Breast Cancer
by Eun Hye Joo, Sangmin Kim, Donghyun Park, Taeseob Lee, Woong-Yang Park, Kyung Yeon Han and Jeong Eon Lee
Int. J. Mol. Sci. 2024, 25(11), 5876; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25115876 - 28 May 2024
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Abstract
Hormone receptor-positive and HER2-negative breast cancer (HR+/HER2-BC) is the most common type with a favorable prognosis under endocrine therapy. However, it still demonstrates unpredictable progression and recurrences influenced by high tumoral diversity and microenvironmental status. To address these heterogeneous molecular characteristics of HR+/HER2-BC, [...] Read more.
Hormone receptor-positive and HER2-negative breast cancer (HR+/HER2-BC) is the most common type with a favorable prognosis under endocrine therapy. However, it still demonstrates unpredictable progression and recurrences influenced by high tumoral diversity and microenvironmental status. To address these heterogeneous molecular characteristics of HR+/HER2-BC, we aimed to simultaneously characterize its transcriptomic landscape and genetic architecture at the same resolution. Using advanced single-cell RNA and DNA sequencing techniques together, we defined four distinct tumor subtypes. Notably, the migratory tumor subtype was closely linked to genomic alterations of EGFR, related to the tumor-promoting behavior of IL6-positive inflammatory tumor-associated fibroblast, and contributing to poor prognosis. Our study comprehensively utilizes integrated analysis to uncover the complex dynamics of this breast cancer subtype, highlighting the pivotal role of the migratory tumor subtype in influencing surrounding cells. This sheds light on potential therapeutic targets by offering enhanced insights for HR+/HER2-BC treatment. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Targeted Therapies of Breast Cancer)
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18 pages, 4780 KiB  
Article
Harnessing Metformin’s Immunomodulatory Effects on Immune Cells to Combat Breast Cancer
by Andjela Petrovic, Ivan Jovanovic, Bojan Stojanovic, Milica Dimitrijevic Stojanovic, Bojana S. Stojanovic, Milena Jurisevic, Bojana Simovic Markovic, Marina Jovanovic, Milan Jovanovic, Mihailo Jovanovic and Nevena Gajovic
Int. J. Mol. Sci. 2024, 25(11), 5869; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25115869 - 28 May 2024
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Abstract
Metformin, a medication known for its anti-glycemic properties, also demonstrates potent immune system activation. In our study, using a 4T1 breast cancer model in BALB/C WT mice, we examined metformin’s impact on the functional phenotype of multiple immune cells, with a specific emphasis [...] Read more.
Metformin, a medication known for its anti-glycemic properties, also demonstrates potent immune system activation. In our study, using a 4T1 breast cancer model in BALB/C WT mice, we examined metformin’s impact on the functional phenotype of multiple immune cells, with a specific emphasis on natural killer T (NKT) cells due to their understudied role in this context. Metformin administration delayed the appearance and growth of carcinoma. Furthermore, metformin increased the percentage of IFN-γ+ NKT cells, and enhanced CD107a expression, as measured by MFI, while decreasing PD-1+, FoxP3+, and IL-10+ NKT cells in spleens of metformin-treated mice. In primary tumors, metformin increased the percentage of NKp46+ NKT cells and increased FasL expression, while lowering the percentages of FoxP3+, PD-1+, and IL-10-producing NKT cells and KLRG1 expression. Activation markers increased, and immunosuppressive markers declined in T cells from both the spleen and tumors. Furthermore, metformin decreased IL-10+ and FoxP3+ Tregs, along with Gr-1+ myeloid-derived suppressor cells (MDSCs) in spleens, and in tumor tissue, it decreased IL-10+ and FoxP3+ Tregs, Gr-1+, NF-κB+, and iNOS+ MDSCs, and iNOS+ dendritic cells (DCs), while increasing the DCs quantity. Additionally, increased expression levels of MIP1a, STAT4, and NFAT in splenocytes were found. These comprehensive findings illustrate metformin’s broad immunomodulatory impact across a variety of immune cells, including stimulating NKT cells and T cells, while inhibiting Tregs and MDSCs. This dynamic modulation may potentiate its use in cancer immunotherapy, highlighting its potential to modulate the tumor microenvironment across a spectrum of immune cell types. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Targeted Therapies of Breast Cancer)
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