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Biomedicines
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Breast Cancer: Mechanisms of Development and Progression and Novel Approaches...
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Breast Cancer: Mechanisms of Development and Progression and Novel Approaches to Clinical Management

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 5145

Special Issue Editors

Dr. Armen Parsyan

E-Mail Website
Guest Editor
General Surgeon and Breast Surgical Oncologist, Clinician-Scientist Assistant Professor, Departments of Surgery and Oncology, St Joseph’s Health Care and London Health Sciences Centre, London Regional Cancer Program, Schulich School of Medicine & Dentistry, Western University London, ON
Interests: breast cancer
Dr. Vasudeva Bhat

E-Mail Website
Guest Editor
Anatomy and Cell Bioligy, University of Western Ontario, London, ON, Canada
Interests: breast cancer stem cells; breast cancer metastasis; patient derived organoids; circulating tumor cells; circulating tumor DNA; liquid biopsies; tumor microenvironment

Special Issue Information

Dear Colleagues,

Breast cancer is a major cause of morbidity and mortality among women worldwide. A significant progress has been made in our understanding of the biology of breast cancer that has served as a foundation for the development of clinically effective diagnostic, prevention, and treatment strategies. While in early-stage breast cancer, excellent outcomes are observed, the metastatic, recurrent, and drug-resistant disease still confers an unacceptably poor prognosis. Certain subtypes of this malignancy, such as its most aggressive triple-negative subtype, lack predictive and treatment biomarkers, which contributes to the relatively poor oncologic outcomes. The significant heterogeneity of breast cancer mandates a nuanced understanding and management that requires further research efforts. This issue discusses mechanisms of breast cancer development and progression, as well as presents recent preclinical studies on novel approaches in treatment of this condition.

Dr. Armen Parsyan
Dr. Vasudeva Bhat
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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; triple-negative breast cancer; cancer progression and development; novel chemotherapies; rediotherapy; immunotherapy

Published Papers (2 papers)

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16 pages, 2795 KiB  
Article
Lung-Derived Selectins Enhance Metastatic Behavior of Triple Negative Breast Cancer Cells
by Sami U. Khan, Ying Xia, David Goodale, Gabriella Schoettle and Alison L. Allan
Biomedicines 2021, 9(11), 1580; https://doi.org/10.3390/biomedicines9111580 - 30 Oct 2021
Cited by 5 | Viewed by 1776
Abstract
The lung is one of the deadliest sites of breast cancer metastasis, particularly for triple negative breast cancer (TNBC). We have previously shown that the lung produces several soluble factors that may enhance the metastatic behavior of TNBC, including E-, L-, and P-selectin. [...] Read more.
The lung is one of the deadliest sites of breast cancer metastasis, particularly for triple negative breast cancer (TNBC). We have previously shown that the lung produces several soluble factors that may enhance the metastatic behavior of TNBC, including E-, L-, and P-selectin. In this paper, we hypothesize that lung-derived selectins promote TNBC metastatic behavior and may serve as a potential therapeutic target. Lungs were isolated from mice and used to generate lung-conditioned media (CM). Lung-derived selectins were immunodepleted and TNBC migration and proliferation were assessed in response to native or selectin-depleted lung-CM. A 3D ex vivo pulmonary metastasis assay (PuMA) was used to assess the metastatic progression of TNBC in the lungs of wild-type versus triple-selectin (ELP-/-) knockout mice. We observed that individual lung-derived selectins enhance in vitro migration (p ≤ 0.05), but not the proliferation of TNBC cells, and that ex vivo metastatic progression is reduced in the lungs of ELP-/- mice compared to wild-type mice (p ≤ 0.05). Treatment with the pan-selectin inhibitor bimosiamose reduced in vitro lung-specific TNBC migration and proliferation (p ≤ 0.05). Taken together, these results suggest that lung-derived selectins may present a potential therapeutic target against TNBC metastasis. Future studies are aimed at elucidating the pro-metastatic mechanisms of lung-derived selectins and developing a lung-directed therapeutic approach. Full article
(This article belongs to the Special Issue Breast Cancer: Mechanisms of Development and Progression and Novel Approaches to Clinical Management)
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8 pages, 1404 KiB  
Perspective
PPARgamma: A Potential Intrinsic and Extrinsic Molecular Target for Breast Cancer Therapy
by Giuseppina Augimeri and Daniela Bonofiglio
Biomedicines 2021, 9(5), 543; https://doi.org/10.3390/biomedicines9050543 - 13 May 2021
Cited by 7 | Viewed by 2624
Abstract
Over the last decades, the breast tumor microenvironment (TME) has been increasingly recognized as a key player in tumor development and progression and as a promising prognostic and therapeutic target for breast cancer patients. The breast TME, representing a complex network of cellular [...] Read more.
Over the last decades, the breast tumor microenvironment (TME) has been increasingly recognized as a key player in tumor development and progression and as a promising prognostic and therapeutic target for breast cancer patients. The breast TME, representing a complex network of cellular signaling—deriving from different stromal cell types as well as extracellular matrix components, extracellular vesicles, and soluble growth factors—establishes a crosstalk with cancer cells sustaining tumor progression. A significant emphasis derives from the tumor surrounding inflammation responsible for the failure of the immune system to effectively restrain breast cancer growth. Thus, effective therapeutic strategies require a deeper understanding of the interplay between tumor and stroma, aimed at targeting both the intrinsic neoplastic cells and the extrinsic surrounding stroma. In this scenario, peroxisome proliferator-activated receptor (PPAR) γ, primarily known as a metabolic regulator, emerged as a potential target for breast cancer treatment since it functions in breast cancer cells and several components of the breast TME. In particular, the activation of PPARγ by natural and synthetic ligands inhibits breast cancer cell growth, motility, and invasiveness. Moreover, activated PPARγ may educate altered stromal cells, counteracting the pro-inflammatory milieu that drive breast cancer progression. Interestingly, using Kaplan–Meier survival curves, PPARγ also emerges as a prognostically favorable factor in breast cancer patients. In this perspective, we briefly discuss the mechanisms by which PPARγ is implicated in tumor biology as well as in the complex regulatory networks within the breast TME. This may help to profile approaches that provide a simultaneous inhibition of epithelial cells and TME components, offering a more efficient way to treat breast cancer. Full article
(This article belongs to the Special Issue Breast Cancer: Mechanisms of Development and Progression and Novel Approaches to Clinical Management)
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