23-01-2012. Horizon Discovery (Horizon), a leading provider of research tools to support the development of personalized medicines, has announced the appointment of Eric Rhodes as Chief Technical Officer, Gene Targeting.Eric has over twenty years’ experience in technology development and senior executive roles, most notably as Vice President of Business Development at Sangamo Biosciences (NASDAQ:SGMO) between 1998 and 2008 and most recently as Business Development Director for Sigma-Aldrich Corp (NASDAQ:SIAL). At Horizon, Eric will be the Company’s primary expert in human and mammalian gene targeting methods, with significant input into R&D and marketing for rAAV-mediated genome editing technology. He will also play a key role in supporting sites participating in Horizon’s Centers of Excellence Program.

Dr Darrin Disley, CEO of Horizon, commented: “Eric has a proven track record of delivery in the biotech industry, backed by a broad knowledge of the gene-editing field, and so brings added perspective to our technology, IP and commercial strategies. I’m delighted to welcome him to Horizon, and look forward to seeing him make an impact within an innovative, dynamic and entrepreneurial environment.”

Plasmid-based homologous recombination techniques have been used primarily to create transgenic mice from embryonic stems cells (an approach that received the Nobel Prize in 2007 for Mario R. Capecchi, Sir Martin J. Evans and Oliver Smithies). However, in these cell-types, recombination frequencies are naturally very high to support DNA repair during cell-division; whereas in non-dividing or differentiated somatic cell types, this process is essentially shut off. This has been a serious restriction in creating genetically defined human disease models; where one cannot utilise the natural process of homologous recombination to precisely and permanently alter any target endogenous gene in the human genome, without eliciting unwanted off-target genetic changes or integration-site errors.

Source: Horizon Discovery / Zyme Communications
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January 13, 2011. The mucosal lining of the intestine is renewed every two to five days. In this process, stem cells in the intestine replace cells of the gut epithelium which have been lost due to injury or normal wear and tear by new cells. Scientists of the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) and Heidelberg University have now discovered, jointly with colleagues of the Fred Hutchinson Cancer Research Center in Seattle, that the cellular EGFR signaling pathway plays an important role in this process: It stimulates stem cells to divide so that their daughter cells replace the damaged intestinal epithelium. This signaling pathway may also be involved in the onset of human intestinal cancer.

“For the intestinal epithelium to be able to renew itself dynamically, the stem cells of the intestine need to respond to the needs of the intestinal tissue,” says Professor Bruce Edgar, who has a bridging professorship within the alliance of DKFZ and the Center for Molecular Biology (ZMBH) of Heidelberg University. “They may divide and produce new intestinal cells only to the extent in which cells of the intestinal epithelium are dying. But how the stem cells are activated has been largely unknown so far.” The investigators have used the fruit fly Drosophila for their experiments. This insect regularly renews its intestinal epithelium with the aid of stem cells, just like man. The researchers used genetic methods to induce death of cells of the intestinal lining or fed the toxic bacterium Pseudomonas entomophila to the animals. In this way, they specifically induced self-renewal of the intestinal epithelium. The gut lining cells under attack produced an increased amount of mediator substances which activate the epidermal growth factor receptor, or EGFR for short. There was a parallel increase in the activity of the cellular EGFR signaling pathway in the intestinal stem cells. Further experiments showed that the EGFR signaling pathway activates the stem cells using the mediators Ras, RAF und MAPK. These molecules cause the stem cells to divide and to renew the damaged intestine. “Our results show that the EGFR/Ras/MAPK signaling pathway plays a key role in the renewal and regeneration of the intestine,” summarizes Bruce Edgar. However, this signaling pathway may also be involved in intestinal cancer. “There is mounting evidence suggesting that the signaling pathway is also activated when intestinal polyps arise,” Edgar added. Such polyps tend to turn into malignant intestinal cancer. “In intestinal cancer cells, the two signaling molecules Ras and BRAF, which are also part of the EGFR signaling pathway, are often hyperactive. However, the exact function of the EGFR signaling pathway in the onset of cancer is not yet understood,” emphasized Edgar. But there already are drugs, so-called antibodies, which are directed against EGFR and which are used, with good results, for treating intestinal cancer.

In a next step, the investigators are now planning to uncover how the EGFR signaling pathway is switched on in stem cells, in order to understand exactly what it is that causes stem cells to replace lost tissue. Biologist and cancer researcher Bruce Edgar has recently been awarded a European Research Council Advanced Grant of 2.6 million euros for his work.

Press Release DKFZ

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