Special Issue "Cancer Stem Cells and Tumor Microenvironment"

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

Deadline for manuscript submissions: closed (15 November 2015)

Special Issue Editor

Guest Editor
Dr. Vita Golubovskaya

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
Website | E-Mail
Interests: Immunotherapy; CAR-T cells; tumor microenvironment; checkpoint protein; hypoxia; tumor survival signaling

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 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

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

Published Papers (5 papers)

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Research

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Open AccessArticle The Effect of Stromal Integrin β3-Deficiency on Two Different Tumors in Mice
Received: 19 August 2015 / Revised: 17 December 2015 / Accepted: 5 January 2016 / Published: 12 January 2016
Cited by 2 | PDF Full-text (1373 KB) | HTML Full-text | XML Full-text
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)
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Review

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Open AccessReview Melanoma Cancer Stem Cells: Markers and Functions
Received: 22 January 2016 / Revised: 2 March 2016 / Accepted: 4 March 2016 / Published: 11 March 2016
Cited by 9 | PDF Full-text (181 KB) | HTML Full-text | XML Full-text
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)
Open AccessFeature PaperReview Cancer Stem Cells and Their Interaction with the Tumor Microenvironment in Neuroblastoma
Received: 21 November 2015 / Revised: 16 December 2015 / Accepted: 21 December 2015 / Published: 31 December 2015
Cited by 9 | PDF Full-text (601 KB) | HTML Full-text | XML Full-text
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)
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Open AccessReview Prostate Cancer Stem-like Cells Contribute to the Development of Castration-Resistant Prostate Cancer
Cancers 2015, 7(4), 2290-2308; https://doi.org/10.3390/cancers7040890
Received: 9 July 2015 / Revised: 30 October 2015 / Accepted: 4 November 2015 / Published: 18 November 2015
Cited by 12 | PDF Full-text (670 KB) | HTML Full-text | XML Full-text
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)
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Other

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Open AccessCommentary The Microenvironment in Gliomas: Phenotypic Expressions
Cancers 2015, 7(4), 2352-2359; https://doi.org/10.3390/cancers7040896
Received: 20 October 2015 / Revised: 25 November 2015 / Accepted: 27 November 2015 / Published: 3 December 2015
Cited by 6 | PDF Full-text (1265 KB) | HTML Full-text | XML Full-text
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)
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