Special Issue "Breast Cancer Stem Cells: Therapy Resistance and Novel Therapeutic Targets"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 15 June 2019

Special Issue Editor

Guest Editor
Dr. Paola Marcato

Department of Pathology, Dalhousie University, Halifax, NS B3H 4G7, Canada
Website | E-Mail
Interests: triple-negative breast cancer; cancer stem cells; aldehyde dehydrogenase 1A3; retinoic acid signaling; precision medicine; therapy resistance

Special Issue Information

Dear Colleagues,

As with other cancers, increasing evidence supports the significance of breast cancer stem cells (CSCs) in the development and progression of breast cancer. Importantly, these cancer drivers also share many of the characteristics of stem cells, including qualities that make them resistant to commonly used cancer treatments. Mechanisms such as increased efflux capacity, higher levels of detoxifying enzymes, enhanced DNA repair, a slower cell-cycle, and increased activation of the embryonic signaling pathways (Notch, Wnt, and Hedgehog) give CSCs an increased resistance to chemotherapeutics and radiation. Clinical evidence also suggests that CSC resistance may contribute to breast tumor recurrence and poorer patient outcomes. Therefore, the development of adjuvant therapies that either target CSCs or sensitize CSCs to chemotherapies has been a major focus of recent drug discovery in the treatment of cancer. We invite original research or review articles that address the mechanisms of breast CSC therapy resistance and anti-breast CSC drug development.

Dr. Paola Marcato
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 papers will be 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. Cancers 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 1800 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
  • cancer stem cells
  • therapy
  • resistance
  • recurrence

Published Papers (1 paper)

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Research

Open AccessArticle Therapeutic Potential of a Novel αvβ3 Antagonist to Hamper the Aggressiveness of Mesenchymal Triple Negative Breast Cancer Sub-Type
Cancers 2019, 11(2), 139; https://doi.org/10.3390/cancers11020139
Received: 8 January 2019 / Revised: 17 January 2019 / Accepted: 20 January 2019 / Published: 24 January 2019
PDF Full-text (3487 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The mesenchymal sub-type of triple negative breast cancer (MES-TNBC) has a highly aggressive behavior and worse prognosis, due to its invasive and stem-like features, that correlate with metastatic dissemination and resistance to therapies. Furthermore, MES-TNBC is characterized by the expression of molecular markers [...] Read more.
The mesenchymal sub-type of triple negative breast cancer (MES-TNBC) has a highly aggressive behavior and worse prognosis, due to its invasive and stem-like features, that correlate with metastatic dissemination and resistance to therapies. Furthermore, MES-TNBC is characterized by the expression of molecular markers related to the epithelial-to-mesenchymal transition (EMT) program and cancer stem cells (CSCs). The altered expression of αvβ3 integrin has been well established as a driver of cancer progression, stemness, and metastasis. Here, we showed that the high levels of αvβ3 are associated with MES-TNBC and therefore exploited the possibility to target this integrin to reduce the aggressiveness of this carcinoma. To this aim, MES-TNBC cells were treated with a novel peptide, named ψRGDechi, that we recently developed and characterized for its ability to selectively bind and inhibit αvβ3 integrin. Notably, ψRGDechi was able to hamper adhesion, migration, and invasion of MES-TNBC cells, as well as the capability of these cells to form vascular-like structures and mammospheres. In addition, this peptide reversed EMT program inhibits mesenchymal markers. These findings show that targeting αvβ3 integrin by ψRGDechi, it is possible to inhibit some of the malignant properties of MES-TNBC phenotype. Full article
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