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Lu Q.,Epigenetic Research Center | Renaudineau Y.,University of Western Brittany | Cha S.,University of Florida | Ilei G.,U.S. National Institutes of Health | And 8 more authors.
Autoimmunity Reviews | Year: 2010

During the 10th International Symposium on Sjögren's Syndrome held in Brest, France, from October 1-3, 2009 (http://www.sjogrensymposium-brest2009.org), the creation of an international epigenetic autoimmune group has been proposed to establish gold standards and to launch collaborative studies. During this "epigenetics session", leading experts in the field presented and discussed the most recent developments of this topic in Sjögren's Syndrome research. The "Brest epigenetic task force" was born and has scheduled a meeting in Ljubljana, Slovenia during the 7th Autoimmunity congress in May 2010.The following is a report of that session. © 2010 Elsevier B.V. Source

Golan A.,Yale University | Golan A.,Technion - Israel Institute of Technology | Pick E.,Yale University | Pick E.,Haifa University | And 5 more authors.
Cell Cycle | Year: 2010

Two major control systems regulate early stages of mitosis: activation of Cdk1 and anaphase control through assembly and disassembly of the mitotic spindle. In parallel to cell cycle progression, centrosomal duplication is regulated through proteins including Nek2. Recent studies suggest that centrosome-localized Chk1 forestalls premature activation of centrosomal Cdc25b and Cdk1 for mitotic entry, whereas Chk2 binds centrosomes and arrests mitosis only after activation by ATM and ATR in response to DNA damage. Here, we show that Chk2 centrosomal binding does not require DNA damage, but varies according to cell cycle progression. These and other data suggest a model in which binding of Chk2 to the centrosome at multiple cell cycle junctures controls co-localization of Chk2 with other cell cycle and centrosomal regulators. © 2010 Landes Bioscience. Source

Flach E.H.,Moffitt Research Institute | Rebecca V.W.,Moffitt Research Institute | Herlyn M.,Wistar Institute | Smalley K.S.M.,Moffitt Research Institute | Anderson A.R.A.,Moffitt Research Institute
Molecular Pharmaceutics | Year: 2011

Figure Persented: The role of tumor-stromal interactions in progression is generally well accepted, but their role in initiation or treatment is less well understood. It is now generally agreed that, rather than consisting solely of malignant cells, tumors consist of a complex dynamic mixture of cancer cells, host fibroblasts, endothelial cells and immune cells that interact with each other and microenvironmental factors to drive tumor progression. We are particularly interested in stromal cells (for example fibroblasts) and stromal factors (for example fibronectin) as important players in tumor progression since they have also been implicated in drug resistance. Here we develop an integrated approach to understand the role of such stromal cells and factors in the growth and maintenance of tumors as well as their potential impact on treatment resistance, specifically in application to melanoma. Using a suite of experimental assays we show that melanoma cells can stimulate the recruitment of fibroblasts and activate them, resulting in melanoma cell growth by providing both structural (extracellular matrix proteins) and chemical support (growth factors). Motivated by these experimental results we construct a compartment model and use it to investigate the roles of both stromal activation and tumor aggressiveness in melanoma growth and progression. We utilize this model to investigate the role fibroblasts might play in melanoma treatment resistance and the clinically observed flare phenomenon that is seen when a patient, who appears resistant to a targeted drug, is removed from that treatment. Our model makes the unexpected prediction that targeted therapies may actually hasten tumor progression once resistance has occurred. If confirmed experimentally, this provocative prediction may bring important new insights into how drug resistance could be managed clinically. © 2011 American Chemical Society. Source

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