PUBLIC RELEASE DATE:

12-Nov-2014

Contact: Elizabeth Dowling newsmedia@mssm.edu 212-241-9200 The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc

The brain's ability to effectively deal with stress or to lack that ability and be more susceptible to depression, depends on a single protein type in each person's brain, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published November 12 in the journal Nature.

The Mount Sinai study findings challenge the current thinking about depression and the drugs currently used to treat the disorder.

"Our findings are distinct from serotonin and other neurotransmitters previously implicated in depression or resilience against it," says the study's lead investigator, Eric J. Nestler, MD, PhD, Nash Family Professor, Chair of the Department of Neuroscience and Director of the Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai. "These data provide a new pathway to find novel and potentially more effective antidepressants."

The protein involved in this new model of depression is beta-catenin (B-catenin), which is expressed throughout the brain and is known to have many biological roles. Using mouse models exposed to chronic social stress, Mount Sinai investigators discovered that it is the activity of the protein in the D2 neurons, a specific set of nerve cells (neurons) in the nucleus accumbens (NAc), the brain's reward and motivation center, which drives resiliency.

Specifically, the research team found that animals whose brains activated B-catenin were protected against stress, while those with inactive B-catenin developed signs of depression in their behavior. The study also showed suppression of this protein in brain tissue of depressed patients examined post mortem.

"Our human data are notable in that we show decreased activation of B-catenin in depressed humans, regardless of whether these individuals were on or off antidepressants at the time of death," says the study's co-lead investigator, Caroline Dias, an MD-PhD student at the Icahn School of Medicine at Mount Sinai. "This implies that the antidepressants were not adequately targeting this brain system."

In the study, researchers blocked B-catenin in the D2 brain cells in mice that had previously shown resilience to depression and found the animals became susceptible to stress. Conversely, activating B-catenin in stress mice bolstered their resilience to stress.

Read this article:

Brain protein influences how the brain manages stress; suggests new model of depression

PUBLIC RELEASE DATE:

12-Nov-2014

Contact: John Wallace wallacej@vcu.edu 804-628-1550 Virginia Commonwealth University @vcunews

VCU Massey Cancer Center and VCU Institute of Molecular Medicine (VIMM) researchers discovered a unique approach to treating pancreatic cancer that may be potentially safe and effective. The treatment method involves immunochemotherapy - a combination of chemotherapy and immunotherapy, which uses the patient's own immune system to help fight against disease. This pre-clinical study, led by Paul B. Fisher, M.Ph., Ph.D., and Luni Emdad, M.B.B.S., Ph.D., found that the delivery of [pIC]PEI - a combination of the already-established immune-modulating molecule, polyinosine-polycytidylic acid (pIC), with delivery molecule polyethlenimine (PEI), a polymer often used in detergents, adhesives and cosmetics - inside pancreatic cancer cells triggers cancer cell death without harming normal pancreatic cells.

Pancreatic cancer is one of the deadliest cancers, with an overall five-year survival rate of less than six percent. Its high fatality is attributed to failure to diagnose the disease before it spreads to other organs, as well as its resistance to current therapies. Surgical removal of the cancer, chemotherapy and radiation each offer little resistance against this aggressive disease.

"Pancreatic cancer is currently the fourth leading cause of cancer death in the US. Developing an effective treatment is a vital step, and immunochemotherapy may be the key," said Emdad, member of the Cancer Molecular Genetics research program at VCU Massey, assistant professor in the Department of Human and Molecular Genetics at VCU School of Medicine and member of the VIMM.

Published in Cancer Research, this is the first study that links the proteins involved in programmed cell death as prime mediators in cancer-specific killing by [pIC]PEI. Emdad and Fisher have found that, in vitro (in cell cultures), [pIC]PEI selectively induces cell death in pancreatic cancer cells, and that, in vivo (in animal models), [pIC]PEI also inhibited tumor growth via cell death.

"Since [pIC]PEI is extremely and selectively toxic to pancreatic cancer cells both in vitro and in vivo, the use of this compound, alone and in combination with other therapeutic agents, could potentially lead to a novel, safe and effective approach for treating pancreatic cancer by directly attacking the cancer cell chemotherapeutically and stimulating the immune system to confront the cancer, an immunochemotherapy approach," said Fisher, Thelma Newmeyer Corman Chair in Cancer Research and co-leader of the Cancer Molecular Genetics research program at VCU Massey, professor and chair of the VCU Department of Human and Molecular Genetics, and director of the VIMM . "The results are promising, and we look forward to conducting more extensive pre-clinical studies. Our ultimate hope is to bring this innovative scheme into the clinic to treat patients with pancreatic cancer."

As the need exists for newer and more effective strategies to treat pancreatic cancer, these findings are critical. And while the current focus of this research is on pancreatic cancer, this approach also has applications for melanoma, breast cancer and hepatocellular carcinoma. Several important questions related to [pIC]PEI will be explored in future research, including assessing its efficacy in additional and expanded in vitro and in vivo studies, and testing it in new combinations with conventional chemotherapies.

###

Continued here:

Innovative approach to treating pancreatic cancer combines chemo- and immuno-therapy

PUBLIC RELEASE DATE:

12-Nov-2014

Contact: Sue McGreevey smcgreevey@partners.org 617-724-2764 Massachusetts General Hospital @MassGeneralNews

A study led by Massachusetts General Hospital (MGH) investigators has identified what appears to be a molecular switch controlling inflammatory processes involved in conditions ranging from muscle atrophy to Alzheimer's disease. In their report published in Science Signaling, the research team found that the action of the signaling molecule nitric oxide on the regulatory protein SIRT1 is required for the induction of inflammation and cell death in cellular and animal models of several aging-related disorders.

"Since different pathological mechanisms have been identified for diseases like type 2 diabetes, atherosclerosis and Parkinson's disease, it has been assumed that therapeutic strategies for those conditions should also differ," says Masao Kaneki, MD, PhD, MGH Department of Anesthesia, Critical Care and Pain Medicine, senior author of the paper. "In contrast, our findings identified nitric oxide-mediated inactivation of SIRT1 - believed to be a longevity gene - as a hub of the inflammatory spiral common to many aging-related diseases, clarifying a new preventive molecular target."

Studies have implicated a role for nitric oxide in diabetes, neurodegeneration, atherosclerosis and other aging-related disorders known to involve chronic inflammation. But exactly how nitric oxide exerts those effects - including activation of the inflammatory factor NF-kappaB and the regulatory protein p53, which can induce the death of damaged cells - was not known. SIRT1 is known to suppress the activity of both NF-kappaB and p53, and since its dysregulation has been associated with models of several aging-related conditions, the research team focused on nitric oxide's suppression of SIRT1 through a process called S-nitrosylation.

Cellular experiments revealed that S-nitrosylation inactivates SIRT1 by interfering with the protein's ability to bind zinc, which in turn increases the activation of p53 and of a protein subunit of NF-kappaB. Experiments in mouse models of systemic inflammation, age-related muscle atrophy and Parkinson's disease found that blocking or knocking out NO synthase - the enzyme that induces nitric oxide generation - prevented the cellular and in the Parkinson's model behavioral effects of the diseases. Additional experiments pinpointed the S-nitrosylation of SIRT1 as a critical point in the chain of events leading from nitric oxide expression to cellular damage and death.

"Regardless of the original event that set off this process, once turned on by SIRT1 inactivation, the same cascade of enhanced inflammation and cell death leads to many different disorders," says Kaneki, an associate professor of Anaesthesia at Harvard Medical School. "While we need to confirm that what we found in rodent models operates in human diseases, I believe this process plays an important role in the pathogenesis of conditions including obesity-related diabetes, atherosclerosis, Alzheimer's disease and the body's response to major trauma. We're now trying to identify small molecules that will specifically inhibit S-nitrosylation of SIRT1 and related proteins and suppress this proinflammatory switch."

###

The co-lead authors of the Science Signaling paper are Shohei Shinozaki, PhD, Tokyo Medical and Dental University, and Kyungho Chang, MD, PhD, University of Tokyo School of Medicine, both of whom previously were research fellows at MGH. Additional co-authors include Michihiro Sakai, Nobuyuki Shimizu, Marina Yamada, Tomokazu Tanaka, MD, PhD, Harumasa Nakazawa, MD and Fumito Ichinose, MD, PhD, all of the MGH Department of Anesthesia, Critical Care and Pain Medicine; and Jonathan S. Stamler, MD, Case Western Reserve University and University Hospital, Cleveland.

Read the original post:

Single molecular switch may contribute to major aging-related diseases

PUBLIC RELEASE DATE:

11-Nov-2014

Contact: Kimberly Brown kbrown@snmmi.org 703-652-6773 Society of Nuclear Medicine @SNM_MI

Reston, Va. (November 11, 2014) - A novel study demonstrates the potential of a novel molecular imaging drug to detect and visualize early prostate cancer in soft tissue, lymph nodes and bone. The research, published in the November issue of the Journal of Nuclear Medicine, compares the biodistribution and tumor uptake kinetics of two Tc-99m labeled ligands, MIP-1404 and MIP-1405, used with SPECT and planar imaging.

Prostate cancer is the most commonly diagnosed non-skin cancer in the United States, and it is second only to lung cancer as the leading cause of cancer deaths in American men. An estimated 233,000 new cases of prostate cancer will be diagnosed in the United States in 2014, and an estimated 29,000 will die of the disease. More than 2 million men are currently living with prostate cancer in the United States.

Under an exploratory investigational new drug, using a cross-over design, researchers compared the pharmacokinetics, biodistribution, and tumor uptake of Tc-99m MIP-1404 and Tc-99m MIP-1405 in 6 healthy men and 6 men with radiographic evidence of metastatic prostate cancer. Whole body images were obtained at 10 minutes and at 1, 2, 4 and 24 hours. SPECT was performed between 3 and 4 hours after injection. Prior to the study, no single target-specific Tc-99m radiopharmaceutical could image prostate cancer in soft tissue, lymph nodes and bone (bone metastasis) based on planar and SPECT. There was no uptake in degenerative bone disease, which often confounds bone scans.

"This research represents an innovative prostate cancer planar and SPECT imaging technology--addressing unmet clinical need for sensitive and selective imaging of loco-regional and distant metastatic prostate cancer," stated Shankar Vallabhajosula, PhD, lead author of the study "99mTc-Labeled Small Molecule Inhibitors of Prostate Specific Membrane Antigen: Pharmacokinetics and Biodistribution Studies in Healthy Subjects and Patients with Metastatic Prostate Cancer." "With respect to imaging, the lack of focal uptake in the normal prostate of healthy volunteers with both compounds further demonstrated that PSMA is a viable targeting mechanism for detection and visualization of prostate cancer and suggests that this imaging approach is highly sensitive and disease specific."

There was good correlation with bone scans in most subjects, although in general, more lesions were visualized with MIP-1404 and MIP-1405 than with bone scans, suggesting this agent may be more sensitive to detecting skeletal or marrow invasion earlier than bone scans. "We also demonstrated that Tc-99m MIP-1404 has favourable pharmacokinetics and biodistribution, which represents a breakthrough in imaging of prostate cancer for the following reasons: Tc-99m MIP-1404 can image prostate cancer in lymph nodes, soft tissue and bone," noted Vallabhajosula.

A multi-center phase II study with Tc-99m MIP-1404 in 100 patients was recently completed, and the data were presented at 2014 SNMMI Annual Meeting in St. Louis, Mo. Progenics Pharmaceuticals has plans to conduct a phase III trial soon.

###

See the rest here:

Novel molecular imaging drug offers better detection of prostate cancer

Uveal Melanomas After Tumor Necrosis Factor- Inhibitors
Dr. Jose Pulido, a professor of ophthalmology and molecular medicine at Mayo Clinic in Rochester, MN, expresses concern in his article appearing in the Novem...

By: Mayo Proceedings

Read the original:

Uveal Melanomas After Tumor Necrosis Factor- Inhibitors - Video

Epigenetics Stem Cells in Development Regenerative Medicine - Allyson Moutri, UC San Diego
Speaker: Alysson Muotri, Ph.D., Assistant Professor, Department of Pediatrics/Cellular Molecular Medicine, UC San Diego.

By: Alliance for Regenerative Medicine

Read the rest here:

Epigenetics & Stem Cells in Development & Regenerative Medicine - Allyson Moutri, UC San Diego - Video

Molecular Partners AG (MOLN) shares rose on the Swiss companys trading debut, the second-biggest biotechnology offering in Europe since 2007, as Allergan (AGN) Inc. supported the sale.

Molecular Partners put its listing on hold two weeks ago, citing a volatile stock market, and resumed book-building for the offer two days ago. Allergan, the Irvine, California-based drugmaker that funds development of Molecular Partners most advanced eye medicine, supported the IPO with an investment, according to the Swiss company.

U.S. investors are increasingly recognizing the attractiveness of European biotech, said Samir Devani, a health-care analyst at Rx Securities.

The stock rose 4.2 percent from the 22.40-franc offer price in Zurich today, after surging as much as 12 percent. Molecular Partners sold almost 23 percent of its shares, raising about 100 million Swiss francs ($104 million), not counting an over-allotment option, according to data compiled by Bloomberg.

Investors filter for quality, so maybe the quantity of IPOs is to decline, but the window for companies with proximity to revenues is not closed yet, Navid Malik, a London-based analyst at Cenkos Securities Plc, said by phone.

Christian Zahn, Molecular Partners chief executive officer, declined to disclose Allergans stake in an interview two days ago and said the company is not seeking a takeover.

Another possible Swiss IPO candidate may be biotechnology company NovImmune SA, newspaper Finanz und Wirtschaft reported. The company hired Andrew Oakley, former chief financial officer of Actelion (ATLN) Ltd., in March as its CFO.

To contact the reporter on this story: Jan-Henrik Frster in Zurich at jforster20@bloomberg.net

To contact the editors responsible for this story: Mariajose Vera at mvera1@bloomberg.net James Kraus

Press spacebar to pause and continue. Press esc to stop.

Go here to read the rest:

Molecular Partners Up in Trading Debut on Allergan Support

04.11.2014 - (idw) University of Gothenburg

An initiative to create a new centre for molecular medicine at the University of Gothenburg has been launched, with funding of at least SEK 620 million (67 million euro) from the Knut and Alice Wallenberg Foundation, the University of Gothenburg, AstraZeneca and Region Vstra Gtaland. Cancer, obesity and diabetes are just some of the areas highlighted for research. Since the beginning of the 20th century Sweden has had a long and distinguished track record in the field of life science research. However, it has lost some of its momentum with the emergence of the global economy.

"We're looking to boost core skills so that Sweden can once again lead the world in this field," says Peter Wallenberg Jr, Vice Chairman of the Knut and Alice Wallenberg Foundation. "The concept pioneered by the University of Gothenburg where young researchers have dealings with both industry and the clinical side of things is an excellent example and something that will make Sweden more competitive in the life sciences."

The Foundation has therefore decided to put SEK 270 million towards a new centre for molecular medicine in Gothenburg to offer tenure track positions for young researchers. The grant is part of a wider drive to strengthen the life sciences in Sweden. Previously the Swedish government, and four universities in the Mlardalen region, set up the Science for Life Laboratory in Stockholm/Uppsala to serve as a national resource for the life sciences in Sweden. The new centre in Gothenburg will complement and bolster this nationwide initiative.

"The Foundation funds only world-class research, and this grant goes to show that the University of Gothenburg is home to such research," says Pam Fredman, Vice-Chancellor of the University of Gothenburg. "We now have the opportunity to take things to the next level by recruiting outstanding young international researchers. This is excellent news."

The research will initially focus on cancer, obesity, diabetes, respiratory diseases and inflammatory diseases. In a bid to ensure that the research quickly translates into new treatments and benefits patients, Region Vstra Gtaland will be contributing a further SEK 150 million, while AstraZeneca will allocate time and resources of at least SEK 40 million for the next four years, with the option of an extension. The University of Gothenburg will also be contributing SEK 160 million.

Region Vstra Gtaland, which is responsible for regional development and health care in the region, also welcomes the initiative:

"The new centre for molecular medicine will create an attractive environment in Vstra Gtaland for international life science researchers and companies," says Ann-Sofi Lodin, CEO of Region Vstra Gtaland. "Our involvement means that health-related problems can be identified and that research results will benefit health care and patients more quickly."

Spanning ten years, the investment will start in 2016. The University of Gothenburg aims to create a leading international research centre that far outlasts the period of funding.

For more information, please contact:

Continue reading here:

SEK 620 million investment in the life sciences in Gothenburg

DUBLIN--(BUSINESS WIRE)--Research and Markets (http://www.researchandmarkets.com/research/3jdj6f/molecular) has announced the addition of Jain PharmaBiotech's new report "Molecular Diagnostics - Technologies, Markets and Companies" to their offering.

This report describes and evaluates the molecular diagnostics technologies that will play an important role in practice of medicine, public health, pharmaceutical industry, forensics and biological warfare in the 21st century. This includes several polymerase chain reaction (PCR)-based technologies, fluorescent in situ hybridization (FISH), peptide nucleic acids (PNA), electrochemical detection of DNA, sequencing, mitochondrial DNA, biochips, nanotechnology and proteomic technologies.

Initial applications of molecular diagnostics were mostly for infections but are now increasing in the areas of genetic disorders, preimplantation screening and cancer. Genetic screening tests, despite some restrictions is a promising area for future expansion of in vitro diagnostic market. Molecular diagnostics is being combined with therapeutics and forms an important component of integrated healthcare. Molecular diagnostic technologies are also involved in development of personalized medicine based on pharmacogenetics and pharmacogenomics. Currently, there has been a considerable interest in developing rapid diagnostic methods for point-of-care and biowarfare agents such as anthrax.

The number of companies involved in molecular diagnostics has increased remarkably during the past few years. More than 1,000 companies have been identified to be involved in developing molecular diagnostics and 340 of these are profiled in the report along with tabulation of 800 collaborations. Despite the strict regulation, most of the development in molecular diagnostics has taken place in the United States, which has the largest number of companies.

The markets for molecular diagnostics technologies are difficult to estimate. Molecular diagnostics markets overlap with markets for non-molecular diagnostic technologies in the in vitro diagnostic market and are less well defined than those for pharmaceuticals. Molecular diagnostic markets are analyzed for 2013 according to technologies, applications and geographical regions. Forecasts are made up to 2023. A major portion of the molecular diagnostic market can be attributed to advances in genomics and proteomics. Biochip and nanobiotechnology are expected to make a significant contribution to the growth of molecular diagnostics.

Benefits of this report

- This report has evolved during the past 19 years, profiting from feedback by numerous readers and experts.

- The most comprehensive and up-to-date one-stop source of information on technical and commercial aspects of molecular diagnostics.

- Includes profiles of 340 companies, the largest number in any report on this topic.

- 600 references, cited in the report are included in the bibliography.

View post:

Research and Markets: Global Molecular Diagnostics Report 2014-2023 - Updated Technologies, Markets and Companies ...

PUBLIC RELEASE DATE:

29-Oct-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

Researchers at the Stanford University School of Medicine have developed a new strategy that they say could detect bladder cancer with more accuracy and sensitivity than standard endoscopy methods. Endoscopy refers to a procedure in which surgeons use an instrument equipped with a lens to see inside the patient.

The researchers identified a protein known as CD47 as a molecular imaging target to distinguish bladder cancer from benign tissues. In the future, this technique could improve bladder cancer detection, guide more precise cancer surgery and reduce unnecessary biopsies, therefore increasing cancer patients' quality of life.

The work is described in a paper that will be published Oct. 29 in Science Translational Medicine.

Bladder cancer, the fifth most common cancer in the United States, is generally identified in the clinic by a procedure called cystoscopy, an endoscopy in the bladder. Then in the operating room, surgeons remove the cancerous tissue for biopsy.

Need for close monitoring

Bladder cancer must be monitored closely because it has one of the highest recurrence rates of all cancers. It is important that cystoscopy imaging be both highly sensitive (able to detect subtle cancer) and specific (able to distinguish between benign and cancerous tumors) so surgeons can remove cancerous tissue at an early stage to prevent invasion into the underlying muscle, which may require complete removal of the bladder. However, standard cystoscopy has insufficient sensitivity and specificity, particularly for flat-appearing cancers that blend in with the bladder and may be confused with inflammation.

"Our motivation is to improve optical diagnosis of bladder cancer that can better differentiate cancer from noncancer, which is exceedingly challenging at times. Molecular imaging offers the possibility of real-time cancer detection at the molecular level during diagnostic cystoscopy and tumor resection," said co-senior author Joseph Liao, MD, an associate professor of urology and the chief of urology at the Veterans Affairs Palo Alto Health Care System. The lead author is Ying Pan, PhD, a research associate in Liao's lab.

View original post here:

New molecular imaging technology could improve bladder-cancer detection

PUBLIC RELEASE DATE:

29-Oct-2014

Contact: Terri Ogan togan@partners.org 617-726-0954 Massachusetts General Hospital @MassGeneralNews

A study led by investigators from Massachusetts General Hospital and the Perelman School of Medicine at the University of Pennsylvania has identified a potential target for therapies to treat cocaine addiction. In their study receiving advance online publication in Molecular Psychiatry, the investigators find evidence that changing one amino acid in a subunit of an important receptor protein alters whether cocaine-experienced animals will resume drug seeking after a period of cocaine abstinence. Increasing expression of the enzyme responsible for that change within the GluA2 subunits of AMPA receptors which receive nerve impulses carried by the neurotransmitter glutamate reduced cocaine seeking in animals allowed to self-administer the drug.

"The critical role of the AMPA receptor in cocaine addiction is clear," says Ghazaleh Sadri-Vakili, PhD, director of the NeuroEpigenetics Laboratory in the MassGeneral Institute for Neurodegenerative Disease, senior author of the report. "We have known that activation of the AMPA receptor in the nucleus accumbens an area of the brain important for drug addiction promotes the resumption of cocaine seeking in animal models, and this study identifies an increased contribution of calcium-permeable AMPA receptors to this process."

AMPA receptors consist of four subunits that can be of four different types GluA1 through GluA4 and their involvement in cocaine addiction was previously described by study co-author, R. Christopher Pierce, PhD, of the Perelman School of Medicine at the University of Pennsylvania. The GluA2 subunit determines whether the receptor is permeable to calcium, which would enhance the strength of signals transmitted through the receptor.

In the normal adult brain, 99 percent of GluA2 subunits have been edited at the RNA processing stage into a form that renders the receptor impermeable to calcium, and disruptions in GluA2 editing that create a calcium-permeable receptor have been associated with disorders including depression, epilepsy and amyotrophic lateral sclerosis. Since chronic cocaine exposure produces major changes in glutamate transmission in the brain including the nucleus accumbens, a structure deep within the brain known to be involved in reward and addiction the research team investigated the relationship of GluA2 editing within the accumbens to cocaine seeking in an animal model.

Study lead author Heath Schmidt, PhD, of the Perelman School of Medicine, first allowed a group of rats to self-administer cocaine for 21 days, then withheld cocaine from the animals for a week. Examination of the animals' brains after 7 days of drug abstinence found that levels within the nucleus accumbens of both edited GluA2 and of the enzyme responsible for editing were reduced, compared with the brains of animals not exposed to cocaine. These findings suggest that activation of AMPA receptors containing unedited GluA2 could potentially stimulate cocaine craving. In a different group of animals, Schmidt found that inducing overexpression in the nucleus accumbens of the editing enzyme, called ADAR2, both increased the presence of edited GluA2 in the AMPA receptor and reduced the resumption of cocaine seeking in habituated animals given access to the drug after 7 days of abstinence.

Sadri-Vakili explains, "Our findings support the novel hypothesis that calcium-permeable AMPA receptors containing unedited GluA2 subunits contribute to cocaine seeking and that repairing the deficient editing of GluA2, possibly by regulation of ADAR2 expression, could be a treatment strategy for cocaine addiction." She is an assistant professor of Neurology at Harvard Medical School; Schmidt is an assistant professor of Psychiatry, and Pierce is a professor of Neuroscience in Psychiatry at the Perelman School of Medicine at the University of Pennsylvania.

###

Read this article:

Study identifies potential treatment target for cocaine addiction

Show #103 - Molecular Medicine II (Topic)
Dr. Proodian continues to discuss the topic of molecular medicine. Subtopics include: - Mad cow disease - Food in information - Obesity is a structural probl...

By: Dr. Proodian

Link:

Show #103 - Molecular Medicine II (Topic) - Video

Care for cancer patients within the NHS will be radically improved through the combined power of such technologies as big data, informatics and Internet of Things-connected devices to sequence the genomes of individual patients.

That's what a collaboration between the University of Oxford and the US-based Chan Soon-Shiong Institute of Molecular Medicine is hoping to achieve.

The plan has the full backing of the government, with Minister for Life Sciences George Freeman MP, who was at the event, likening its ambition to that of NASA when it was aiming for the Moon.

"This is a project to sequence the full genome of 100,000 patient volunteers in the NHS and combine it with the hospital clinical data," he said.

"We're creating the world's first at-scale dataset [of the genome], the NASA of biomedicine, which will help to shape the precision medicine landscape in the 21st century. Pulling together the two transformational technologies of genomics and informatics will allow us to practise in our health system a much more targeted, precise model of medicine for the benefit of patients," Freeman added.

When Computing asked about the technology behind the genome project, Dr Patrick Soon-Shiong, founder and chairman of the Chan Soon-Shiong Institute for Molecular Medicine, gave some insights into the computing power that will be harnessed to diagnose and treat cancer.

He explained that examining the genome of just one patient represents half a terabyte of data. Therefore, to collect and analyse data from many thousands of patients will require the resources of a supercomputer.

"If you look at the US, there's 13 million cancer survivors, which translates to 4,000 or 5,000 a day. That's equivalent to 50 to 60 times the download of information from Facebook every day," Dr Soon-Shiong said.

This is why a phenomenal amount of computing power is required to extract data from the "tiny matter" of the genome.

"The first thing that was needed was an infrastructure of data transfer which had never actually been considered on this planet before. So we had to actually create an infrastructure which could move all that data; this is now active," Dr Soon-Shiong told Computing.

Read the original here:

Oxford University's big data and Internet of Things project to 'create the NASA of biomedicine'

Care for cancer patients within the NHS will be radically improved through the combined power of such technologies as big data, informatics and Internetof Things-connected devices to sequence the genomes of individual patients.

That's what a collaboration between the University of Oxford and the US-based Chan Soon-Shiong Institute of Molecular Medicine is hoping to achieve, with the two organisations announcing their partnership today at an event in London.

The plan has the full backing of the government, with Minister for Life Sciences George Freeman MP, who was at the event, likening its ambition to that of NASA when it was aiming for the Moon.

"This is a project to sequence the full genome of 100,000 patient volunteers in the NHS and combine it with the hospital clinical data," he said.

"We're creating the world's first at-scale dataset [of the genome], the NASA of biomedicine, which will help to shape the precision medicine landscape in the 21st century. Pulling together the two transformational technologies of genomics and informatics will allow us to practise in our health system a much more targeted, precise model of medicine for the benefit of patients," Freeman added.

When Computing asked about the technology behind the genome project, Dr Patrick Soon-Shiong, founder and chairman of the Chan Soon-Shiong Institute for Molecular Medicine, gave some insights into the computing power that will be harnessed to diagnose and treat cancer.

He explained that examining the genome of just one patient represents half a terabyte of data. Therefore, to collect and analyse data from many thousands of patients will require the resources of a supercomputer.

"If you look at the United States there's 13 million cancer survivors, which translates to 4,000 or 5,000 a day. That's equivalent to 50 to 60 times the download of information from Facebook every day," Dr Soon-Shiong explained.

This is why a phenomenal amount of computing power is required to extract data from the "tiny matter" of the genome.

"The first thing that was needed was an infrastructure of data transfer which had never actually been considered on this planet before. So we had to actually create an infrastructure which could move all that data; this is now active," Dr Soon-Shiong told Computing.

Originally posted here:

Oxford University big data and IoT project to 'create the NASA of biomedicine'

Contact Information

Available for logged-in reporters only

Newswise WASHINGTON (Oct. 23, 2014) The George Washington University School of Medicine and Health Sciences (SMHS), in collaboration with the University of Rome Tor Vergata, is pleased to host the Fourth International Symposium on Thymosins in Health and Disease in Rome, Oct. 23-25. This meeting will bring together many of the leading researchers in the U.S., Europe, and Asia, to report on advances that have been made in the chemistry, biology, and clinical application of the thymosins in health and disease.

Thymosins have significant promise and may be key to new approaches for the treatment of a number of difficult to treat human diseases, ranging from severe sepsis to neurothrophic keratitis, said Allan L. Goldstein, Ph.D., Emeritus Professor and Chairman of the Department Biochemistry and Molecular Medicine at SMHS and co-chair of the symposium. Based on recent discoveries in host immunity and regenerative medicine, thymosins, and other biological response modifiers, have already given us additional weapons in the fight against cancer and a number of infectious diseases. This conference will bring together the greatest minds in the field, allowing us to collaborate and look forward to additional breakthroughs.

Thymosins are a family of biologically active peptides with hormone-like properties that were first isolated in 1966. Since that time, significant progress has been made in understanding the role of these molecules in immunity and the nature of the physiological processes they regulate. Several of these small peptides, such as thymosin alpha 1 and thymosin beta 4, have been synthesized and shown to have important clinical applications. The physiological processes that these peptides affect include stimulation or suppression of immune responses, regulation of actin dynamics and cell motility, neuroplasticity, repair and remodeling of vessels of the heart and other injured tissues, angiogenesis, and stem cell differentiation. Several of these molecules have also been shown to be useful as molecular markers and as potential diagnostics in areas ranging from cancer and infectious diseases to autoimmune diseases and aging.

These experts will review the most current data and focus on recent advances and future prospects for the use of thymosins in clinical medicine. The scientific themes of the symposium will include both experimental and clinical data and the latest molecular, cellular, and gene approaches using combined therapies.

As part of the symposium, the 2014 Abraham White Scientific, Humanitarian, and Public Service Awards, which honor individuals who have made unique contributions to science and medicine, will be presented. Notable past recipients include Nobel laureates Bengt Samuelsson, M.D.; Julius Axelrod, M.D.; Michael Brown, M.D.; Joseph Goldstein, M.D.; and Tim Hunt, Ph.D., in addition to a number of other distinguished scientists. This year, the award will be presented to the following awardees:

- Michael Chopp, Ph.D. and Barbara Ensoli, M.D., Ph.D. will be honored as the 2014 Abraham White Distinguished Scientific Awardees. Chopp is being honored for his pioneering studies and scientific contributions, which have significantly advanced understanding of the role of Thymosin 4 in the treatment of a number of neurological diseases. Ensoli is also being honored for her pioneering studies and scientific contributions, which have significantly advanced understanding of the role of the HIV-1 Tat protein antigen in the development of both preventive and therapeutic HIV vaccines.

- Guido Rasi, M.D., executive director of the European Medicines Agency, will be honored as the 2014 Abraham White Lifetime Public Service Awardee for his lifetime of scientific and medical accomplishments in advancing the development of new pre-clinical models in oncology, including the use of novel combinations of chemo-immunotherapeutic approaches and nanosystem drug delivery.

Leticia Hall-Salam, director of the Office of Continuing Education in the Health Professions at SMHS, and Jessica R. Sa-Reed, lab assistant in the Department of Biochemistry and Molecular Medicine at SMHS, were also instrumental in the organization of this international meeting. Hynda Kleinman, Ph.D., adjunct professor of biochemistry and molecular medicine at SMHS, along with Goldstein, will speak at the symposium.

Read more:

George Washington University Researchers Help Organize International Symposium on Thymosins in Health and Disease

By Duke Medicine News and Communications

DURHAM, N.C. Mary E. Klotman, M.D., chairwoman of the Department of Medicine at the Duke University School of Medicine, has been elected as one of 70 new members to the prestigious Institute of Medicine (IOM). Klotman is an expert in infectious diseases and the human immunodeficiency virus (HIV).

Election to the Institute of Medicine is considered one of the highest honors in medicine, said Nancy C. Andrews, M.D., Ph.D., dean of Duke University School of Medicine. Dr. Klotmans election is a notable achievement and recognition of her important contributions as a leader and as a physician-scientist focused on the molecular pathogenesis of HIV-1 infection.

Klotman attended Duke University for both her undergraduate degree in zoology (1976) and her medical degree (1980) and then completed her internal medicine residency and a fellowship in infectious diseases in the Department of Medicine at Duke.

She started her career at Duke in 1985 as an associate faculty member in medicine, before moving to the National Institutes of Health, where she was a member of the Public Health Service. At NIH, she trained and worked in the Laboratory of Tumor Cell Biology under the direction of renowned HIV researcher Robert C. Gallo, M.D.

Go here to see the original:

Klotman, chair of Medicine, Named to Institute of Medicine

In a sample of patients with undiagnosed, suspected genetic conditions, a certain type of exome sequencing method was associated with a higher molecular diagnostic yield than traditional molecular diagnostic methods, according to a study appearing in JAMA. The study is being released to coincide with the American Society of Human Genetics annual meeting.

Exome sequencing, which sequences the proteincoding region of the genome (the complete set of genes or genetic material present in a cell or organism), has been rapidly applied in research settings and recent increases in accuracy have enabled the development of clinical exome sequencing (CES) for mutation identification in patients with suspected genetic diseases. Early in 2012, the Clinical Genomics Center at the University of California, Los Angeles, launched a CES program with the goal of delivering a more comprehensive method for determining a molecular diagnosis for patients with presumed rare Mendelian disorders (a genetic disease showing a certain pattern of inheritance) that have remained undiagnosed despite exhaustive genetic, biochemical, and radiological testing. Researchers at this center have introduced a new test, called trio-CES, in which the whole exome of the affected proband (first identified individual affected with the disorder among other family members) and both parents are sequenced, according to background information in the article.

Hane Lee, Ph.D., of the University of California, Los Angeles, and colleagues report the results of clinical exome sequencing performed on 814 patients with undiagnosed, suspected genetic conditions at the Clinical Genomics Center between January 2012 and August 2014. Clinical exome sequencing was conducted as trio-CES (both parents and their affected child sequenced simultaneously) or as proband-CES (only the affected individual sequenced) when parental samples were not available.

Overall, a molecular diagnosis (with the causative variant(s) identified in a well-established clinical gene) was provided for 213 of the 814 total cases (26 percent). There was a significantly higher molecular diagnostic yield from cases performed as trio-CES (127 of 410 cases; 31 percent) relative to proband-CES (74 of 338 cases; 22 percent) in the overall group of cases.

In cases of developmental delay in children (<5 years, n = 138), the molecular diagnosis rate was 41 percent (45 of 109) for trio-CES cases and 9 percent (2 of 23) for proband-CES cases.

"In this sample of patients with undiagnosed, suspected genetic conditions, trio-CES was associated with higher molecular diagnostic yield than proband-CES or traditional molecular diagnostic methods. Additional studies designed to validate these findings and to explore the effect of this approach on clinical and economic outcomes are warranted. Clinical implications of these findings need to be better understood before CES should be routinely adopted," the authors conclude.

Editorial: Genome-Scale Sequencing in Clinical Care

In an accompanying editorial, Jonathan S. Berg, M.D., Ph.D., of the University of North Carolina at Chapel Hill, comments on the two JAMA studies that examined exome sequencing.

"Ultimately, it will be essential to know who will benefit from clinical genomic sequencing, including the role of sequencing in a variety of settings, such as oncology, prenatal diagnosis, newborn screening, or population screening in healthy adults. The National Institutes of Health and other funding agencies are supporting a broad portfolio of research projects investigating these and other questions about genomic medicine. In the meantime, physicians should be judicious in considering when to obtain clinical exome sequencing; should effectively communicate the risks, benefits, and limitations of such testing; should be able to clearly communicate the results to patients and their families; and should avoid unnecessarily burdening patients with the cost of such testing if not covered by insurance. The application of genomic sequencing will ultimately contribute to progress in clinical care, from molecular diagnosis to improved outcomes, but there is much to learn before it can be applied more universally."

Story Source:

Here is the original post:

Study examines type of exome sequencing, molecular diagnostic yield

Show #102 - Molecular Medicine I (Topic)
Dr. Proodian discusses the following subjects when talking about the topic of molecular medicine: - Structure and Protein function - Get the structure right...

By: Dr. Proodian

Read more:

Show #102 - Molecular Medicine I (Topic) - Video

16.10.2014 - (idw) Max-Delbrck-Centrum fr Molekulare Medizin (MDC) Berlin-Buch

On October 16, 2014, Professor Walter Rosenthal, former Chair of the Board of Directors and Scientific Director of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch since 2009, assumed his new position as President of the Friedrich Schiller University Jena. He was elected on May 23, 2014 as successor of Professor Klaus Dicke by the University Council in consultation with the Senate of the University. On October 15, 2014, Professor Thomas Sommer became Interim Chair of the MDC Board of Directors until the appointment of a successor. From 2004 to the present, Sommer held the position of Deputy Scientific Director of the MDC. Following Professor Rosenthals departure, Professor Sommer also assumed the vacant positions of member of the Board of Directors of the Berlin Institute of Health (BIH), which was founded in 2013 by the MDC and the Charit, and member of the Board of Directors of the German Centre for Cardiovascular Research (DZHK).

Thomas Sommer studied biology at Freie Universitt Berlin. In 1988 he received his doctorate from the same university with a dissertation at the Max Planck Institute of Molecular Genetics in Berlin-Dahlem in the department of Professor Thomas A. Trautner. He then began working on the mechanisms of protein quality control as a postdoctoral fellow in the laboratory of Professor Stefan Jentsch at the Friedrich Miescher Laboratory of the Max Planck Society in Tbingen.

In 2003 Sommer was elected a member of the European Molecular Biology Organization (EMBO); in 2006 he received an honorary professorship at the Charit. In 2012, together with Professor Glickman, he received the Science Prize of the German Technion Society (Hannover).

In recent years Sommer has also become engaged in issues of the self-administration of research. Since 2014 he has been a member of the scientific advisory board of the Center for Biotechnology of the University of Duisburg-Essen. From 2006 to 2008 he was a member in the Senate Committee for Graduate Programs of the German Research Foundation (DFG), and from 2008 to 2014 he was a member in the Senate Committee for Collaborative Research Centres of the DFG.

Contact: Barbara Bachtler Press Department Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch in the Helmholtz Association Robert-Rssle-Strae 10 13125 Berlin Germany Phone: +49 (0) 30 94 06 - 38 96 Fax: +49 (0) 30 94 06 - 38 33 e-mail: presse@mdc-berlin.de http://www.mdc-berlin.de/en

Follow this link:

Walter Rosenthal Assumes Presidency of Jena University Thomas Sommer Becomes MDC Interim Director

16.10.2014 - (idw) Max-Delbrck-Centrum fr Molekulare Medizin (MDC) Berlin-Buch

In their search for the earliest possible stage of development of human embryonic stem cells (hESCs) that still have the potential to develop into any types of body cells and tissue, researchers from the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch, Germany, and the University of Bath, United Kingdom, have apparently been successful. Jichang Wang, Gangcai Xie, and Dr. Zsuzsanna Izsvk (MDC), together with Professor Laurence D. Hurst (University of Bath), report the discovery of a subtype of cells in culture dishes with hESCs and human induced pluripotent stem cells (hiPSCs) that resemble this very early, pluripotent or nave state (Nature, doi:10.1038/nature13804)*. They also discovered the mechanism that turns human ES cells into nave-like human stem cells. While this has potential implications for medicine and for understanding early human development, an evolutionary enigma still remains unsolved.

Human embryonic stem cells (hESCs) differ considerably from those of mice. Mouse nave cultures resemble the inner cell mass which gives rise to the embryo, while none of the cultured hESC lines do. Nave ESCs of mice are easy to maintain, but not human ESCs isolated from pre-implantation embryos. The hESC lines, researchers work with in their laboratories are considered to be less nave, and have limited differentiation potential. Researchers hypothesize that they have partially lost their pluripotency. Why this is so remains unclear.

What properties characterize human nave stem cells? Can they be identified and proliferated in the laboratory and retained in culture? Researchers in Europe, Asia and the USA are trying to find the answers to these questions in order to be able to use these cells for therapy in the future.

Evolution pointed the way It was evolution that showed the researchers in Bath and Berlin the way to the successful approach. They pinpointed one particular class of ancient viruses called HERVH (human endogenous retrovirus H). HERVH integrated into our DNA millions of years ago, and although it does not function as a virus any longer, it is not silent.

HERVH-derived sequences appear at a very early stage in human embryos, that is, HERVH is highly expressed at just the right time and place in human embryos where one would expect to see nave stem cells. This was also observed by Professor Kazutoshi Takahashi (Kyoto University, Kyoto, Japan), almost at the same time when Dr. Izsvk and Professor Hurst made their discovery.**

Dr. Izsvk and Professor Hurst succeeded in going one step further. They were able to identify the switch that regulates HERVH. In hESC cultures they identified a transcription factor called LBP9 as being central to the activity of HERVH in early embryos. Using a reporter system that made cells expressing HERVH via LBP9 glow green, the Berlin and Bath team found that they had purified human ESCs that showed all the hallmarks of nave mouse stem cells.

This transcription factor was not previously known to be important to human stem cells. However, unknown to them at the time, the same transcription factor was shown by Austin Smiths group (University of Cambridge, UK) to have a role in mouse nave cells***.

Our human nave-like cells look remarkably like the mouse ones, and are close to human inner cell mass (ICM), said Jichang Wang (PhD student, MDC), first author of the Nature publication. With our HERVH-based reporter system we can easily isolate nave-like human ESCs from any human ESC culture. These cells grow like the mouse nave stem cells and express many of the same genes such as NANOG, KLF4 and OCT4 that are associated with murine navet. When we knockdown LBP9 or HERVH, these cells no longer resemble nave-like human stem cells, he added.

To explore a potential role in stem cell-based therapeutics, the next task will be to keep these isolated human nave-like stem cells in culture and proliferate them. HERVH would also be particularly useful in identifying optimal conditions for long-term culturing. As HERVH inhibits differentiation, its expression should be transient, otherwise it might be detrimental to normal embryo development. What factors keep this delicate process in balance is yet to be determined.

Read more:

Researchers in Berlin and Bath Identify Nave-Like Human Stem Cells