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Human Longevity, Inc. Signs Collaborative Agreement with King’s College London to Access TwinsUK Registry

Human Longevity, Inc. (HLI), a biological data-driven human health technology and cell therapy company, recently announced a collaborative agreement with King’s College London to access their TwinsUK Registry.

New Research from SRI Points to Biomarker that Could Track Huntington’s Disease Progression

A hallmark of neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s is that by the time symptoms appear, significant brain damage has already occurred—and currently there are no treatments that can reverse it. A team of SRI International researchers has demonstrated that measurements of electrical activity in the brains of mouse models of Huntington’s disease could indicate the presence of disease before the onset of major symptoms. The findings, “Longitudinal Analysis of the Electroencephalogram and Sleep Phenotype in the R6/2 Mouse Model of Huntington’s Disease,” are published in the July 2013 issue of the neurology journal Brain, published by Oxford University Press.

SRI researchers led by Stephen Morairty, Ph.D., a director in the Center for Neuroscience in SRI Biosciences, and Simon Fisher, Ph.D., a postdoctoral fellow at SRI, used electroencephalography (EEG), a noninvasive method commonly used in humans, to measure changes in neuronal electrical activity in a mouse model of Huntington’s disease. Identification of significant changes in the EEG prior to the onset of symptoms would add to evidence that the EEG can be used to identify biomarkers to screen for the presence of a neurodegenerative disease. Further research on such potential biomarkers might one day enable the tracking of disease progression in clinical trials and could facilitate drug development.

“EEG signals are composed of different frequency bands such as delta, theta and gamma, much as light is composed of different frequencies that result in the colors we call red, green and blue,” explained Thomas Kilduff, Ph.D., senior director, Center for Neuroscience, SRI Biosciences. “Our research identified abnormalities in all three of these bands in Huntington’s disease mice. Importantly, the activity in the theta and gamma bands slowed as the disease progressed, indicating that we may be tracking the underlying disease process.”

EEG has shown promise as an indicator of underlying brain dysfunction in neurodegenerative diseases, which otherwise occurs surreptitiously until symptoms appear. Until now, most investigations of EEG in patients with neurodegenerative diseases and in animal models of neurodegenerative diseases have shown significant changes in EEG patterns only after disease symptoms occurred.

“Our breakthrough is that we have found an EEG signature that appears to be a biomarker for the presence of disease in this mouse model of Huntington’s disease that can identify early changes in the brain prior to the onset of behavioral symptoms,” said Morairty, the paper’s senior author. “While the current study focused on Huntington’s disease, many neurodegenerative diseases produce changes in the EEG that are associated with the degenerative process. This is the first step in being able to use the EEG to predict both the presence and progression of neurodegenerative diseases.”

Although previous studies have shown there are distinct and extensive changes in EEG patterns in Alzheimer’s and Huntington’s disease patients, researchers are looking for changes that may occur decades before disease onset.

Huntington’s disease is an inherited disorder that causes certain nerve cells in the brain to die, resulting in motor dysfunction, cognitive decline and psychiatric symptoms. It is the only major neurodegenerative disease where the cause is known with certainty: a genetic mutation that produces a change in a protein that is toxic to neurons.

Study: Longitudinal Analysis of the Electroencephalogram and Sleep Phenotype in the R6/2 Mouse Model of Huntington’s Disease

Source: SRI International

MET Protein Levels Show Promise as Biomarker for Aggressive Colon Cancer

MET protein levels correlate strongly with epithelial-mesenchymal transition (EMT) phenotype, a treatment-resistant type of colorectal cancer and may be used as a surrogate biomarker, according to new research from The University of Texas MD Anderson Cancer Center.

The study results, which compared MET protein expression with protein/gene expression of EMT markers and evaluated impact on survival, were released recently at the annual meeting of the American Society of Clinical Oncology.

“When the epithelial cells that line the colon become cancerous, some of them develop special features to allow migration, causing the cancer to be more aggressive,” said Kanwal Pratap Singh Raghav, M.D., fellow in MD Anderson’s Division of Cancer Medicine. “Although EMT is a dominant molecular subtype, a biomarker suitable for clinical use has not been found. This research gives us an important step toward learning more about treating this colorectal cancer subtype.”

In a bigger picture view, the study provides another piece of the puzzle of personalized cancer diagnosis and treatment.

“While we know there are many of types of colorectal cancer, we’re not as advanced as we’d like to be in our understanding of them,” said Scott Kopetz, M.D., Ph.D., associate professor in MD Anderson’s Department of Gastrointestinal Medical Oncology and senior author of the study. “One of the larger goals of our research is to classify simple biomarkers that can be used by doctors in the community to identify subtypes. We want to condense sophisticated gene signatures down to single markers and simple tests that can be used to guide therapy.”

The data were tested with:

  • Mann-Whitney U-test and Spearman rank correlation to determine association between MET protein expression and protein/gene expression of EMT markers and EMT gene signature scores
  • Regression tree method and Kaplan-Meier estimates to assess overall survival

Results of the analysis showed higher MET levels were found more often in colon tumors than rectal tumors.

Overexpression of MET was associated with:

  • Decreased overall survival
  • Higher gene expression of 28 EMT markers
  • Higher gene scores derived from three published EMT gene signatures

The researchers also determined that MET protein expression did not correlate with MET gene expression.

Next steps

Going forward, the group plans to apply this approach to other colorectal cancer subtypes, hopefully defining other simple and readily available biomarkers.

“The ultimate success in targeting colorectal cancer requires understanding molecular subsets of the disease,” Kopetz said. “If we can identify and group cancers with similar behaviors, we’ll be closer to identifying vulnerabilities and optimal therapies for each subset.”

Source: EurekAlert!

Empire Genomics Licenses Novel DNA Biomarker for Use in Diagnosing and Creating a Companion Diagnostic Test for Neuroendocrine Prostate Cancer

Empire Genomics recently announced that it has acquired an exclusive license for a patent pending novel genomic biomarker from Cornell University for use in developing a molecular diagnostic test that could help in diagnosing and determining treatment for patients with neuroendocrine (NEPC) prostate cancer.

Neuroendocrine prostate cancer (NEPC) is a lethal variant of prostate adenocarcinoma (PCA) that can arise de novo, but more commonly arises after hormonal therapy for PCA. Little is known about the underlying molecular biology of NEPC or how and why some patients with PCA progress to a predominantly neuroendocrine phenotype. There is currently no effective therapy for NEPC, and most patients survive less than one year. The poor molecular characterization of NEPC accounts in part for the lack of disease specific therapeutics.

“Each year, approximately, 30,000 men will die of advanced prostate cancer, most of whom will be treated with androgen suppression therapy, however, it is impossible to know just how many of them developed NEPC because patients are not typically biopsied at that stage of their disease,” said Dr. Brian Kelly , Director of Technology Commercialization and Liaison at the Weill Cornell Medical College office of the Cornell Center for Technology Enterprise and Commercialization (CCTEC). “We are delighted that Empire Genomics is now going to make this important diagnostic test available to this patient population and we look forward to working with the company and its seasoned management team.”

“We are delighted to work with Empire Genomics to help develop a commercial grade assay to test for abnormalities one of the key driving genes of the most aggressive form of prostate cancer. This clinical tool will be important as we move forward with precision medicine clinical trials for aggressive castration resistant prostate cancer lead by Dr. Himisha Beltran,” said Mark Rubin , Homer T. Hirst Professor of Pathology in Oncology and the Director of the Institute for Precision Medicine.

Empire Genomics will launch a genetic test for NEPC that will diagnose NEPC Prostate Cancer later this year and seek to partner with pharmaceutical companies to use this assay for accelerating patient stratification in clinical trials.

“We are very pleased to work with Drs. Rubin and Beltran and Cornell to commercialize this technology,” said Anthony Johnson , CEO of Empire Genomics. “It is another exciting genomic tool that we have added to our exclusive precision medicine portfolio.”

Source: Empire Genomics

AgedBrainSYSBIO, a Medium-scale Research Initiative Against Neurodegenerative Diseases

The AgedBrainSYSBIO project on systems biology of synapse proteins & ageing was officially launched recently in Paris, France. AgedBrainSYSBIO is a European collaborative research project funded by the European Commission under the Health Work Programme of the 7th Framework Programme. This multidisciplinary consortium assembles 14 academic and industrial internationally renowned research teams from Belgium, Estonia, France, Germany, Israel, United Kingdom and Switzerland.

Ageing is undisputedly a complex process because it affects the deterioration of most (if not all) aspects of life. Cognitive decline is emerging as one of the greatest public health challenges of the old age, with nearly 50% of adults over 85 afflicted by Alzheimer’s disease, the most common type of dementia.

As other chronic and neurodegenerative diseases, Alzheimer’s disease develops slowly and gradually; but is distinctive in that it forces patients to endure many years of steadily-lessening contact with others, because of memory loss, difficulty with orientation, loss of language and speaking abilities, judging things and depression amongst numerous other symptoms. In 2013, it is estimated that there are worldly more than 24 million people with Alzheimer’s disease, with 4.6 million new cases each year, which means a new case each 7 seconds. It is thus one of the greatest challenges in public health for modern societies, in terms of costs but also in terms of cause, cure and care. To address all these issues, European Commission-funded research effort is crucial as there are still no curative drugs, with only symptomatic treatment able to delay the disease progression.

Over the last years, Genome-Wide Association Studies (GWAS) have been instrumental to identify genes that mediate genetic risk associated to Late-Onset Alzheimer Diseases (LOAD). These approaches based on the genetic comparison of large cohorts of patients and healthy aged persons, and for which three academic partners have been involved (Inserm U894; Institut Pasteur Lille, University of Antwerpen), have been largely funded by Europe. Additionally, a variety of new sets of data have been built and have delivered the state-of-the art of protein-protein interactions, their localisation in subregions of human neurons and genome-wide transcriptome analysis of human neurons derived from aged patient fibroblasts. In another field, new drosophila and mouse models have been also generated via academic partners involved in European Commission-supported large-scale programmes. Finally, the analysis of genes displaying an accelerated evolution in humans as non-human primates do not display these human-specific neurodegenerative diseases has open interesting research paths. So far however, in spite of a huge amount of data available and existing in vitro and in vivo models, these approaches have not been successfully translated into the clinic separately.

The AgedBrainSYSBIO will take advantage of these large set of data, will cross them to other large-scale ageing databases and will include all of these know-how, technologies and results. Thanks to the involvement of four European SMEs, this program is expected to get results readily translated into preclinical studies.

AgedBrainSYSBIO project assembles 13 well-established research teams both from academia and industry. The scientists will share results and know how on LOAD GWAS gene discovery, comparative functional genomics in mouse and drosophila models, in mouse transgenic approaches research on human induced pluripotent stem cells (hiPSC) and their differentiation in vitro and modelling pathways with emphasis on comparative and evolutionary aspects. Importantly, the four European SMEs involved will bring their complementary expertise. QURETEC (Estonia) will be a key partner for data management solutions and bioinformatics data analyses; HYBRIGENICS (France) is a world leader in comparative proteomics and protein-protein interaction analyses; GENEBRIDGES (Germany) is marketing novel strategies for DNA engineering in mammalian cells; reMYND (Belgium) is a leader for development of protein misfolding-modifying treatments against LOAD .

Together, researchers will address the basis of brain ageing by studying the pathways involved in Late-Onset Alzheimer Diseases combining integrative systems biology and comparative genomics. One of the first steps will be to identify the interactions through which the ageing phenotype develops in normal and in disease conditions; on this basis, novel pathways and their evolutionary properties will be modelled and experimentally tested in order to identify druggable targets. This work will finally allow the validation of new druggable targets and markers as a proof-of-concept towards the prevention and cure of aging cognitive defects.

Michel Simonneau, MD PhD, Professor at Ecole Normale Supérieure de Cachan, who coordinates this effort states that “this ambitious project integrates the numerous European initiatives, such as JPND , as well as national research programmes, which addresse the scientific and societal challenge of neurodegenerative diseases. This project receives the decisive input of 4 small to medium size enterprises (SMEs) that allow us to get candidate solutions for curing and preventing common age-related diseases. The links between academia and industry is the driving force of this work programme and in the end will hopefully benefit to all of us.”

Source: EurekAlert!