{"228451":{"#nid":"228451","#data":{"type":"news","title":"New Evidence that Cancer Cells Change While Moving throughout Body","body":[{"value":"\u003Cp\u003EFor the majority of cancer patients, it\u2019s not the primary tumor that is deadly, but the spread or \u201cmetastasis\u201d of cancer cells from the primary tumor to secondary locations throughout the body that is the problem. That\u2019s why a major focus of contemporary cancer research is how to stop or fight metastasis.\u003C\/p\u003E\u003Cp\u003EPrevious lab studies suggest that metastasizing cancer cells undergo a major molecular change when they leave the primary tumor \u2013 a process called epithelial-to-mesenchymal transition (EMT). As the cells travel from one site to another, they pick up new characteristics. More importantly, they develop a resistance to chemotherapy that is effective on the primary tumor. But confirmation of the EMT process has only taken place in test tubes or in animals.\u003C\/p\u003E\u003Cp\u003EIn a new study, \u003Ca href=\u0022http:\/\/www.ovarianresearch.com\/content\/6\/1\/49\/abstract\u0022\u003Epublished\u003C\/a\u003E in the Journal of Ovarian Research, Georgia Tech scientists have direct evidence that EMT takes place in humans, at least in ovarian cancer patients. The findings suggest that doctors should treat patients with a combination of drugs: those that kill cancer cells in primary tumors and drugs that target the unique characteristics of cancer cells spreading through the body.\u003C\/p\u003E\u003Cp\u003EThe researchers looked at matching ovarian and abdominal cancerous tissues in seven patients. Pathologically, the cells looked exactly the same, implying that they simply fell off the primary tumor and spread to the secondary site with no changes. But on the molecular level, the cells were very different. Those in the metastatic site displayed genetic signatures consistent with EMT. The scientists didn\u2019t see the process take place, but they know it happened.\u003C\/p\u003E\u003Cp\u003E\u201cIt\u2019s like noticing that a piece of cake has gone missing from your kitchen and you turn to see your daughter with chocolate on her face,\u201d said John McDonald, director of Georgia Tech\u2019s Integrated Cancer Research Center and lead investigator on the project. \u201cYou didn\u2019t see her eat the cake, but the evidence is overwhelming. The gene expression patterns of the metastatic cancers displayed gene expression profiles that unambiguously identified them as having gone through EMT.\u201d\u003C\/p\u003E\u003Cp\u003EThe EMT process is an essential component of embryonic development and allows for reduced cell adhesiveness and increased cell movement.\u003C\/p\u003E\u003Cp\u003EAccording to Benedict Benigno, collaborating physician on the paper, CEO of the Ovarian Cancer Institute and director of gynecological oncology at Atlanta\u2019s Northside Hospital, \u201cThese results clearly indicate that metastasizing ovarian cancer cells are very different from those comprising the primary tumor and will likely require new types of chemotherapy if we are going to improve the outcome of these patients.\u201d\u003C\/p\u003E\u003Cp\u003EOvarian cancer is the most malignant of all gynecological cancers and responsible for more than 14,000 deaths annually in the United States alone. It often reveals no early symptoms and isn\u2019t typically diagnosed until after it spreads.\u003C\/p\u003E\u003Cp\u003E\u201cOur team is hopeful that, because of the new findings, the substantial body of knowledge that has already been acquired on how to block EMT and reduce metastasis in experimental models may now begin to be applied to humans,\u201d said Georgia Tech graduate student Loukia Lili, co-author of the study.\u003C\/p\u003E\u003Cp\u003E\u0026nbsp;\u003C\/p\u003E\u003Cp\u003E\u0026nbsp;\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":"","field_summary_sentence":[{"value":"Ovarian cancer research indicates that cells undergo genetic changes while spreading."}],"uid":"27560","created_gmt":"2013-08-12 12:24:49","changed_gmt":"2016-10-08 03:14:42","author":"Jason Maderer","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2013-08-12T00:00:00-04:00","iso_date":"2013-08-12T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"99761":{"id":"99761","type":"image","title":"John McDonald, co-director of the Ovarian Cancer I","body":null,"created":"1449178150","gmt_created":"2015-12-03 21:29:10","changed":"1475894715","gmt_changed":"2016-10-08 02:45:15","alt":"John McDonald, co-director of the Ovarian Cancer I","file":{"fid":"193959","name":"tcp55643.jpg","image_path":"\/sites\/default\/files\/images\/tcp55643_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/tcp55643_0.jpg","mime":"image\/jpeg","size":39191,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/tcp55643_0.jpg?itok=YEtwWbGK"}}},"media_ids":["99761"],"related_links":[{"url":"http:\/\/www.ovarianresearch.com\/content\/6\/1\/49\/abstract","title":"Journal Article"},{"url":"http:\/\/www.cos.gatech.edu\/","title":"College of Sciences"},{"url":"http:\/\/www.biology.gatech.edu\/","title":"School of Biology"}],"groups":[{"id":"1183","name":"Home"}],"categories":[{"id":"140","name":"Cancer Research"},{"id":"135","name":"Research"}],"keywords":[{"id":"2371","name":"John McDonald"},{"id":"2372","name":"ovarian cancer"}],"core_research_areas":[{"id":"39441","name":"Bioengineering and Bioscience"}],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EJason Maderer\u003Cbr \/\u003EMedia Relations\u003Cbr \/\u003E\u003Ca href=\u0022mailto:maderer@gatech.edu\u0022\u003Emaderer@gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-385-2966\u003C\/p\u003E","format":"limited_html"}],"email":["maderer@gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"167921":{"#nid":"167921","#data":{"type":"news","title":"Blood Testing Predicts Level of Enzymes that Facilitate Disease Progression","body":[{"value":"\u003Cp\u003EPredicting how atherosclerosis, osteoporosis or cancer will progress or respond to drugs in individual patients is difficult. In a new study, researchers took another step toward that goal by developing a technique able to predict from a blood sample the amount of cathepsins\u2014protein-degrading enzymes known to accelerate these diseases\u2014a specific person would produce.\u003C\/p\u003E\u003Cp\u003EThis patient-specific information may be helpful in developing personalized approaches to treat these tissue-destructive diseases.\u003C\/p\u003E\u003Cp\u003E\u201cWe measured significant variability in the amount of cathepsins produced by blood samples we collected from healthy individuals, which may indicate that a one-size-fits-all approach of administering cathepsin inhibitors may not be the best strategy for all patients with these conditions,\u201d said Manu Platt, an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.\u003C\/p\u003E\u003Cp\u003EThe study was published online on Oct. 19, 2012 in the journal \u003Cem\u003EIntegrative Biology\u003C\/em\u003E. This work was supported by the National Institutes of Health, Georgia Cancer Coalition, Atlanta Clinical and Translational Science Institute, and the Emory\/Georgia Tech Regenerative Engineering and Medicine Center.\u003C\/p\u003E\u003Cp\u003EPlatt and graduate student Keon-Young Park collected blood samples from 14 healthy individuals, removed white blood cells called monocytes from the samples and stimulated those cells with certain molecules so that they would become macrophages or osteoclasts in the laboratory. By doing this, the researchers recreated what happens in the body\u2014monocytes receive these cues from damaged tissue, leave the blood, and become macrophages or osteoclasts, which are known to contribute to tissue changes that occur in atherosclerosis, cancer and osteoporosis.\u003C\/p\u003E\u003Cp\u003EThen the researchers developed a model that used patient-varying kinase signals collected from the macrophages or osteoclasts to predict patient-specific activity of four cathepsins: K, L, S and V. \u0026nbsp;\u003C\/p\u003E\u003Cp\u003E\u201cKinases are enzymes that integrate stimuli from different soluble, cellular and physical cues to generate specific cellular responses,\u201d explained Platt, who is also a Georgia Cancer Coalition Distinguished Cancer Scholar. \u201cBy using a systems biology approach to link cell differentiation cues and responses through integration of signals at the kinase level, we were able to mathematically predict relative amounts of cathepsin activity and distinguish which blood donors exhibited greater cathepsin activity compared to others.\u201d\u003C\/p\u003E\u003Cp\u003EPredictability for all cathepsins ranged from 90 to 95 percent for both macrophages and osteoclasts, despite a range in the level of each cathepsin among the blood samples tested.\u003C\/p\u003E\u003Cp\u003E\u201cWe were pleased with the results because our model achieved very high predictability from a simple blood draw and overcame the challenge of incorporating the complex, unknown cues from individual patients\u2019 unique genetic and biochemical backgrounds,\u201d said Platt.\u003C\/p\u003E\u003Cp\u003EAccording to Platt, the next step will be to assess the model\u2019s ability to predict cathepsin activity using blood samples from individuals with the diseases of interest: atherosclerosis, osteoporosis or cancer.\u003C\/p\u003E\u003Cp\u003E\u201cOur ultimate goal is to create an assay that will inform a clinician whether an individual\u2019s case of cancer or other tissue-destructive disease will be very aggressive from the moment that individual is diagnosed, which will enable the clinician to develop and begin the best personalized treatment plan immediately,\u201d added Platt.\u003C\/p\u003E\u003Cp\u003EWeiwei A. Li, who received her bachelor\u2019s degree from the Coulter Department in 2010, also contributed to this study.\u003C\/p\u003E\u003Cp\u003E\u003Cem\u003EResearch reported in this publication was supported in part by the National Center for Advancing Translational Sciences of the National Institutes of Health (NIH) under award number UL1TR000454 and the Office of the Director of the NIH under award number 1DP2OD007433. The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NIH.\u003C\/em\u003E\u003C\/p\u003E\u003Cp\u003E\u003Cstrong\u003ECITATION\u003C\/strong\u003E: Park, Keon-Young et al., \u201cPatient specific proteolytic activity of monocyte-derived macrophages and osteoclasts predicted with temporal kinase activation states during differentiation,\u201d Integrative Biology (2012): \u003Ca href=\u0022http:\/\/dx.doi.org\/10.1039\/C2IB20197F\u0022 title=\u0022http:\/\/dx.doi.org\/10.1039\/C2IB20197F\u0022\u003Ehttp:\/\/dx.doi.org\/10.1039\/C2IB20197F\u003C\/a\u003E.\u003Cbr \/\u003E\u003Cbr \/\u003E\u003Cstrong\u003EResearch News \u0026amp; Publications Office\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003EGeorgia Institute of Technology\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003E177 North Avenue\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003EAtlanta, Georgia\u0026nbsp; USA\u0026nbsp; 30332-0177\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cbr \/\u003E\u003Cstrong\u003EMedia Relations Contact\u003C\/strong\u003E: John Toon (404-894-6986)(\u003Ca href=\u0022mailto:jtoon@gatech.edu\u0022\u003Ejtoon@gatech.edu\u003C\/a\u003E).\u003Cbr \/\u003E\u003Cstrong\u003EWriter\u003C\/strong\u003E: Abby Robinson\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"\u003Cp\u003EResearchers are developing a technique for predicting from a simple blood sample the amount of cathepsins\u2014protein-degrading enzymes known to accelerate certain diseases\u2014a specific person would produce. This patient-specific information may be helpful in developing personalized approaches to treat these tissue-destructive diseases.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"Researchers are developing a technique for predicting the amount of protein-degrading enzymes a specific person would produce."}],"uid":"27303","created_gmt":"2012-11-01 14:12:05","changed_gmt":"2016-10-08 03:13:06","author":"John Toon","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2012-11-01T00:00:00-04:00","iso_date":"2012-11-01T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"167891":{"id":"167891","type":"image","title":"Cathepsin prediction","body":null,"created":"1449178968","gmt_created":"2015-12-03 21:42:48","changed":"1475894806","gmt_changed":"2016-10-08 02:46:46","alt":"Cathepsin prediction","file":{"fid":"195633","name":"cathepsin-prediction41.jpg","image_path":"\/sites\/default\/files\/images\/cathepsin-prediction41_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/cathepsin-prediction41_0.jpg","mime":"image\/jpeg","size":1287075,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/cathepsin-prediction41_0.jpg?itok=8Dh7au-_"}},"167901":{"id":"167901","type":"image","title":"Cathepsin prediction2","body":null,"created":"1449178968","gmt_created":"2015-12-03 21:42:48","changed":"1475894806","gmt_changed":"2016-10-08 02:46:46","alt":"Cathepsin prediction2","file":{"fid":"195634","name":"cathepsin-prediction96.jpg","image_path":"\/sites\/default\/files\/images\/cathepsin-prediction96_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/cathepsin-prediction96_0.jpg","mime":"image\/jpeg","size":1113462,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/cathepsin-prediction96_0.jpg?itok=P0KeURw0"}}},"media_ids":["167891","167901"],"groups":[{"id":"1188","name":"Research Horizons"}],"categories":[{"id":"135","name":"Research"}],"keywords":[{"id":"7270","name":"atherosclerosis"},{"id":"385","name":"cancer"},{"id":"40431","name":"cathepsin"},{"id":"11533","name":"Department of Biomedical Engineering"},{"id":"7735","name":"enzyme"},{"id":"48841","name":"kinase"},{"id":"10832","name":"Manu Platt"},{"id":"48851","name":"osteopororis"}],"core_research_areas":[{"id":"39441","name":"Bioengineering and Bioscience"}],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EJohn Toon\u003C\/p\u003E\u003Cp\u003EResearch News \u0026amp; Publications Office\u003C\/p\u003E\u003Cp\u003E(404) 894-6986\u003C\/p\u003E\u003Cp\u003E\u003Ca href=\u0022mailto:jtoon@gatech.edu\u0022\u003Ejtoon@gatech.edu\u003C\/a\u003E\u003C\/p\u003E","format":"limited_html"}],"email":["jtoon@gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"159261":{"#nid":"159261","#data":{"type":"news","title":"Squeezing Ovarian Cancer Cells to Predict Metastatic Potential","body":[{"value":"\u003Cp\u003ENew Georgia Tech research shows that cell stiffness could be a valuable clue for doctors as they search for and treat cancerous cells before they\u2019re able to spread. The findings, which are \u003Ca href=\u0022http:\/\/dx.plos.org\/10.1371\/journal.pone.0046609\u0022\u003Epublished\u003C\/a\u003E in the journal PLoS One, found that highly metastatic ovarian cancer cells are several times softer than less metastatic ovarian cancer cells.\u003C\/p\u003E\u003Cp\u003EAssistant Professor Todd Sulchek and Ph.D. student Wenwei Xu used a process called atomic force microscopy (AFM) to study the mechanical properties of various ovarian cell lines. A soft mechanical probe \u201ctapped\u201d healthy, malignant and metastatic ovarian cells to measure their stiffness.\u003C\/p\u003E\u003Cp\u003E\u201cIn order to spread, metastatic cells must push themselves into the bloodstream. As a result, they must be highly deformable and softer,\u201d said Sulchek, a faculty member in the George W. Woodruff School of Mechanical Engineering. \u201cOur results indicate that cell stiffness may be a useful biomarker to evaluate the relative metastatic potential of ovarian and perhaps other types of cancer cells.\u201d\u003C\/p\u003E\u003Cp\u003EJust as previous studies on other types of epithelial cancers have indicated, Sulchek also found that cancerous ovarian cells are generally softer and display lower intrinsic variability in cell stiffnesss than non-malignant cells.\u003C\/p\u003E\u003Cp\u003ESulchek\u2019s lab partnered with the molecular cancer lab of Biology Professor John McDonald, who is also director of Georgia Tech\u2019s newly established Integrated Cancer Research Center.\u003C\/p\u003E\u003Cp\u003E\u201cThis is a good example of the kinds of discoveries that only come about by integrating skills and knowledge from traditionally diverse fields such as molecular biology and bioengineering,\u201d said McDonald. \u201cAlthough there are a number of developing methodologies to identify circulating cancer cells in the blood and other body fluids, this technology offers the added potential to rapidly determine if these cells are highly metastatic or relatively benign.\u201d\u003C\/p\u003E\u003Cp\u003ESulchek and McDonald believe that, when further developed, this technology could offer a huge advantage to clinicians in the design of optimal chemotherapies, not only for ovarian cancer patients but also for patients of other types of cancer.\u003C\/p\u003E\u003Cp\u003E\u003Cem\u003EThis project was supported in part by the National Science Foundation (NSF) (Award Number CBET-0932510). The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NSF. \u003C\/em\u003E\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":[{"value":"New Research Lists Cell Stiffness as Possible Biomarker"}],"field_summary":[{"value":"\u003Cp\u003ENew Georgia Tech research shows that cell stiffness could be a valuable clue for doctors as they search for and treat cancerous cells before they\u2019re able to spread. The findings, which are published in the journal PLoS One, found that highly metastatic ovarian cancer cells are several times softer than less metastatic ovarian cancer cells.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"New Georgia Tech research shows that cell stiffness could be a valuable clue for doctors as they search for and treat cancerous cells before they\u2019re able to spread."}],"uid":"27560","created_gmt":"2012-10-04 10:55:06","changed_gmt":"2016-10-08 03:12:54","author":"Jason Maderer","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2012-10-05T00:00:00-04:00","iso_date":"2012-10-05T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"159221":{"id":"159221","type":"image","title":"Squeezing Cancer Cells 1","body":null,"created":"1449178896","gmt_created":"2015-12-03 21:41:36","changed":"1475894794","gmt_changed":"2016-10-08 02:46:34","alt":"Squeezing Cancer Cells 1","file":{"fid":"195382","name":"13p1000-p5-007.jpg","image_path":"\/sites\/default\/files\/images\/13p1000-p5-007_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/13p1000-p5-007_0.jpg","mime":"image\/jpeg","size":1867947,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/13p1000-p5-007_0.jpg?itok=d_bhPgTO"}},"159211":{"id":"159211","type":"image","title":"Squeezing Cancer Cells 2","body":null,"created":"1449178896","gmt_created":"2015-12-03 21:41:36","changed":"1475894794","gmt_changed":"2016-10-08 02:46:34","alt":"Squeezing Cancer Cells 2","file":{"fid":"195381","name":"heya8_m23_0000.jpg","image_path":"\/sites\/default\/files\/images\/heya8_m23_0000_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/heya8_m23_0000_0.jpg","mime":"image\/jpeg","size":61778,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/heya8_m23_0000_0.jpg?itok=0Wocm7NQ"}},"159231":{"id":"159231","type":"image","title":"Todd Sulchek and John McDonald","body":null,"created":"1449178896","gmt_created":"2015-12-03 21:41:36","changed":"1475894794","gmt_changed":"2016-10-08 02:46:34","alt":"Todd Sulchek and John McDonald","file":{"fid":"195383","name":"13p1000-p5-004.jpg","image_path":"\/sites\/default\/files\/images\/13p1000-p5-004_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/13p1000-p5-004_0.jpg","mime":"image\/jpeg","size":2089143,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/13p1000-p5-004_0.jpg?itok=m770Dcms"}},"159251":{"id":"159251","type":"image","title":"Todd Sulchek","body":null,"created":"1449178896","gmt_created":"2015-12-03 21:41:36","changed":"1475894794","gmt_changed":"2016-10-08 02:46:34","alt":"Todd Sulchek","file":{"fid":"195384","name":"13p1000-p5-006.jpg","image_path":"\/sites\/default\/files\/images\/13p1000-p5-006_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/13p1000-p5-006_0.jpg","mime":"image\/jpeg","size":2264455,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/13p1000-p5-006_0.jpg?itok=qZKma9NL"}}},"media_ids":["159221","159211","159231","159251"],"groups":[{"id":"1183","name":"Home"}],"categories":[{"id":"135","name":"Research"}],"keywords":[],"core_research_areas":[{"id":"39441","name":"Bioengineering and Bioscience"}],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EJason Maderer\u003Cbr \/\u003EMedia Relations\u003Cbr \/\u003E\u003Ca href=\u0022mailto:maderer@gatech.edu\u0022\u003Emaderer@gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-385-2966\u003C\/p\u003E","format":"limited_html"}],"email":["maderer@gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"146041":{"#nid":"146041","#data":{"type":"news","title":"Cathepsin Cannibalism: Enzymes Attack One Another Instead of Harming Proteins","body":[{"value":"\u003Cp\u003EResearchers for the first time have shown that members of a family of enzymes known as cathepsins \u2013 which are implicated in many disease processes \u2013 may attack one another instead of the bodily proteins they normally degrade. Dubbed \u201ccathepsin cannibalism,\u201d the phenomenon may help explain problems with drugs that have been developed to inhibit the effects of these powerful proteases.\u003C\/p\u003E\u003Cp\u003ECathepsins are involved in disease processes as varied as cancer metastasis, atherosclerosis, cardiovascular disease, osteoporosis and arthritis. Because cathepsins have harmful effects on critical proteins such as collagen and elastin, pharmaceutical companies have been developing drugs to inhibit activity of the enzymes, but so far these compounds have had too many side effects to be useful and have failed clinical trials.\u003C\/p\u003E\u003Cp\u003EUsing a combination of modeling and experiments, researchers from the Georgia Institute of Technology and Emory University have shown that one type of cathepsin preferentially attacks another, reducing the enzyme\u2019s degradation of collagen. The work could affect not only the development of drugs to inhibit cathepsin activity, but could also lead to a better understanding of how the enzymes work together.\u003C\/p\u003E\u003Cp\u003E\u201cThese findings provide a new way of thinking about how these proteases are working with and against each other to remodel tissue \u2013 or fight against each other,\u201d said Manu Platt, an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. \u201cThere has been an assumption that these cathepsins have been inert in relationship to one another, when in actuality they have been attacking one another. We think this may have broader implications for other classes of proteases.\u201d\u003C\/p\u003E\u003Cp\u003EThe research was supported by the National Institutes of Health, the National Science Foundation and the Georgia Cancer Coalition. Details of the study were reported August 10 in the \u003Cem\u003EJournal of Biological Chemistry.\u003C\/em\u003E\u003C\/p\u003E\u003Cp\u003EPlatt and student Zachary Barry made their discovery accidentally while investigating the effects of cathepsin K and cathepsin S \u2013 two of the 11-member cathepsin family. Cathepsin K degrades both collagen and elastin, and is one of the most powerful proteases. Cathepsin S degrades elastin, and does not strongly attack collagen.\u003C\/p\u003E\u003Cp\u003EWhen the researchers combined the two cathepsins and allowed them to attack samples of elastin, they expected to see increased degradation of the protein. What they saw, however, was not much more damage than cathepsin K did by itself.\u003C\/p\u003E\u003Cp\u003EPlatt at first believed the experiment was flawed, and asked Barry \u2013 an undergraduate student in his lab who specializes in modeling \u2013 to examine what possible conditions could account for the experimental result. Barry\u2019s modeling suggested that effects observed could occur if cathepsin S were degrading cathepsin K instead of attacking the elastin \u2013 a protein essential in arteries and the cardiovascular system.\u003C\/p\u003E\u003Cp\u003EThat theoretical result led to additional experiments in which the researchers measured a direct correlation between an increase in the amount of cathepsin S added to the experiment and a reduction in the degradation of collagen. By increasing the amount of cathepsin S ten-fold over the amount used in the original experiment, Platt and Barry were able to completely block the activity of cathepsin K, preventing damage to the collagen sample.\u003C\/p\u003E\u003Cp\u003E\u201cWe saw that the cathepsin K was going away much faster when there was cathepsin S present than when it was by itself,\u201d said Platt, who is also a Georgia Cancer Coalition Distinguished Scholar and a Fellow of the Keystone Symposia on Molecular and Cellular Biology. \u201cWe kept increasing the amount of cathepsin S until the collagen was not affected at all because all of the cathepsin K was eaten by the cathepsin S.\u201d\u003C\/p\u003E\u003Cp\u003EThe researchers used a variety of tests to determine the amount of each enzyme, including fluorogenic substrate analysis, Western blotting and multiplex cathepsin zymography \u2013 a sensitive technique developed in the Platt laboratory.\u003C\/p\u003E\u003Cp\u003EBeyond demonstrating for the first time that cathepsins can attack one another, the research also shows the complexity of the body\u2019s enzyme system \u2013 and may suggest why drugs designed to inhibit cathepsins haven\u2019t worked as intended.\u003C\/p\u003E\u003Cp\u003E\u201cThe effect of the cathepsins on one another complicates the system,\u201d said Platt. \u201cIf you are targeting this system pharmaceutically, you may not have the types or quantities of cathepsins that you expect, which could cause off-target binding and side effects that were not anticipated.\u201d\u003C\/p\u003E\u003Cp\u003EPlatt\u2019s long-term research has focused on cathepsins, including the development of sensitive tools and assays to quantify their activity in cells and tissue, as well as potential diagnostic applications for breast, lung and cervical cancer. Cathepsins normally operate within cells to carry out housekeeping tasks such as breaking down proteins that are no longer needed.\u003C\/p\u003E\u003Cp\u003E\u201cThese enzymes are very powerful, but they have been overlooked because they are difficult to study,\u201d said Platt. \u201cWe are changing the way that people view them.\u201d\u003C\/p\u003E\u003Cp\u003EFor the future, Platt plans to study interactions of additional cathepsins \u2013 as many as three or four are released during certain disease processes \u2013 and to develop a comprehensive model of how these proteases interact while they degrade collagen and elastin. That model could be useful to the designers of future drugs.\u003C\/p\u003E\u003Cp\u003E\u201cAs we build toward a comprehensive model of how these enzymes work, we can begin to understand how they behave in the extracellular matrix around these cells,\u201d said Platt. \u201cThat will help us be smarter about how we go about treating diseases and designing new drugs.\u201d\u003C\/p\u003E\u003Cp\u003E\u003Cem\u003EThe project described was supported by Award Number DP2OD007433 from the Office of the Director, National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Office of the Director, National Institutes of Health, or the National lnstitutes of Health. This material is also based on work supported by the National Science Foundation under the Science and Technology Center Emergent Behaviors of Integrated Cellular systems (EBICS) Grant No. CBET-0939511.\u003C\/em\u003E\u003Cbr \/\u003E\u003Cbr \/\u003E\u003Cstrong\u003EResearch News \u0026amp; Publications Office\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003EGeorgia Institute of Technology\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003E75 Fifth Street, N.W, Suite 309\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cstrong\u003EAtlanta, Georgia\u0026nbsp; 30308\u0026nbsp; USA\u003C\/strong\u003E\u003Cbr \/\u003E\u003Cbr \/\u003E\u003Cstrong\u003EMedia Relations Assistance\u003C\/strong\u003E: John Toon (404-894-6986)(\u003Ca href=\u0022mailto:jtoon@gatech.edu\u0022\u003Ejtoon@gatech.edu\u003C\/a\u003E).\u003C\/p\u003E\u003Cp\u003E\u003Cstrong\u003EWriter\u003C\/strong\u003E: John Toon\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"\u003Cp\u003EResearchers for the first time have shown that members of a family of enzymes known as cathepsins \u2013 which are implicated in many disease processes \u2013 may attack one another instead of the proteins they normally degrade. Dubbed \u201ccathepsin cannibalism,\u201d the phenomenon may help explain problems with drugs that have been developed to inhibit the effects of these powerful proteases.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"Researchers for the first time have shown that enzymes that normally degrade proteins may attack each other instead."}],"uid":"27303","created_gmt":"2012-08-13 12:45:14","changed_gmt":"2016-10-08 03:12:40","author":"John Toon","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2012-08-13T00:00:00-04:00","iso_date":"2012-08-13T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"68625":{"id":"68625","type":"image","title":"Manu Platt, PhD - Assistant Professor, Department of Biomedical Engineering","body":null,"created":"1449177185","gmt_created":"2015-12-03 21:13:05","changed":"1475894597","gmt_changed":"2016-10-08 02:43:17","alt":"Manu Platt, PhD - Assistant Professor, Department of Biomedical Engineering","file":{"fid":"192620","name":"platt_2010.jpg","image_path":"\/sites\/default\/files\/images\/platt_2010_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/platt_2010_0.jpg","mime":"image\/jpeg","size":1277779,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/platt_2010_0.jpg?itok=EC2Vbd9_"}},"146021":{"id":"146021","type":"image","title":"Manu Platt - Cathepsin Cannibalism","body":null,"created":"1449178751","gmt_created":"2015-12-03 21:39:11","changed":"1475894779","gmt_changed":"2016-10-08 02:46:19","alt":"Manu Platt - Cathepsin Cannibalism","file":{"fid":"195075","name":"manu-platt.jpg","image_path":"\/sites\/default\/files\/images\/manu-platt_1.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/manu-platt_1.jpg","mime":"image\/jpeg","size":1025829,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/manu-platt_1.jpg?itok=xgN8-nrO"}}},"media_ids":["68625","146021"],"groups":[{"id":"1214","name":"News Room"}],"categories":[{"id":"140","name":"Cancer Research"},{"id":"146","name":"Life Sciences and Biology"}],"keywords":[{"id":"40431","name":"cathepsin"},{"id":"12515","name":"College of Engineering; Wallace H. Coulter Department of Biomedical Engineering; Emory; Children\u0027s Healthcare of Atlanta; pediatric nanomedicine;  Gang Bao"},{"id":"7735","name":"enzyme"},{"id":"40451","name":"inhibitor"},{"id":"10832","name":"Manu Platt"},{"id":"40441","name":"protease"}],"core_research_areas":[{"id":"39441","name":"Bioengineering and Bioscience"}],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EJohn Toon\u003C\/p\u003E\u003Cp\u003EResearch News \u0026amp; Publications Office\u003C\/p\u003E\u003Cp\u003E(404) 894-6986\u003C\/p\u003E\u003Cp\u003E\u003Ca href=\u0022mailto:jtoon@gatech.edu\u0022\u003Ejtoon@gatech.edu\u003C\/a\u003E\u003C\/p\u003E","format":"limited_html"}],"email":["jtoon@gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"120171":{"#nid":"120171","#data":{"type":"news","title":"Novel Compound Halts Tumor Spread, Improves Brain Cancer Treatment in Animal Studies","body":[{"value":"\u003Cp\u003ETreating invasive brain tumors with a combination of chemotherapy and radiation has improved clinical outcomes, but few patients survive longer than two years after diagnosis. The effectiveness of the treatment is limited by the tumor\u2019s aggressive invasion of healthy brain tissue, which restricts chemotherapy access to the cancer cells and complicates surgical removal of the tumor.\u003C\/p\u003E\u003Cp\u003ETo address this challenge, researchers from the Georgia Institute of Technology and Emory University have designed a new treatment approach that appears to halt the spread of cancer cells into normal brain tissue in animal models. The researchers treated animals possessing an invasive tumor with a vesicle carrying a molecule called imipramine blue, followed by conventional doxorubicin chemotherapy. The tumors ceased their invasion of healthy tissue and the animals survived longer than animals treated with chemotherapy alone.\u003C\/p\u003E\u003Cp\u003E\u201cOur results show that imipramine blue stops tumor invasion into healthy tissue and enhances the efficacy of chemotherapy, which suggests that chemotherapy may be more effective when the target is stationary,\u201d said \u003Ca href=\u0022http:\/\/www.bme.gatech.edu\/facultystaff\/faculty_record.php?id=59\u0022 target=\u0022_blank\u0022\u003ERavi Bellamkonda\u003C\/a\u003E, a professor in the \u003Ca href=\u0022http:\/\/www.bme.gatech.edu\u0022 target=\u0022_blank\u0022\u003EWallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University\u003C\/a\u003E. \u201cThese results reveal a new strategy for treating brain cancer that could improve clinical outcomes.\u201d\u003C\/p\u003E\u003Cp\u003EThe results of this work were published on March 28, 2012 in the journal \u003Ca href=\u0022http:\/\/stm.sciencemag.org\/content\/4\/127\/127ra36\u0022 target=\u0022_blank\u0022\u003E\u003Cem\u003EScience Translational Medicine\u003C\/em\u003E\u003C\/a\u003E. The research was supported primarily by the Ian\u2019s Friends Foundation and partially by the Georgia Cancer Coalition, the Wallace H. Coulter Foundation and a National Science Foundation graduate research fellowship.\u003C\/p\u003E\u003Cp\u003EIn addition to Bellamkonda, collaborators on the project include Jack Arbiser, a professor in the Emory University Department of Dermatology; Daniel Brat, a professor in the Emory University Department of Pathology and Laboratory Medicine; and the paper\u2019s lead author, Jennifer Munson, a former Fulbright Scholar who was a bioengineering graduate student in the \u003Ca href=\u0022http:\/\/www.chbe.gatech.edu\u0022 target=\u0022_blank\u0022\u003EGeorgia Tech School of Chemical \u0026amp; Biomolecular Engineering\u003C\/a\u003E when the research was conducted.\u003C\/p\u003E\u003Cp\u003EArbiser designed the novel imipramine blue compound, which is an organic triphenylmethane dye. After \u003Cem\u003Ein vitro\u003C\/em\u003E experiments showed that imipramine blue effectively inhibited movement of several cancer cell lines, the researchers tested the compound in an animal model of aggressive cancer that exhibited attributes similar to a human brain tumor called glioblastoma.\u003C\/p\u003E\u003Cp\u003E\u201cThere were many reasons why we chose to use the RT2 astrocytoma rat model for these experiments,\u201d said Brat. \u201cThe tumor exhibited properties of aggressive growth, invasiveness, angiogenesis and necrosis that are similar to human glioblastoma; the model utilized an intact immune system, which is seen in the human disease; and the model enabled increased visualization by MRI because it was a rat model, rather than a mouse.\u201d\u003C\/p\u003E\u003Cp\u003EBecause imipramine blue is hydrophobic and doxorubicin is cytotoxic, the researchers encapsulated each compound in an artificially-prepared vesicle called a liposome so that the drugs would reach the brain. The liposomal drug delivery vehicle also ensured that the drugs would not be released into tissue until they passed through leaky blood vessel walls, which are only present where a tumor is growing.\u003C\/p\u003E\u003Cp\u003EAnimals received one of the following four treatments: liposomes filled with saline, liposomes filled with imipramine blue, liposomes filled with doxorubicin chemotherapy, or liposomes filled with imipramine blue followed by liposomes filled with doxorubicin chemotherapy.\u003C\/p\u003E\u003Cp\u003EAll of the animals that received the sequential treatment of imipramine blue followed by doxorubicin chemotherapy survived for 200 days -- more than 6 months -- with no observable tumor mass. Of the animals treated with doxorubicin chemotherapy alone, 33 percent were alive after 200 days with a median survival time of 44 days. Animals that received capsules filled with saline or imipramine blue \u2013 but no chemotherapy -- did not survive more than 19 days.\u003C\/p\u003E\u003Cp\u003E\u201cOur results show that the increased effectiveness of the chemotherapy treatment is not because of a synergistic toxicity between imipramine blue and doxorubicin. Imipramine blue is not making the doxorubicin more toxic, it\u2019s simply stopping the movement of the cancer cells and containing the cancer so that the chemotherapy can do a better job,\u201d explained Bellamkonda, who is also the Carol Ann and David D. Flanagan Chair in Biomedical Engineering and a Georgia Cancer Coalition Distinguished Cancer Scholar.\u003C\/p\u003E\u003Cp\u003EMRI results showed a reduction and compaction of the tumor in animals treated with imipramine blue followed by doxorubicin chemotherapy, while animals treated with chemotherapy alone presented with abnormal tissue and glioma cells. MRI also indicated that the blood-brain barrier breach often seen during tumor growth was present in the animals treated with chemotherapy alone, but not the group treated with chemotherapy and imipramine blue.\u003C\/p\u003E\u003Cp\u003EAccording to the researchers, imipramine blue appears to improve the outcome of brain cancer treatment by altering the regulation of actin, a protein found in all eukaryotic cells. Actin mediates a variety of essential biological functions, including the production of reactive oxygen species. Most cancer cells exhibit overproduction of reactive oxygen species, which are thought to stimulate cancer cells to invade healthy tissue. The dye\u2019s reorganization of the actin cytoskeleton is thought to inhibit production of enzymes that produce reactive oxygen species.\u003C\/p\u003E\u003Cp\u003E\u201cI formulated the imipramine blue compound as a triphenylmethane dye because I knew that another triphenylmethane dye, gentian violet, exhibited anti-cancer properties, and I decided to use imipramine -- a drug used to treat depression -- as the starting material because I knew it could get into the brain,\u201d said Arbiser.\u003C\/p\u003E\u003Cp\u003EFor future studies, the researchers are planning to test imipramine blue\u2019s effect on animal models with invasive brain tumors, metastatic tumors, and other types of cancer such as prostate and breast.\u003C\/p\u003E\u003Cp\u003E\u201cWhile we need to conduct future studies to determine if the effect of imipramine blue is the same for different types of cancer diagnosed at different stages, this initial study shows the possibility that imipramine blue may be useful as soon as any tumor is diagnosed, before anti-cancer treatment begins, to create a more treatable tumor and enhance clinical outcome,\u201d noted Bellamkonda.\u0026nbsp;\u003C\/p\u003E\u003Cp\u003E\u003Cstrong\u003EResearch News \u0026amp; Publications Office\u003Cbr \/\u003E Georgia Institute of Technology\u003Cbr \/\u003E 75 Fifth Street, N.W., Suite 314\u003Cbr \/\u003E Atlanta, Georgia 30308 USA\u003C\/strong\u003E\u003C\/p\u003E\u003Cp\u003E\u003Cstrong\u003EMedia Relations Contacts:\u003C\/strong\u003E Abby Robinson (abby@innovate.gatech.edu; 404-385-3364) or John Toon (jtoon@gatech.edu; 404-894-6986)\u003C\/p\u003E\u003Cp\u003E\u003Cstrong\u003EWriter: \u003C\/strong\u003EAbby Robinson\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"\u003Cp\u003EBy stopping the spread of cancer cells into normal brain tissue in animal models, researchers from Georgia Tech and Emory University have developed a new strategy for treating brain cancer that could improve clinical outcomes. The researchers treated animals possessing an invasive tumor with a novel molecule called imipramine blue, followed by conventional doxorubicin chemotherapy. The tumors ceased their invasion of healthy tissue and the animals survived longer than animals treated with chemotherapy alone.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"Researchers have designed a new treatment approach that appears to halt the spread of cancer cells into normal brain tissue in animal models."}],"uid":"27206","created_gmt":"2012-03-28 15:18:40","changed_gmt":"2016-10-08 03:11:56","author":"Abby Vogel Robinson","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2012-03-28T00:00:00-04:00","iso_date":"2012-03-28T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"120181":{"id":"120181","type":"image","title":"Imipramine blue","body":null,"created":"1449178268","gmt_created":"2015-12-03 21:31:08","changed":"1475894741","gmt_changed":"2016-10-08 02:45:41","alt":"Imipramine blue","file":{"fid":"194355","name":"imipramine_blue_hires.jpg","image_path":"\/sites\/default\/files\/images\/imipramine_blue_hires_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/imipramine_blue_hires_0.jpg","mime":"image\/jpeg","size":90121,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/imipramine_blue_hires_0.jpg?itok=x00IaSfV"}},"120191":{"id":"120191","type":"image","title":"Imipramine blue inhibits glioblastoma cells","body":null,"created":"1449178268","gmt_created":"2015-12-03 21:31:08","changed":"1475894741","gmt_changed":"2016-10-08 02:45:41","alt":"Imipramine blue inhibits glioblastoma cells","file":{"fid":"194356","name":"ib-effect-glioblastoma-cells-hires.jpg","image_path":"\/sites\/default\/files\/images\/ib-effect-glioblastoma-cells-hires_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/ib-effect-glioblastoma-cells-hires_0.jpg","mime":"image\/jpeg","size":226151,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/ib-effect-glioblastoma-cells-hires_0.jpg?itok=iL84lBXA"}},"120201":{"id":"120201","type":"image","title":"Imipramine blue tumor invasion","body":null,"created":"1449178268","gmt_created":"2015-12-03 21:31:08","changed":"1475894741","gmt_changed":"2016-10-08 02:45:41","alt":"Imipramine blue tumor invasion","file":{"fid":"194357","name":"ib-effect-tumor_invasion-hires.jpg","image_path":"\/sites\/default\/files\/images\/ib-effect-tumor_invasion-hires_0.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/ib-effect-tumor_invasion-hires_0.jpg","mime":"image\/jpeg","size":1511508,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/ib-effect-tumor_invasion-hires_0.jpg?itok=3k96CjPZ"}}},"media_ids":["120181","120191","120201"],"groups":[{"id":"1188","name":"Research Horizons"}],"categories":[{"id":"140","name":"Cancer Research"},{"id":"145","name":"Engineering"},{"id":"146","name":"Life Sciences and Biology"},{"id":"135","name":"Research"}],"keywords":[{"id":"28591","name":"Actin"},{"id":"28521","name":"Brain Cancer"},{"id":"10365","name":"Brain Tumor"},{"id":"8084","name":"Cancer treatment"},{"id":"1439","name":"chemotherapy"},{"id":"594","name":"college of engineering"},{"id":"11533","name":"Department of Biomedical Engineering"},{"id":"1445","name":"doxorubicin"},{"id":"28561","name":"Glioblastoma"},{"id":"28581","name":"Glioma"},{"id":"28571","name":"Liposome"},{"id":"2471","name":"Ravi Bellamkonda"},{"id":"28601","name":"triphenylmethane dye"},{"id":"1442","name":"tumor"}],"core_research_areas":[],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EAbby Robinson\u003Cbr \/\u003E Research News and Publications\u003Cbr \/\u003E \u003Ca href=\u0022mailto:abby@innovate.gatech.edu\u0022\u003Eabby@innovate.gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E 404-385-3364\u003C\/p\u003E","format":"limited_html"}],"email":[],"slides":[],"orientation":[],"userdata":""}},"108801":{"#nid":"108801","#data":{"type":"news","title":"Georgia Tech Develops Computational Algorithm to Assist in Cancer Treatments","body":[{"value":"\u003Cp\u003EHigh-throughput DNA sequencing technologies are leading to\na revolution in how clinicians diagnose and treat cancer. The molecular\nprofiles of individual tumors are beginning to be used in the design of\nchemotherapeutic programs optimized for the treatment of individual patients. The\nreal revolution, however, is coming with the emerging capability to\ninexpensively and accurately sequence the entire genome of cancers, allowing\nfor the identification of specific mutations responsible for the disease in\nindividual patients.\u003C\/p\u003E\n\n\u003Cp\u003EThere is only one downside. Those sequencing technologies\nprovide massive amounts of data that are not easily processed and translated by\nscientists. That\u2019s why Georgia Tech has created a new data analysis algorithm\nthat quickly transforms complex RNA sequence data into usable content for\nbiologists and clinicians. The RNA-Seq analysis pipeline (R-SAP) was developed\nby School of Biology Professor John McDonald and Ph.D. Bioinformatics candidate\nVinay Mittal. Details of the pipeline are published in the journal \u003Ca href=\u0022http:\/\/nar.oxfordjournals.org\/cgi\/reprint\/gks047?%20ijkey=Fd2USew6iX9nbaM\u0026amp;keytype=ref\u0022\u003ENucleic\nAcids Research\u003C\/a\u003E. \n\n\u003C\/p\u003E\u003Cp\u003E\u201cA major bottleneck in the realization of the dream of\npersonalized medicine is no longer technological. It\u2019s computational,\u201d said\nMcDonald, director of Georgia Tech\u2019s newly created Integrated Cancer Research\nCenter. \u201cR-SAP follows a hierarchical decision-making procedure to accurately characterize\nvarious classes of gene transcripts in cancer samples.\u201d \n\n\u003C\/p\u003E\u003Cp\u003EThere are at least 23,000 pieces of RNA in the human\ngenome that encode the sequence of proteins. Millions of other pieces help\nregulate the production of proteins. R-SAP is able to quickly determine every\ngene\u2019s level of RNA expression and provide information about splice variants,\nbiomarkers and chimeric RNAs. Biologists and clinicians will be able to more\nreadily use this data to compare the RNA profiles or \u201ctranscriptomes\u201d of normal\ncells with those of individual cancers and thereby be in a better position to\ndevelop optimized personal therapies. \n\n\u003C\/p\u003E\u003Cp\u003EPersonalized approaches to cancer medicine are already in\nwidespread use for a few \u201ccancer biomarkers\u201d including variants of the BRAC 1\ngene that can be used to identify women with a high risk of developing breast\nand ovarian cancer. \n\n\u003C\/p\u003E\u003Cp\u003E\u201cOur goal was to design a pipeline that is easily\ninstallable with parallel processing capabilities,\u201d said Mittal. \u201cR-SAP can\nmake 100 million reads in just 90 minutes. Running the program simultaneously\non multiple CPUs can further decrease that time.\u201d\n\n\u003C\/p\u003E\u003Cp\u003ER-SAP is open source software, freely accessible at the\nMcDonald Lab \u003Ca href=\u0022http:\/\/www.mcdonaldlab.biology.gatech.edu\/r-sap.htm\u0022\u003Ewebsite\u003C\/a\u003E.\n\n\n\u003C\/p\u003E\u003Cp\u003E\u201cThis is another example of Georgia Tech\u2019s ability to\nmerge computer technology with science to create an essential feature of\nnext-generation bioinformatics tools,\u201d said McDonald. \u201cWe hope that R-SAP will\nbe a useful and user-friendly instrument for scientists and clinicians in the\nfield of cancer biology.\u201d \n\n\u003C\/p\u003E\u003Cp\u003E\u0026nbsp;\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":[{"value":"New software key for personalized cancer medicine"}],"field_summary":[{"value":"\u003Cp\u003EGeorgia Tech has created a new data analysis algorithm that quickly \ntransforms complex RNA sequence data into usable content for biologists \nand clinicians. Scientists will be able to more readily use this data to\n compare the RNA profiles or \u201ctranscriptomes\u201d of normal cells with those\n of individual cancers and thereby be in a better position to develop \noptimized personal therapies.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"Georgia Tech has created a new data analysis algorithm that quickly transforms complex RNA sequence data into usable content for cancer biologists and clinicians."}],"uid":"27560","created_gmt":"2012-02-13 13:30:19","changed_gmt":"2016-10-08 03:11:40","author":"Jason Maderer","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2012-02-13T00:00:00-05:00","iso_date":"2012-02-13T00:00:00-05:00","tz":"America\/New_York"},"extras":[],"hg_media":{"101211":{"id":"101211","type":"image","title":"John McDonald","body":null,"created":"1449178159","gmt_created":"2015-12-03 21:29:19","changed":"1475894717","gmt_changed":"2016-10-08 02:45:17"}},"media_ids":["101211"],"related_links":[{"url":"http:\/\/www.cos.gatech.edu\/","title":"College of Sciences"},{"url":"http:\/\/www.biology.gatech.edu\/","title":"School of Biology"}],"groups":[{"id":"1183","name":"Home"}],"categories":[{"id":"140","name":"Cancer Research"}],"keywords":[{"id":"2546","name":"bioinformatics"},{"id":"4896","name":"College of Sciences"},{"id":"2371","name":"John McDonald"}],"core_research_areas":[],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003EJason Maderer\u003Cbr \/\u003EGeorgia Tech Media Relations\u003Cbr \/\u003E404-385-2966\u003Cbr \/\u003E\u003Ca href=\u0022mailto:maderer@gatech.edu\u0022\u003Emaderer@gatech.edu\u003C\/a\u003E\u003C\/p\u003E","format":"limited_html"}],"email":["maderer@gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"73311":{"#nid":"73311","#data":{"type":"news","title":"Study Identifies Mechanisms Cells Use to Remove Bits of RNA from DNA Strands","body":[{"value":"\u003Cp\u003EWhen RNA component units called ribonucleotides become embedded in genomic DNA, which contains the complete genetic data for an organism, they can cause problems for cells. It is known that ribonucleotides in DNA can potentially distort the DNA double helix, resulting in genomic instability and altered DNA metabolism, but not much is known about the fate of these ribonucleotides.\u003C\/p\u003E\n\u003Cp\u003EA new study provides a mechanistic explanation of how ribonucleotides embedded in genomic DNA are recognized and removed from cells. Two mechanisms, enzymes called ribonucleases (RNases) H and the DNA mismatch repair system, appear to interplay to root out the RNA components.\n\u003C\/p\u003E\n\u003Cp\u003E\u0022We believe this is the first study to show that cells utilize independent repair pathways to remove mispaired ribonucleotides embedded in chromosomal DNA, which can be sources of genetic modification if not removed,\u0022 said Francesca Storici, an assistant professor in the School of Biology at the Georgia Institute of Technology. \u0022The results also highlight a novel case of genetic redundancy, where the mismatch repair system and RNase H mechanisms compete with each other to remove misincorporated ribonucleotides and restore DNA integrity.\u0022\n\u003C\/p\u003E\n\u003Cp\u003EThe findings were reported Dec. 4, 2011 in the advance online publication of the journal \u003Cem\u003ENature Structural \u0026amp; Molecular Biology\u003C\/em\u003E. The research was supported by the Georgia Cancer Coalition, National Science Foundation and Georgia Tech Integrative BioSystems Institute.\n\u003C\/p\u003E\n\u003Cp\u003EStorici and Georgia Tech biology graduate students Ying Shen and Kyung Duk Koh conducted the study in collaboration with Bernard Weiss, a professor emeritus in the Department of Pathology and Laboratory Medicine at Emory University.\u003C\/p\u003E\n\u003Cp\u003E\u0022We wanted to understand how cells of the bacterium \u003Cem\u003EEscherichia coli\u003C\/em\u003E and the yeast \u003Cem\u003ESaccharomyces cerevisiae\u003C\/em\u003E tolerate the presence of different ribonucleotides embedded in their genomic DNA. We found that the structure of a ribonucleotide tract embedded in DNA influenced its ability to cause genetic mutations more than the tract\u0027s length,\u0022 said Storici.\n\u003C\/p\u003E\n\u003Cp\u003EWith double-stranded DNA, when wrong bases are paired or one or few nucleotides are in excess or missing on one of the strands, a mismatch is generated. If mismatches are not corrected, they can lead to mutations.\n\u003C\/p\u003E\n\u003Cp\u003EThe researchers found that single mismatched ribonucleotides in chromosomal DNA were removed by either the mismatch repair system or RNase H type 2. Mismatched ribonucleotides in the middle of at least four other ribonucleotides required RNase H type 1 for removal.\n\u003C\/p\u003E\n\u003Cp\u003E\u0022We were excited to find that a DNA repair mechanism like mismatch repair was activated by RNA\/DNA mismatches and could remove ribonucleotides embedded in chromosomal DNA,\u0022 explained Storici. \u0022In future studies, we plan to test whether other DNA repair mechanisms, such as nucleotide-excision repair and base-excision repair, can also locate and remove ribonucleotides in DNA.\u0022\n\u003C\/p\u003E\n\u003Cp\u003EUsing gene correction assays driven by short nucleic acid polymers called oligonucleotides, the researchers showed that when ribonucleotides embedded in DNA were not removed, they served as templates for DNA synthesis and produced a mutation in the DNA. If both the mismatch repair system and RNase H repair mechanisms are disabled, ribonucleotide-driven gene modification increased by a factor of 47 in the yeast and 77,000 in the bacterium. \n\u003C\/p\u003E\n\u003Cp\u003EDefects in the mismatch repair system are known to predispose a person to certain types of cancer. Because the mismatch repair system is conserved from unicellular to multicellular organisms, such as humans, this study\u0027s findings open up the possibility that defects in the mismatch repair system could have consequences more critical than previously thought given the newly identified function of mismatch repair to target RNA\/DNA mispairs. \n\u003C\/p\u003E\n\u003Cp\u003EThe results also provide new information on the capacity of RNA to play an active role in DNA editing and remodeling, which could be the basis of an unexplored process of RNA-driven DNA evolution. \n\u003C\/p\u003E\n\u003Cp\u003E\u003Cem\u003EThis project was supported by the National Science Foundation (NSF) (Award No. MCB-1021763). The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NSF.\u003C\/em\u003E\n\u003C\/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EResearch News \u0026amp; Publications Office\u003Cbr \/\u003E\nGeorgia Institute of Technology\u003Cbr \/\u003E\n75 Fifth Street, N.W., Suite 314\u003Cbr \/\u003E\nAtlanta, Georgia  30308  USA\u003C\/strong\u003E\n\u003C\/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMedia Relations Contacts:\u003C\/strong\u003E Abby Robinson (abby@innovate.gatech.edu; 404-385-3364) or John Toon (jtoon@gatech.edu; 404-894-6986)\n\u003C\/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWriter:\u003C\/strong\u003E Abby Robinson\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"\u003Cp\u003EWhen RNA ribonucleotides become embedded in genomic DNA, they can cause problems for cells, but not much is known about the fate of these ribonucleotides. A new study identifies two mechanisms cells use to recognize and remove ribonucleotides from DNA.\u003C\/p\u003E","format":"limited_html"}],"field_summary_sentence":[{"value":"Study identifies two mechanisms cells use to remove RNA from DNA."}],"uid":"27206","created_gmt":"2011-12-04 01:00:00","changed_gmt":"2016-10-08 03:10:42","author":"Abby Vogel Robinson","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2011-12-04T00:00:00-05:00","iso_date":"2011-12-04T00:00:00-05:00","tz":"America\/New_York"},"extras":[],"hg_media":{"73312":{"id":"73312","type":"image","title":"Ying Shen, Francesca Storici \u0026 Kyung Duk Koh","body":null,"created":"1449178002","gmt_created":"2015-12-03 21:26:42","changed":"1475894676","gmt_changed":"2016-10-08 02:44:36"},"73313":{"id":"73313","type":"image","title":"Ying Shen \u0026 Francesca Storici","body":null,"created":"1449178002","gmt_created":"2015-12-03 21:26:42","changed":"1475894676","gmt_changed":"2016-10-08 02:44:36"},"73314":{"id":"73314","type":"image","title":"Ying Shen, Francesca Storici \u0026 Kyung Duk Koh","body":null,"created":"1449178002","gmt_created":"2015-12-03 21:26:42","changed":"1475894676","gmt_changed":"2016-10-08 02:44:36"}},"media_ids":["73312","73313","73314"],"related_links":[{"url":"http:\/\/www.biology.gatech.edu\/","title":"School of Biology"},{"url":"http:\/\/www.biology.gatech.edu\/people\/index.php?id=francesca-storici","title":"Francesca Storici"}],"groups":[{"id":"1188","name":"Research Horizons"}],"categories":[{"id":"146","name":"Life Sciences and Biology"}],"keywords":[{"id":"4896","name":"College of Sciences"},{"id":"1041","name":"dna"},{"id":"13560","name":"Francesca Storici"},{"id":"15258","name":"oligonucleotides"},{"id":"15259","name":"ribonucleotides"},{"id":"984","name":"RNA"}],"core_research_areas":[],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003E\u003Cstrong\u003EAbby Robinson\u003C\/strong\u003E\u003Cbr \/\u003EResearch News and Publications\u003Cbr \/\u003E\u003Ca href=\u0022http:\/\/www.gatech.edu\/contact\/index.html?id=avogel6\u0022\u003EContact Abby Robinson\u003C\/a\u003E\u003Cbr \/\u003E\u003Cstrong\u003E404-385-3364\u003C\/strong\u003E\u003C\/p\u003E","format":"limited_html"}],"email":["abby@innovate.gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"52903":{"#nid":"52903","#data":{"type":"news","title":"Attacking Cancer Cells with Hydrogel Nanoparticles","body":[{"value":"\u003Cp\u003EOne of the difficulties of fighting cancer is that drugs\noften hit other non-cancerous cells, causing patients to get sick. But what if\nresearchers could sneak cancer-fighting particles into just the cancer cells?\nResearchers at the Georgia Institute of Technology and the Ovarian Cancer\nInstitute are working on doing just that. In the online journal \u003Cem\u003EBMC\u003C\/em\u003E \u003Cem\u003ECancer\n\u003C\/em\u003Ethey detail a method that uses hydrogels - less than 100 nanometers in size\n- to sneak a particular type of small interfering RNA(siRNA) into cancer cells.\nOnce in the cell the siRNA turns on the programmed cell death the body uses to\nkill mutated cells and help traditional chemotherapy do its job.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;Many cancers are characterized by an over abundance of\nepidermal growth factor receptors (EGFR). When the EGFR level in a cell is\nelevated it tells the cell to replicate at a rapid rate. It also turns down\napoptosis, or programmed cell death.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cWith our technique we\u2019re inhibiting EGFR\u2019s growth, with\nsmall interfering RNA. And by inhibiting it\u2019s growth, we\u2019re increasing the\ncells\u2019s apoptotic function. If we hit the cell with chemotherapy at the same time,\nwe should be able to kill the cancer cells more effectively,\u201d said John\nMcDonald, professor\nat the School of Biology at Georgia Tech and chief research scientist at the\nOvarian Cancer Institute.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;Small interfering RNA is good at shutting down EGFR\nproduction, but once inside the cell siRNA has a limited life span. Keeping it\nprotected inside the hydrogel nanoparticles allows them to get into the cancer\ncell safely and acts as a protective barrier around them. The hydrogel releases\nonly a small amount of siRNA at a time, ensuring that while some are out in the\ncancer cell doing their job, reinforcements are held safely inside the\nnanoparticle until it\u2019s time to do their job.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cIt\u2019s like a Trojan horse,\u201d said L. Andrew Lyon, professor\nin the School of Chemistry and Biochemistry at Georgia Tech. \u201cWe\u2019ve decorated\nthe surface of these hydrogels with a ligand that tricks the cancer cell into\ntaking it up. Once inside, the particles have a slow release profile that leaks\nout the siRNA over a timescale of days, allowing it to have a therapeutic\neffect.\u201d\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;Cells use the\nmessenger RNA (mRNA) to generate proteins, which help to keep the cell growing.\nOnce the siRNA enters the cell, it binds to the mRNA and recruits proteins that attack the siRNA-mRNA complex. But the\ncancer cell\u0027s not finished; it keeps generating proteins, so without a\ncontinuous supply of siRNA, the cell recovers. Using the hydrogel to slowly\nrelease the siRNA allows it to keep up a sustained attack so that it can continue to interrupt the\nproduction of proteins.\u0026nbsp;\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cWe\u2019ve shown that\nyou can get knock down out to a few days time frame, which could present a\nclinical window to come in and do multiple treatments in a combination\nchemotherapy approach,\u201d said Lyon.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cThe fact that this\nsystem is releasing the siRNA slowly, without giving the cell time to immediately\nrecover, gives us much better efficiency at killing the cancer cells with\nchemotherapy,\u201d added McDonald.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;Previous techniques\nhave involved using antibodies to knock down the proteins.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cBut oftentimes, a\nmutation may arise in the targeted gene such that the antibody will no longer\nhave the effect it once did, thereby increasing the chance for recurrence,\u201d\nsaid McDonald.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;The team used hydrogels because they\u2019re non-toxic, have a\nrelatively slow release rate, and can survive in the body long enough to reach\ntheir target.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;\u201cIt\u2019s a well-defined architecture that you\u2019re using the\nintrinsic porosity of that material to load things into, and since our\nparticles are about 98 percent water by volume, there\u2019s plenty of internal\nvolume in which to load things,\u201d said Lyon.\u003C\/p\u003E\n\n\u003Cp\u003E\u0026nbsp;Currently, the tests have been shown to work \u003Cem\u003Ein vitro\u003C\/em\u003E, but the team will be\ninitiating tests \u003Cem\u003Ein vivo\u003C\/em\u003E shortly.\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"Researchers at Georgia Tech are using hydrogels - less than 100 nanometers in size - to sneak a particular type of small interfering RNA into cancer cells. Once in the cell the siRNA turns on the programmed cell death the body uses to kill mutated cells and help traditional chemotherapy do its job.","format":"limited_html"}],"field_summary_sentence":[{"value":"Researchers at Georgia Tech are using hydrogel nanoparticles to kill cancer cells"}],"uid":"27310","created_gmt":"2010-02-15 09:54:14","changed_gmt":"2016-10-08 03:05:33","author":"David Terraso","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2010-02-15T00:00:00-05:00","iso_date":"2010-02-15T00:00:00-05:00","tz":"America\/New_York"},"extras":[],"hg_media":{"52904":{"id":"52904","type":"image","title":"Hydrogel Nanoparticles","body":null,"created":"1449175459","gmt_created":"2015-12-03 20:44:19","changed":"1475894476","gmt_changed":"2016-10-08 02:41:16","alt":"Hydrogel Nanoparticles","file":{"fid":"190171","name":"CSR_Lyon_scale.jpg","image_path":"\/sites\/default\/files\/images\/CSR_Lyon_scale.jpg","image_full_path":"http:\/\/www.tlwarc.hg.gatech.edu\/\/sites\/default\/files\/images\/CSR_Lyon_scale.jpg","mime":"image\/jpeg","size":575934,"path_740":"http:\/\/www.tlwarc.hg.gatech.edu\/sites\/default\/files\/styles\/740xx_scale\/public\/images\/CSR_Lyon_scale.jpg?itok=N68VGW4D"}}},"media_ids":["52904"],"groups":[{"id":"1183","name":"Home"}],"categories":[{"id":"140","name":"Cancer Research"},{"id":"141","name":"Chemistry and Chemical Engineering"},{"id":"146","name":"Life Sciences and Biology"},{"id":"149","name":"Nanotechnology and Nanoscience"}],"keywords":[{"id":"8462","name":"hydro"},{"id":"3356","name":"hydrogel"},{"id":"3355","name":"Lyon"},{"id":"281","name":"mcdonald"},{"id":"2286","name":"nano"},{"id":"2054","name":"nanoparticle"},{"id":"2973","name":"nanoparticles"}],"core_research_areas":[],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003E\u003Cstrong\u003EGeorgia Tech Media Relations\u003C\/strong\u003E\u003Cbr \/\u003ELaura Diamond\u003Cbr \/\u003E\u003Ca href=\u0022mailto:laura.diamond@comm.gatech.edu\u0022\u003Elaura.diamond@comm.gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-894-6016\u003Cbr \/\u003EJason Maderer\u003Cbr \/\u003E\u003Ca href=\u0022mailto:maderer@gatech.edu\u0022\u003Emaderer@gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-660-2926\u003C\/p\u003E","format":"limited_html"}],"email":["david.terraso@comm.gatech.edu"],"slides":[],"orientation":[],"userdata":""}},"71185":{"#nid":"71185","#data":{"type":"news","title":"Computer Predicts Anti-Cancer Molecules","body":[{"value":"\u003Cp\u003EA new computer-based method of analyzing cellular activity has correctly predicted the anti-tumour activity of several molecules. Research published today in BioMed Central\u0027s open access journal, Molecular Cancer, describes \u0027CoMet\u0027 - a tool that studies the integrated machinery of the cell and predicts those components that will have an effect on cancer.\n\u003C\/p\u003E\n\u003Cp\u003EJeffery Skolnick, professor in the School of Biology and director of the Center for the Study of Systems Biology, in collaboration with John McDonald, chair of the School of Biology, led a team from the Georgia Institute of Technology who have developed this new strategy. \n\u003C\/p\u003E\n\u003Cp\u003E\u0022This opens up the possibility of novel therapeutics for cancer and develops our understanding of why such metabolites work. CoMet provides a deeper understanding of the molecular mechanisms of cancer,\u0022 said Skolnick.\n\u003C\/p\u003E\n\u003Cp\u003EThe small molecules that are naturally produced in cells are called metabolites. Enzymes, the biological catalysts that produce and consume these metabolites, are created according to a cell\u0027s genetic blueprints. Importantly, however, the metabolites can also affect the expression of genes. \n\u003C\/p\u003E\n\u003Cp\u003E\u0022By comparing the gene expression levels of cancer cells relative to normal cells and converting that information into the enzymes that produce metabolites,\u0022 said Skolnick,  \u0022CoMet predicts metabolites that have lower concentrations in cancer relative to normal cells.\u0022\n\u003C\/p\u003E\n\u003Cp\u003EThe research proves that when such putatively depleted metabolites are added to cancer cells, they exhibit anticancer properties. In this case, growth of leukemia cells was slowed by all nine of the metabolites suggested by CoMet. \n\u003C\/p\u003E\n\u003Cp\u003EThe future for this treatment looks bright, added McDonald. \u0022While we have only performed cell proliferation assays, it is reasonable to speculate that some metabolites may also exhibit many other anticancer properties,\u0022 he said. \u0022These could be important steps on the road to a cure.\u0022\n\u003C\/p\u003E","summary":null,"format":"limited_html"}],"field_subtitle":"","field_summary":[{"value":"A new computer-based method of analyzing cellular activity has correctly predicted the anti-tumour activity of several molecules. Research published today in BioMed Central\u0027s open access journal, Molecular Cancer, describes \u0027CoMet\u0027 - a tool that studies the integrated machinery of the cell and predicts those components that will have an effect on cancer.","format":"limited_html"}],"field_summary_sentence":[{"value":"CoMet predicts which cell components have effect on cancer"}],"uid":"27310","created_gmt":"2008-06-17 00:00:00","changed_gmt":"2016-10-08 03:01:15","author":"David Terraso","boilerplate_text":"","field_publication":"","field_article_url":"","dateline":{"date":"2008-06-17T00:00:00-04:00","iso_date":"2008-06-17T00:00:00-04:00","tz":"America\/New_York"},"extras":[],"hg_media":{"71186":{"id":"71186","type":"image","title":"Tech Tower","body":null,"created":"1449177358","gmt_created":"2015-12-03 21:15:58","changed":"1475894630","gmt_changed":"2016-10-08 02:43:50"}},"media_ids":["71186"],"related_links":[{"url":"http:\/\/www.biology.gatech.edu\/","title":"School of Biology"},{"url":"http:\/\/cssb.biology.gatech.edu\/index.html","title":"Center for the Study of Systems Biology"}],"groups":[{"id":"1214","name":"News Room"}],"categories":[{"id":"140","name":"Cancer Research"},{"id":"146","name":"Life Sciences and Biology"},{"id":"135","name":"Research"}],"keywords":[{"id":"2070","name":"cancer cell"},{"id":"2069","name":"CoMet"},{"id":"281","name":"mcdonald"},{"id":"2071","name":"molecule"},{"id":"169252","name":"skolnick"}],"core_research_areas":[],"news_room_topics":[],"event_categories":[],"invited_audience":[],"affiliations":[],"classification":[],"areas_of_expertise":[],"news_and_recent_appearances":[],"phone":[],"contact":[{"value":"\u003Cp\u003E\u003Cstrong\u003EGeorgia Tech Media Relations\u003C\/strong\u003E\u003Cbr \/\u003ELaura Diamond\u003Cbr \/\u003E\u003Ca href=\u0022mailto:laura.diamond@comm.gatech.edu\u0022\u003Elaura.diamond@comm.gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-894-6016\u003Cbr \/\u003EJason Maderer\u003Cbr \/\u003E\u003Ca href=\u0022mailto:maderer@gatech.edu\u0022\u003Emaderer@gatech.edu\u003C\/a\u003E\u003Cbr \/\u003E404-660-2926\u003C\/p\u003E","format":"limited_html"}],"email":["david.terraso@comm.gatech.edu"],"slides":[],"orientation":[],"userdata":""}}}