Special Issue "Tumor Cell Genesis and Its Microenvironment: Chicken or the Egg"

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

Deadline for manuscript submissions: closed (30 September 2011)

Special Issue Editors

Guest Editor
Dr. Constantine S. Mitsiades

450 Brookline Ave, Room HIM346, Harvard Institutes of Medicine Building, Boston, MA 02115, USA
Website | E-Mail
Fax: +1 617 812 7701
Interests: hematologic malignancies; novel therapeutics; signal transduction inhibitors; tumor microenvironment; bone metastases; clinical trial design; prognostic markers; multiple myeloma; plasma cell dyscrasias; insulin-like growth factor; IGF1R; heat shock protein; proteasome; histone deacetylase; kinase
Guest Editor
Prof. Dr. Margareta Mueller

Head, Molecular Cell Biology Laboratory, Hochschule Furtwangen University, Campus Villingen-Schwenningen, Jakob Kienzle Str 17, 78054 Villingen-Schwenningen, Germany
E-Mail
Fax: +49 7720 307 4207
Interests: tumor stroma interaction; angiogenesis; inflammation and cancer; growth factors and cytokines; proteases; IL-6 signalling

Published Papers (4 papers)

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Research

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Open AccessArticle Tumor-Promoting Circuits That Regulate a Cancer-Related Chemokine Cluster: Dominance of Inflammatory Mediators Over Oncogenic Alterations
Cancers 2012, 4(1), 55-76; doi:10.3390/cancers4010055
Received: 2 November 2011 / Revised: 13 January 2012 / Accepted: 17 January 2012 / Published: 20 January 2012
Cited by 3 | PDF Full-text (526 KB) | HTML Full-text | XML Full-text
Abstract
Here, we investigated the relative contribution of genetic/signaling components versus microenvironmental factors to the malignancy phenotype. In this system, we took advantage of non-transformed fibroblasts that carried defined oncogenic modifications in Ras and/or p53. These cells were exposed to microenvironmental pressures, and the
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Here, we investigated the relative contribution of genetic/signaling components versus microenvironmental factors to the malignancy phenotype. In this system, we took advantage of non-transformed fibroblasts that carried defined oncogenic modifications in Ras and/or p53. These cells were exposed to microenvironmental pressures, and the expression of a cancer-related chemokine cluster was used as readout for the malignancy potential (CCL2, CCL5, CXCL8, CXCL10). In cells kept in-culture, synergism between Ras hyper-activation and p53 dysfunction was required to up-regulate the expression of the chemokine cluster. The in vivo passage of RasHigh/p53Low-modified cells has led to tumor formation, accompanied by potentiation of chemokine release, implicating a powerful role for the tumor microenvironment in up-regulating the chemokine cluster. Indeed, we found that inflammatory mediators which are prevalent in tumor sites, such as TNFa and IL-1β, had a predominant impact on the release of the chemokines, which was substantially higher than that obtained by the oncogenic modifications alone, possibly acting through the transcription factors AP-1 and NF-kB. Together, our results propose that in the unbiased model system that we were using, inflammatory mediators of the tumor milieu have dominating roles over oncogenic modifications in dictating the expression of a pro-malignancy chemokine readout. Full article
(This article belongs to the Special Issue Tumor Cell Genesis and Its Microenvironment: Chicken or the Egg)
Open AccessArticle Tertiary Intratumor Lymphoid Tissue in Colo-Rectal Cancer
Cancers 2012, 4(1), 1-10; doi:10.3390/cancers4010001
Received: 11 October 2011 / Revised: 15 November 2011 / Accepted: 21 December 2011 / Published: 28 December 2011
Cited by 16 | PDF Full-text (634 KB) | HTML Full-text | XML Full-text
Abstract
Ectopic (or tertiary) lymphoid tissue develops at sites of inflammation or infection in non lymphoid organs and is associated with chronic inflammation. In colon mucosa, small lymphoid aggregates are already present in homeostatic conditions, as part of the gut-associated lymphoid tissue and play
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Ectopic (or tertiary) lymphoid tissue develops at sites of inflammation or infection in non lymphoid organs and is associated with chronic inflammation. In colon mucosa, small lymphoid aggregates are already present in homeostatic conditions, as part of the gut-associated lymphoid tissue and play an essential role in the immune response to perturbations of the mucosal microenvironment. Despite the recognized role of inflammation in tumor progression, the presence and biological function of lymphoid tissue in cancer has been poorly investigated. We identified aggregates of lymphocytes resembling tertiary lymphoid tissue in human colorectal cancer specimens; intratumor accumulations of lymphocytes display a high degree of compartmentalization, with B and T cells, mature dendritic cells and a network of CD21+ follicular dendritic cells (FDC). We analyzed the adaptation of colon lymphoid tissue in a murine model of colitis-associated cancer (AOM/DSS). B cell follicle formation increases in the context of the chronic inflammation associated to intestinal neoplasia, in this model. A network of lymphatic and haematic vessels surrounding B cell follicles is present and includes high endothelial venules (HEV). Future task is to determine whether lymphoid tissue contributes to the persistence of the tumor-associated inflammatory reaction, rather than represent a functional immune compartment, potentially participating to the anti tumor response. Full article
(This article belongs to the Special Issue Tumor Cell Genesis and Its Microenvironment: Chicken or the Egg)

Review

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Open AccessReview Tumor Microenvironment in the Brain
Cancers 2012, 4(1), 218-243; doi:10.3390/cancers4010218
Received: 9 December 2011 / Revised: 29 January 2012 / Accepted: 16 February 2012 / Published: 22 February 2012
Cited by 18 | PDF Full-text (885 KB) | HTML Full-text | XML Full-text
Abstract
In addition to malignant cancer cells, tumors contain a variety of different stromal cells that constitute the tumor microenvironment. Some of these cell types provide crucial support for tumor growth, while others have been suggested to actually inhibit tumor progression. The composition of
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In addition to malignant cancer cells, tumors contain a variety of different stromal cells that constitute the tumor microenvironment. Some of these cell types provide crucial support for tumor growth, while others have been suggested to actually inhibit tumor progression. The composition of tumor microenvironment varies depending on the tumor site. The brain in particular consists of numerous specialized cell types such as microglia, astrocytes, and brain endothelial cells. In addition to these brain-resident cells, primary and metastatic brain tumors have also been shown to be infiltrated by different populations of bone marrow-derived cells. The role of different cell types that constitute tumor microenvironment in the progression of brain malignancies is only poorly understood. Tumor microenvironment has been shown to be a promising therapeutic target and diagnostic marker in extracranial malignancies. A better understanding of tumor microenvironment in the brain would therefore be expected to contribute to the development of improved therapies for brain tumors that are urgently required due to a poor availability of treatments for these malignancies. This review summarizes some of the known interactions between brain tumors and different stromal cells, and also discusses potential therapeutic approaches within this context. Full article
(This article belongs to the Special Issue Tumor Cell Genesis and Its Microenvironment: Chicken or the Egg)
Open AccessReview Actin—Towards a Deeper Understanding of the Relationship Between Tissue Context, Cellular Function and Tumorigenesis
Cancers 2011, 3(4), 4269-4280; doi:10.3390/cancers3044269
Received: 17 October 2011 / Revised: 26 November 2011 / Accepted: 7 December 2011 / Published: 14 December 2011
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Abstract
It is well-established that the actin cytoskeleton plays an important role in tumor development yet the contribution made by nuclear actin is ill-defined. In a recent study, nuclear actin was identified as a key mediator through which laminin type III (LN1) acts to
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It is well-established that the actin cytoskeleton plays an important role in tumor development yet the contribution made by nuclear actin is ill-defined. In a recent study, nuclear actin was identified as a key mediator through which laminin type III (LN1) acts to control epithelial cell growth. In the breast, epithelial tumors are surrounded by an environment which lacks LN1. These findings point to actin as a potential mediator of tumor development. Here our current understanding of the roles of cytoplasmic and nuclear actin in normal and tumor cell growth is reviewed, relating these functions to cell phenotype in a tissue context. Full article
(This article belongs to the Special Issue Tumor Cell Genesis and Its Microenvironment: Chicken or the Egg)

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