Special Issue "Cancer Invasion and Metastasis"

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

Deadline for manuscript submissions: 30 September 2019

Special Issue Editors

Guest Editor
Prof. Dr. Yitzhak Zimmer

Department of Radiation Oncology, Universitat Bern, Bern, Switzerland
Website | E-Mail
Interests: MET receptor, protein phosphorylation, (phospho-)proteomics, tumor radiosensitization, precision radiation oncology, integrated omics analysis
Guest Editor
PD. Dr. Michaela Medova

Department for BioMedical Research (DBMR), Universitat Bern, Bern, Switzerland
Website | E-Mail
Interests: DNA damage response, receptor tyrosine kinases, systems biology, cancer resistance mechanisms, head and neck cancer, single cell proteomics
Guest Editor
Prof. Deborah Stroka

Department for BioMedical Research (DBMR), Universitat Bern, Bern, Switzerland
Website | E-Mail
Interests: Hepatocellular carcinoma, Liver regeneration, Hippo pathway, tumor hypoxia, stem cells, mass cytometry

Special Issue Information

Dear Colleagues,

The aberrant invasion pathways that are activated in cancer cells underlie the establishment of metastatic programs across numerous malignant disorders. With revolutionary recent breakthroughs in primary cancer management, metastasis continues to present as a major prognostic hurdle. Systemic dissemination represents the final stage of tumor progression, as well as the principal cause of cancer-associated deaths. Over the recent years, scientific advancements continue to shed new light and provide critical insight into the mechanisms associated with metastasis that are needed for designing the next generation of therapeutic modalities. Major innovative insights derived from large-scale sequencing efforts, novel research technologies, various omics-based studies, and integrative analyses of omics data will be fundamental for our understanding of the networks that drive the deregulated invasion and metastatic processes.

In that respect, zooming into the differences of the global cellular landscapes between primary and metastatic tumors are key determinants for the identification of metastasis-driving events. Understanding how various regulatory mechanisms, for example those that involve microRNAs, autophagy, and long non-coding RNAs, are abnormally regulated, and sustaining metastasis will be of utmost importance. The current Special Issue invites contributions that provide novel aspects related to the onset and maintenance of metastasis, with special focus, but not limited to, precision medicine aspects. Particular insights describing the genomics, transcriptomics, proteomics, and posttranslational modifications-related proteomics, metabolomics, and single-cell omics with respect to the biology of metastasis are of great interest. Likewise, research topics focusing on efforts combining novel therapeutic approaches with existing modalities to manage systemic dissemination will also be welcome.

Prof. Dr. Yitzhak Zimmer
PD. Dr. Michaela Medova
Prof. Deborah Stroka
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 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.

Published Papers (2 papers)

View options order results:
result details:
Displaying articles 1-2
Export citation of selected articles as:

Research

Jump to: Review

Open AccessArticle Targeting the mDia Formin-Assembled Cytoskeleton Is an Effective Anti-Invasion Strategy in Adult High-Grade Glioma Patient-Derived Neurospheres
Cancers 2019, 11(3), 392; https://doi.org/10.3390/cancers11030392
Received: 23 January 2019 / Revised: 4 March 2019 / Accepted: 15 March 2019 / Published: 20 March 2019
PDF Full-text (14564 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
High-grade glioma (HGG, WHO Grade III–IV) accounts for the majority of adult primary malignant brain tumors. Failure of current therapies to target invasive glioma cells partly explains the minimal survival advantages: invasive tumors lack easily-defined surgical margins, and are inherently more chemo- and [...] Read more.
High-grade glioma (HGG, WHO Grade III–IV) accounts for the majority of adult primary malignant brain tumors. Failure of current therapies to target invasive glioma cells partly explains the minimal survival advantages: invasive tumors lack easily-defined surgical margins, and are inherently more chemo- and radioresistant. Much work centers upon Rho GTPase-mediated glioma invasion, yet downstream Rho effector roles are poorly understood and represent potential therapeutic targets. The roles for the mammalian Diaphanous (mDia)-related formin family of Rho effectors have emerged in invasive/metastatic disease. mDias assemble linear F-actin to promote protrusive cytoskeletal structures underlying tumor cell invasion. Small molecule mDia intramimic (IMM) agonists induced mDia functional activities including F-actin polymerization. mDia agonism inhibited polarized migration in Glioblastoma (WHO Grade IV) cells in three-dimensional (3D) in vitro and rat brain slice models. Here, we evaluate whether clinically-relevant high-grade glioma patient-derived neuro-sphere invasion is sensitive to formin agonism. Surgical HGG samples were dissociated, briefly grown as monolayers, and spontaneously formed non-adherent neuro-spheres. IMM treatment dramatically inhibited HGG patient neuro-sphere invasion, both at neuro-sphere embedding and mid-invasion assay, inducing an amoeboid morphology in neuro-sphere edge cells, while inhibiting actin- and tubulin-enriched tumor microtube formation. Thus, mDia agonism effectively disrupts multiple aspects of patient-derived HGG neuro-sphere invasion. Full article
(This article belongs to the Special Issue Cancer Invasion and Metastasis)
Figures

Figure 1

Review

Jump to: Research

Open AccessReview Triple Negative Breast Cancer Profile, from Gene to microRNA, in Relation to Ethnicity
Cancers 2019, 11(3), 363; https://doi.org/10.3390/cancers11030363
Received: 26 January 2019 / Revised: 1 March 2019 / Accepted: 6 March 2019 / Published: 13 March 2019
PDF Full-text (5086 KB) | HTML Full-text | XML Full-text
Abstract
Breast cancer is the most frequent cause of cancer-related deaths among women worldwide. It is classified into four major molecular subtypes. Triple-negative breast cancers (TNBCs), a subgroup of breast cancer, are defined by the absence of estrogen and progesterone receptors and the lack [...] Read more.
Breast cancer is the most frequent cause of cancer-related deaths among women worldwide. It is classified into four major molecular subtypes. Triple-negative breast cancers (TNBCs), a subgroup of breast cancer, are defined by the absence of estrogen and progesterone receptors and the lack of HER-2 expression; this subgroup accounts for ~15% of all breast cancers and exhibits the most aggressive metastatic behavior. Currently, very limited targeted therapies exist for the treatment of patients with TNBCs. On the other hand, it is important to highlight that knowledge of the molecular biology of breast cancer has recently changed the decision-making process regarding the course of cancer therapies. Thus, a number of new techniques, such as gene profiling and sequencing, proteomics, and microRNA analysis have been used to explore human breast carcinogenesis and metastasis including TNBC, which consequently could lead to new therapies. Nevertheless, based on evidence thus far, genomics profiles (gene and miRNA) can differ from one geographic location to another as well as in different ethnic groups. This review provides a comprehensive and updated information on the genomics profile alterations associated with TNBC pathogenesis associated with different ethnic backgrounds. Full article
(This article belongs to the Special Issue Cancer Invasion and Metastasis)
Figures

Figure 1

Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top