Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.0
4.5
Journals
Cancers
Special Issues
Cancer Stem Cells and Tumor Microenvironment
share announcement

Cancer Stem Cells and Tumor Microenvironment

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

Deadline for manuscript submissions: closed (15 November 2015) | Viewed by 39995

Special Issue Editor

Dr. Vita Golubovskaya

E-Mail Website
Guest Editor
1. Research and Business Development, Promab Biotechnologies, 2600 Hilltop Drive, Richmond, CA 94806, USA
2. Department of Medicine, University of Oklahoma, Oklahoma City, OK 73126, USA
Interests: Immunotherapy; CAR-T cells; tumor microenvironment; checkpoint protein; hypoxia; tumor survival signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues

Cancer stem cells or tumor initiating cells overexpress specific intra- and extra-cellular markers that result in their tumorigenic and high metastatic activity. In addition, the unique intracellular signaling and metabolism of cancer stem cells drive aggressive behavior of these cells. Cancer stem cells cross talk with microenvironment components: immune cells, blood vessels, fibroblasts, extracellular matrix proteins), which is important to understand for future development of anti-cancer therapeutics. The genomics, proteomics, and metabolomics technology should be applied to the characterization of these cells and microenvironment to develop personalized medicine approaches.

Dr. Vita Golubovskaya
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 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 semimonthly 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 2900 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

  • cancer stem cells;
  • microenvironment;
  • extracellular matrix;
  • immune cells;
  • blood vessels;
  • metabolism;
  • signaling

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

1373 KiB  
Article
The Effect of Stromal Integrin β3-Deficiency on Two Different Tumors in Mice
by Inga Reigstad, Kristina Sortland, Trude Skogstrand, Rolf K. Reed and Linda Stuhr
Cancers 2016, 8(1), 14; https://doi.org/10.3390/cancers8010014 - 12 Jan 2016
Cited by 4 | Viewed by 5305
Abstract
There is an increasing focus on the tumor microenvironment in carcinogenesis. Integrins are important receptors and adhesion molecules in this environment and have been shown to be involved in cell adhesion, proliferation, differentiation and migration. The present study aimed to evaluate the effect [...] Read more.
There is an increasing focus on the tumor microenvironment in carcinogenesis. Integrins are important receptors and adhesion molecules in this environment and have been shown to be involved in cell adhesion, proliferation, differentiation and migration. The present study aimed to evaluate the effect of stromal integrin β3-deficiency on tumor growth, angiogenesis, interstitial fluid pressure (PIF), fibrosis and metastasis in a murine breast cancer (4T1) and a prostate tumor (RM11) model. We showed that stromal integrin β3-deficiency led to an elevation in PIF that correlated to a shift towards thicker collagen fibrils in the 4T1 mammary tumor. In the RM11 prostate carcinoma model there was no effect of integrin β3-deficiency on PIF and collagen fibril thickness. These findings support the notion that changes in the collagen scaffold influence PIF, and also indicate that there must be important crosstalk between the stroma and tumor cells, in a tumor cell line specific manner. Furthermore, stromal integrin β3-deficiency had no effect on tumor growth or angiogenesis in both tumor models and no effect on lung metastasis in the 4T1 mammary tumor model. In conclusion, the stromal β3 integrin influence PIF, possibly via its effect on the structure of the collagen network, in a tumor cell line dependent manner. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Tumor Microenvironment)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

181 KiB  
Review
Melanoma Cancer Stem Cells: Markers and Functions
by Giorgio Parmiani
Cancers 2016, 8(3), 34; https://doi.org/10.3390/cancers8030034 - 11 Mar 2016
Cited by 43 | Viewed by 10249
Abstract
The discovery of cancer stem cells (CSCs) in human solid tumors has allowed a better understanding of the biology and neoplastic transformation of normal melanocytes, and the possible mechanisms by which melanoma cells acquire tumorigenicity. In this review I summarize the literature findings [...] Read more.
The discovery of cancer stem cells (CSCs) in human solid tumors has allowed a better understanding of the biology and neoplastic transformation of normal melanocytes, and the possible mechanisms by which melanoma cells acquire tumorigenicity. In this review I summarize the literature findings on the potential biomarkers of melanoma CSCs, their presence in the melanoma cell populations, the interaction with the immune system (with both T and NK cells) and the role of melanoma CSCs in the clinics. Given the extraordinary progress in the therapy of melanoma caused by immune checkpoint antibodies blockade, I discuss how these antibodies can work by the activation of melanoma infiltrating T cells specifically recognizing neo-antigens expressed even by melanoma CSCs. This is the mechanism that can induce a regression of the metastatic melanomas. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Tumor Microenvironment)
601 KiB  
Review
Cancer Stem Cells and Their Interaction with the Tumor Microenvironment in Neuroblastoma
by Evan F. Garner and Elizabeth A. Beierle
Cancers 2016, 8(1), 5; https://doi.org/10.3390/cancers8010005 - 31 Dec 2015
Cited by 38 | Viewed by 13385
Abstract
Neuroblastoma, a solid tumor arising from neural crest cells, accounts for over 15% of all pediatric cancer deaths. The interaction of neuroblastoma cancer-initiating cells with their microenvironment likely plays an integral role in the maintenance of resistant disease and tumor relapse. In this [...] Read more.
Neuroblastoma, a solid tumor arising from neural crest cells, accounts for over 15% of all pediatric cancer deaths. The interaction of neuroblastoma cancer-initiating cells with their microenvironment likely plays an integral role in the maintenance of resistant disease and tumor relapse. In this review, we discuss the interaction between neuroblastoma cancer-initiating cells and the elements of the tumor microenvironment and how these interactions may provide novel therapeutic targets for this difficult to treat disease. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Tumor Microenvironment)
►▼ Show Figures

Figure 1

670 KiB  
Review
Prostate Cancer Stem-like Cells Contribute to the Development of Castration-Resistant Prostate Cancer
by Diane Ojo, Xiaozeng Lin, Nicholas Wong, Yan Gu and Damu Tang
Cancers 2015, 7(4), 2290-2308; https://doi.org/10.3390/cancers7040890 - 18 Nov 2015
Cited by 55 | Viewed by 5827
Abstract
Androgen deprivation therapy (ADT) has been the standard care for patients with advanced prostate cancer (PC) since the 1940s. Although ADT shows clear benefits for many patients, castration-resistant prostate cancer (CRPC) inevitably occurs. In fact, with the two recent FDA-approved second-generation anti-androgens abiraterone [...] Read more.
Androgen deprivation therapy (ADT) has been the standard care for patients with advanced prostate cancer (PC) since the 1940s. Although ADT shows clear benefits for many patients, castration-resistant prostate cancer (CRPC) inevitably occurs. In fact, with the two recent FDA-approved second-generation anti-androgens abiraterone and enzalutamide, resistance develops rapidly in patients with CRPC, despite their initial effectiveness. The lack of effective therapeutic solutions towards CRPC largely reflects our limited understanding of the underlying mechanisms responsible for CRPC development. While persistent androgen receptor (AR) signaling under castration levels of serum testosterone (<50 ng/mL) contributes to resistance to ADT, it is also clear that CRPC evolves via complex mechanisms. Nevertheless, the physiological impact of individual mechanisms and whether these mechanisms function in a cohesive manner in promoting CRPC are elusive. In spite of these uncertainties, emerging evidence supports a critical role of prostate cancer stem-like cells (PCSLCs) in stimulating CRPC evolution and resistance to abiraterone and enzalutamide. In this review, we will discuss the recent evidence supporting the involvement of PCSLC in CRPC acquisition as well as the pathways and factors contributing to PCSLC expansion in response to ADT. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Tumor Microenvironment)
►▼ Show Figures

Figure 1

Other

Jump to: Research, Review

1265 KiB  
Commentary
The Microenvironment in Gliomas: Phenotypic Expressions
by Davide Schiffer, Laura Annovazzi, Marta Mazzucco and Marta Mellai
Cancers 2015, 7(4), 2352-2359; https://doi.org/10.3390/cancers7040896 - 3 Dec 2015
Cited by 17 | Viewed by 4337
Abstract
The microenvironment of malignant gliomas is described according to its definition in the literature. Beside tumor cells, a series of stromal cells (microglia/macrophages, pericytes, fibroblasts, endothelial cells, normal and reactive astrocytes) represents the cell component, whereas a complex network of molecular signaling represents [...] Read more.
The microenvironment of malignant gliomas is described according to its definition in the literature. Beside tumor cells, a series of stromal cells (microglia/macrophages, pericytes, fibroblasts, endothelial cells, normal and reactive astrocytes) represents the cell component, whereas a complex network of molecular signaling represents the functional component. Its most evident expressions are perivascular and perinecrotic niches that are believed to be the site of tumor stem cells or progenitors in the tumor. Phenotypically, both niches are not easily recognizable; here, they are described together with a critical revision of their concept. As for perinecrotic niches, an alternative interpretation is given about their origin that regards the tumor stem cells as the residue of those that populated hyperproliferating areas in which necroses develop. This is based on the concept that the stem-like is a status and not a cell type, depending on the microenvironment that regulates a conversion of tumor non-stem cells and tumor stem cells through a cell reprogramming. Full article
(This article belongs to the Special Issue Cancer Stem Cells and Tumor Microenvironment)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop