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

Guest Editor
Dr. Constantine S. Mitsiades
Department of Medical Oncology, Dana-Farber Cancer Institute; and Department of Medicine, Harvard Medical School, 44 Binney Street, Mayer Building, Room M555, Boston, MA 02115, USA
Website: http://www.dfhcc.harvard.edu/membership/profile/member/485/0/
E-Mail: constantine_mitsiades@dfci.harvard.edu
Phone: +1 617 632 1962
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: muem@hs-furtwangen.de
Phone: +49 7720 307 4231
Fax: +49 7720 307 4207
Interests: tumor stroma interaction; angiogenesis; inflammation and cancer; growth factors and cytokines; proteases; IL-6 signalling

Submission

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Type of Paper: Review
Title: Tumor Microenvironment in the Brain
Author: Mihaela Lorger
Affiliation: Leeds Institute of Molecular Medicine, University of Leeds, UK; E-Mail: M.Lorger@leeds.ac.uk (M.L.)
Abstract: Growth and behavior of tumour cells is driven by intrinsic factors, for example aberrantly activated signaling pathways, as well as by extrinsic factors originating from the microenvironment of tumour cells. Tumour microenvironment is very complex: it consists of blood vessels that supply tumour cells with nutrients and oxygen, organ-specific stromal cells, infiltrating cells like macrophages and other bone marrow-derived cells, as well as extracellular matrix deposited by cancer and non-cancer cells. Notably, the tumour microenvironment differs significantly between different organs and increasing body of literature demonstrates that these differences are reflected in the growth and behavior of cancer cells. In this review we will summarize what is known about the tumour microenvironment and its cross-talk with tumour cells specifically in the brain. We will describe evidence for the brain-specific behavior of tumour cells and also discuss potential approaches for the therapeutic targeting of tumour microenvironment in the brain.

Type of Paper: Review
Title: Towards a Deeper Understanding of the Relationship Between Tissue Context, Cellular Function and Tumorigenesis
Author: Virginia A. Spencer
Affiliation: Cell Culture Essentials, Life Technologies, Frederick, MD, USA; E-Mail: Virginia.Spencer@lifetech.com
Abstract: Breast epithelial tumors appear to abide by a unique set of rules when it comes to growing in vivo. They are also surrounded by an environment which lacks laminin type III, an extracellular matrix protein that restricts the growth of ductal epithelial cells in the mammary gland. In a recent study, nuclear actin was identified as a key mediator through which LN1 acts to control epithelial cell growth. These findings combined with the inherent differences between the normal and diseased breast tissue environment point to cytoskeletal proteins as potential mediators of tumor development. With a particular emphasis on nuclear actin and the breast epithelial cell model, here I will review our current understanding of the roles of nuclear cytoskeletal proteins in normal and tumor cell function, relating these functions to cell phenotype in a tissue context.