From UCLA: “Using big data, scientists discover biomarkers that could help give cancer patients better survival estimates”

UCLA bloc

UCLA

June 09, 2016
Stuart Wolpert

1
A SURVIV analysis of breast cancer isoforms developed at UCLA. Blue lines are associated with longer survival times, and magenta lines with shorter survival times. Courtesy of Yi Xing

People with cancer are often told by their doctors approximately how long they have to live, and how well they will respond to treatments, but what if there were a way to improve the accuracy of doctors’ predictions?

A new method developed by UCLA scientists could eventually lead to a way to do just that, using data about patients’ genetic sequences to produce more reliable projections for survival time and how they might respond to possible treatments. The technique is an innovative way of using biomedical big data — which gleans patterns and trends from massive amounts of patient information — to achieve precision medicine — giving doctors the ability to better tailor their care for each individual patient.

The approach is likely to enable doctors to give more accurate predictions for people with many types of cancers. In this research, the UCLA scientists studied cancers of the breast, brain (glioblastoma multiforme, a highly malignant and aggressive form; and lower grade glioma, a less aggressive version), lung, ovary and kidney.

In addition, it may allow scientists to analyze people’s genetic sequences and determine which are lethal and which are harmless.

The new method analyzes various gene isoforms — combinations of genetic sequences that can produce an enormous variety of RNAs and proteins from a single gene — using data from RNA molecules in cancer specimens. That process, called RNA sequencing, or RNA-seq, reveals the presence and quantity of RNA molecules in a biological sample. In the method developed at UCLA, scientists analyzed the ratios of slightly different genetic sequences within the isoforms, enabling them to detect important but subtle differences in the genetic sequences. In contrast, the conventional analysis aggregates all of the isoforms together, meaning that the technique misses important differences within the isoforms.

2
Yi Xing. Courtesy of Yi Xing

SURVIV (for “survival analysis of mRNA isoform variation”) is the first statistical method for conducting survival analysis on isoforms using RNA-seq data, said senior author Yi Xing, a UCLA associate professor of microbiology, immunology and molecular genetics. The research is published today in the journal Nature Communications.

The researchers report having identified some 200 isoforms that are associated with survival time for people with breast cancer; some predict longer survival times, others are linked to shorter times. Armed with that knowledge, scientists might eventually be able to target the isoforms associated with shorter survival times in order to suppress them and fight disease, Xing said.

The researchers evaluated the performance of survival predictors using a metric called C-index and found that across the six different types of cancer they analyzed, their isoform-based predictions performed consistently better than the conventional gene-based predictions.

The result was surprising because it suggests, contrary to conventional wisdom, that isoform ratios provide a more robust molecular signature of cancer patients than overall gene abundance, said Xing, director of UCLA’s bioinformatics doctoral program and a member of the UCLA Institute for Quantitative and Computational Biosciences.

“Our finding suggests that isoform ratios provide a more robust molecular signature of cancer patients in large-scale RNA-seq datasets,” he said.

The researchers studied tissues from 2,684 people with cancer whose samples were part of the National Institutes of Health’s Cancer Genome Atlas, and they spent more than two years developing the algorithm for SURVIV.

According to Xing, a human gene typically produces seven to 10 isoforms.

“In cancer, sometimes a single gene produces two isoforms, one of which promotes metastasis and one of which represses metastasis,” he said, adding that understanding the differences between the two is extremely important in combatting cancer.

“We have just scratched the surface,” Xing said. “We will apply the method to much larger data sets, and we expect to learn a lot more.”

Co-authors of the research are lead author Shihao Shen, a senior research scientist in Xing’s laboratory; Ying Nian Wu, a UCLA professor of statistics; Yuanyuan Wang, and Chengyang Wang, UCLA doctoral students.

The research was funded by the National Institutes of Health (grants R01GM088342 and R01GM105431) and the National Science Foundation (grant DMS1310391). Xing’s research is also supported by an Alfred Sloan Research Fellowship.

See the full article here .

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UC LA Campus

For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

#applied-research-technology, #cancer, #scientists-discover-biomarkers-that-could-help-give-cancer-patients-better-survival-estimates, #ucla, #using-big-data

From U Glasgow: “Scientists identify drugs to target ‘Achilles heel’ of Chronic Myeloid Leukaemia cells”

U Glasgow bloc

University of Glasgow

08 Jun 2016
ali.howard@glasgow.ac.uk
0141 330 6557

elizabeth.mcmeekin@glasgow.ac.uk
0141 330 4831

New research, by the Universities of Glasgow and Manchester, has revealed an ‘Achilles heel’ of Chronic Myeloid Leukaemia (CML) and found drugs to successfully target this weakness and eradicate the disease in mice.

The study*, which is published in Nature today, analysed both CML and normal blood stem cells and found two proteins that were key to the survival of CML stem cells. The group, which has been working on this research for more than six years, then developed a drug combination to simultaneously target these critical proteins and kill the cancer stem cells, while largely sparing normal cells.

The interdisciplinary research team, led by Professor Tessa Holyoake from the University of Glasgow and Professor Tony Whetton from the University of Manchester, used a range of techniques to show that these two proteins (p53 and c-Myc) act as ‘gateway controllers’ in CML.

Guided by the concept of precision medicine (the right drug, at the right time, for the right effect in the patient), the team designed a new treatment to exploit this critical weakness in the cancer. Using CML cells transplanted into mice, the authors demonstrated that drugs targeting these two proteins killed the cells that cause the leukaemia, effectively eradicating the disease.

The results have potential implications for other cancers including acute myeloid leukaemia and brain tumours. The researchers are now keen to build on their work by beginning human trials in patients with drug-resistant CML.

Professor Holyoake, who led the team from the Paul O’Gorman Leukaemia Research Centre, said: “We are certainly excited by the results shown in the study. The research – a fantastic example of precision medicine in action – is at an early stage, but the data we collected has revealed two weaknesses in CML and a potential drug approach to eradicating these key stem cells.

“We also could not have achieved such an excellent result without all the generous stem cell donations from both CML patients and other members of the public, so it is important to say thank you to them.”

The team used a range of techniques in their research including proteomics (the large scale study of quantities, structures and functions of proteins).

Professor Whetton said: “We have found a way to kill leukaemia stem cells which could lead to a cure of chronic myeloid leukaemia instead of managing the disease. We are really excited that our new proteomics approaches helped to achieve this.

“There are so many other diseases where we can use the same proteomics approach to find precision medicine solutions for patients. We have the largest clinical proteomics centre in Europe in Manchester so we really look forward to contributing to this work.”

Current therapy for CML is with tyrosine kinase inhibitors (TKIs) which effectively hold back the disease, but do not cure it. If the therapy is stopped, the leukaemia relapses in the majority of patients, requiring CML patients to remain on treatment for their lifetime. These drugs, as well as being costly to administer, can cause a number of side effects including diabetes and vascular problems. It is the dual issues of cost and toxicity in current CML treatment that has driven this particular piece of research.

Dr Matt Kaiser, Head of Research at Bloodwise, said: “Advances made in treatment for this type of leukaemia have, thanks to research, been one of the great medical success stories of recent years, with the transformation of a usually fatal cancer into a lifelong manageable condition for most patients. The only hope of a permanent cure at the moment is a gruelling stem cell transplant, which doesn’t always work and would not be suitable for many patients to even consider. Although it’s early days, these hugely significant findings suggest that targeted drugs could be developed to cut the cancer off at its roots while sparing healthy cells, providing hope of more effective and kinder treatments.”

Dr Áine McCarthy, senior science information officer at Cancer Research UK, said: “By recognising the important roles p53 and MYC play in helping chronic myeloid leukaemia stem cells to survive, this study has identified two new ways to target and kill these cells. Excitingly, this early-stage laboratory work also showed that two experimental drugs which target the effects of these molecules can kill CML stem cells in mice. The next step will be to test if this combination works the same way in people, and if it is safe to use.”

The study, ‘Dual targeting of p53 and c-Myc selectively eliminates leukaemic stem cells’ is published in Nature. The research was funded by Bloodwise, Cancer Research UK, The Howat Foundation, Roche, Constellation Pharmaceuticals, the Medical Research Council (MRC), the Scottish Government Chief Scientist Office, Friends of Paul O’Gorman, and the British Society for Haematology start-up fund.

About the Research

The research team used an unbiased approach to their work, which involved a series of laboratory tests complemented with computational analyses and proteomics. Human stem cell samples were collected from CML donors and tested against donated stem cells from healthy individuals.

After gathering protein and RNA data from CML and healthy cell types, they used computational analyses to identify the likely protein interactions controlling CML stem cells. The proteins p53 and c-Myc were revealed as controllers in cancer but not in the normal stem cells. Using CML cells transplanted into mice they demonstrated that drugs targeting this dual hub killed the CML stem cells.

About CML

CML is a blood cancer affecting less than 1% of the population with more than 700 new patients diagnosed in the UK each year. It causes the body to make too many white blood cells, which over time fill the bone marrow and reduce the number of healthy white blood cells.

As a result of CML sufferers surviving longer (85% live for more than five years after being diagnosed) there is a growing economic cost associated with current therapy costing between 40,000 and 70,000 Euros for one patient per year in Europe.

CML was also the first cancer found to have a genetic mutation. As a result science has used CML as a learning model to understand how other cancers work, and importantly how patients become resistant to drug therapy.

*Science paper:
There is no link to the science paper in the article. I have requested a link. If I get a link I will update the article.

See the full article here .

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U Glasgow campus

The University of Glasgow (Scottish Gaelic: Oilthigh Ghlaschu, Latin: Universitas Glasguensis) is the fourth oldest university in the English-speaking world and one of Scotland’s four ancient universities. It was founded in 1451. Along with the University of Edinburgh, the University was part of the Scottish Enlightenment during the 18th century. It is currently a member of Universitas 21, the international network of research universities, and the Russell Group.

In common with universities of the pre-modern era, Glasgow originally educated students primarily from wealthy backgrounds, however it became a pioneer[citation needed] in British higher education in the 19th century by also providing for the needs of students from the growing urban and commercial middle class. Glasgow University served all of these students by preparing them for professions: the law, medicine, civil service, teaching, and the church. It also trained smaller but growing numbers for careers in science and engineering.[4]

Originally located in the city’s High Street, since 1870 the main University campus has been located at Gilmorehill in the West End of the city.[5] Additionally, a number of university buildings are located elsewhere, such as the University Marine Biological Station Millport on the Island of Cumbrae in the Firth of Clyde and the Crichton Campus in Dumfries.

Alumni or former staff of the University include philosopher Francis Hutcheson, engineer James Watt, philosopher and economist Adam Smith, physicist Lord Kelvin, surgeon Joseph Lister, 1st Baron Lister, seven Nobel laureates, and two British Prime Ministers.

#applied-research-technology, #cancer, #scientists-identify-drugs-to-target-achilles-heel-of-chronic-myeloid-leukaemia-cells, #u-glasgow

From Science Alert: “Scientists have performed the first trials of a ‘universal cancer vaccine’ “

ScienceAlert

Science Alert

2 JUN 2016
FIONA MACDONALD

1
Cancer Research UK via Henry Scowcroft/YouTube

It’s really happening.

Scientists just took a big, “very positive” step towards developing what could be the first ‘universal cancer vaccine’.

The results from early trials in humans, along with research in mice, have just been published, and they suggest that the new technique could be used to activate patients’ immune systems against any type of tumour, no matter where it is in the body.

Unlike the vaccines we’re familiar with, this potential vaccine would be given to patients who already have cancer, rather than those at risk of getting it. It basically works by shooting tiny ‘darts’ containing pieces of RNA extracted from the patient’s cancer cells at the body’s own immune system, convincing them to launch an all-out attack on any tumours they come across.

By just changing the RNA inside those darts, the team can, in theory, mobilise the immune system against any kind of cancer. “[Such] vaccines are fast and inexpensive to produce, and virtually any tumour antigen can be encoded by RNA,” the team, led by researchers at Johannes Gutenberg University of Mainz in Germany, reports in Nature.

“Thus, the nanoparticulate RNA immunotherapy approach introduced here may be regarded as a universally applicable novel vaccine class for cancer immunotherapy.”

Immunotherapy, which involves using the patient’s own immune system to attack cancer, isn’t in itself new – researchers are already using it against different cancer types with great results.

But until now, researchers have mostly done this by genetically engineering special, cancer-targeting immune cells in the lab, and then injecting them back into a patient – which is a time-consuming and expensive process.

The difference with this technique is that the vaccine is made in the lab, and it introduces the cancer DNA into the immune cells within the body, which is a lot less invasive. It also means that the vaccine can be tweaked to hunt a range of cancer types.

So why isn’t the immune system naturally taking out these cancer types?

“One reason is that cancer cells are similar in many ways to normal cells and the immune system avoids attacking the self,” explain Dutch immunologists Jolanda de Vries and Figdor in a commentary accompanying the Nature paper.

That means that when you develop a vaccine, you need to use an antigen – a foreign molecule that works like a ‘mugshot’ for the immune system – that’s not expressed in normal cells, too.

“Only relatively modest immune responses occur with vaccines containing antigens that are also expressed on healthy tissue,” write de Vries and Carl Figdor. “Strong immune responses can be expected only when cancer cells express antigens that are not usually expressed in normal adult cells.”

It’s this kind of cancer-specific antigen that the new vaccine is designed to deliver to the immune system. It works by coating the cancer RNA in a simple, fatty acid membrane, and giving it a slightly negative charge.

This means that once the vaccine is injected into a patient, it’s drawn via electric charge towards dendritic immune cells in the spleen, lymph nodes, and bone marrow.

These dendritic cells then ‘show’ the cancer RNA to the body’s T cells and, to anthropomorphise the situation, pretty much tell them, “Hey, this is the guy we’re after, go get him.” The goal is that the T cells will then go out and mass murder all the cancer cells in the body.

And this is what early research by the German team has demonstrated in mice. Once injected with the vaccine, the immune system was able to fight “aggressively growing” tumours, the research found.

Of course, many results in mice don’t translate to humans, so we can’t get too excited just yet.

The team has also now trialled a version of the vaccine in three patients with melanoma. The point of the trial was only to test whether the vaccine was safe to use in humans, not whether it was effective, and so far, the results are promising. The side effects were limited to flu-like symptoms, which is better than most chemotherapy treatments.

The team is now waiting 12 months for follow-up results from this safety trial, and if all goes well, will start a larger clinical trial after that to see if the vaccine really works.

“By combining laboratory-based studies with results from an early-phase clinical trial, this research shows that a new type of treatment vaccine could be used to treat patients with melanoma by boosting the effects of their immune systems,” Aine McCarthy, the senior science information officer at Cancer Research UK, told The Telegraph.

“Because the vaccine was only tested in three patients, larger clinical trials are needed to confirm it works and is safe, while more research will determine if it could be used to treat other types of cancer.”

Although it’s still very early days, we have another reason to feel hopeful about the future of cancer treatment. And that’s always a good thing.

See the full article here .

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From UCLA: “Researchers prove lung cancer mutations can be detected in saliva”

UCLA bloc

UCLA

June 08, 2016
Brianna Aldrich

1
The EFIRM machine was developed at UCLA. EZLife BioSciTech Co., Ltd

IMPACT

Confirming that saliva is just as accurate as biopsied tissues to detect treatable cancer mutations is a major step forward in the field of salivary diagnostics. Collecting and analyzing saliva is a non-invasive, inexpensive method in the early detection of many types of cancer. Lung cancer patients can particularly benefit from this method as lung cancer tends to be diagnosed in advanced stages and may be mistaken for other problems.

METHOD

Researchers from the UCLA School of Dentistry and their collaborators performed a double-blind study on 37 people who have non-small cell lung cancer at three lung cancer centers in Chengdu, China. For each person, pre- and post-biopsy samples were collected for tissue and saliva cells. The researchers began by cataloging the biopsied plasma cells (from the lungs) using digital polymerase chain reaction. Next, the team cataloged the saliva cells using a proprietary UCLA-developed technology, called electric field-induced release and measurement (EFIRM) liquid biopsy, to see whether they could detect the same mutations as they did with the plasma cells.

They were looking for epidermal growth factor receptor (EGFR) mutations, which are early cellular signals for cancer. More specifically, they were looking for epidermal growth factor receptor L858R and exon 19del — two types of cancer mutations.

FINDINGS

The team found saliva detection correctly predicted the mutations in all 37 pre- and post-surgery saliva samples with 100 percent accuracy. The biopsied tissue predicted mutations with 70 percent accuracy. Furthermore, they found that the mutation signals in saliva were cleaner than in the biopsied tissue for L858R; and the tissue and saliva samples had clean separation for exon 19del.

“This study has confirmed the performance of EFIRM liquid biopsy using as little as 40 microliters of saliva for detecting EGFR mutations,” said Dr. David Wong, lead author on the study and the associate dean for research at the UCLA School of Dentistry. “We are confident that EFIRM liquid biopsy is just as effective at detecting cancer mutations as the current dPCR method of testing tissue. The results from this study show that we are even closer to using saliva to detect cancer mutations; and that saliva can be just as accurate as tissue.”

BACKGROUND

According to the World Health Organization, lung cancer is the leading cause of cancer deaths worldwide. In the United States alone, there are projected to be 225,000 new cases diagnosed in 2016. There is also a growing concern about the rise of lung cancer in women and in Asian countries where the frequency of cancer mutations is three times higher.

The clinical gold standard for detecting non-small cell lung cancer mutations is to perform a tissue biopsy. However, performing a biopsy incurs the risk of puncturing a lung, and for elderly patients the recovery time is long and difficult.

AUTHORS

Other authors on the study were Fang Wei and Yong Kim from the UCLA School of Dentistry; David Chia from the UCLA Department of Pathology and Laboratory Medicine; Wei Liao from EZLife BioSciTech Co., Ltd.; Ziding Feng from the University of Texas MD Anderson Cancer Center; Dr. Youlin Qiao from Peking Union Medical College and Dr. Qinghua Zhou from Sichuan University.

Wong is the Felix and Mildred Yip Endowed Chair in Dentistry and the director for UCLA Center for Oral/Head & Neck Oncology Research at the UCLA School of Dentistry. He is also a member of the UCLA Jonsson Comprehensive Cancer Center.

PRESENTATION

Wong presented the team’s findings at the American Society of Clinical Oncology’s 2016 Annual Meeting on June 4. Prototypes of point-of-care and reference lab high-throughput platforms were on display at the exhibit hall at ASCO 2016.

DISCLOSURE

David Wong is co-founder of RNAmeTRIX Inc., a molecular diagnostic company. He holds equity in RNAmeTRIX, and serves as a company director and scientific advisor. The University of California also holds equity in RNAmeTRIX. Intellectual property that Wong invented and which was patented by the University of California has been licensed to RNAmeTRIX. Wong is a consultant to GlaxoSmithKlein, PeriRx, Wrigley and Colgate-Palmolive.

See the full article here .

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UC LA Campus

For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

#applied-research-technology, #cancer, #researchers-prove-lung-cancer-mutations-can-be-detected-in-saliva, #ucla

From EPFL: “Portable probes hunt down cancer cells during surgery”

EPFL bloc

École Polytechnique Fédérale de Lausanne EPFL

08.06.16
Laure-Anne Pessina


Access mp4 video here .
Light, wireless probes the size of a large pen have been developed to identify cancer cells and suspicious lymph nodes during surgery. The probes, which EPFL helped develop, are now being tested by surgeons at the University Hospital of Lausanne (CHUV) and across Europe.

When surgeons remove a malignant tumor, they have to be sure to get all the cancer cells. Just as crucial, they have to determine whether the tumor has already sent micrometastases into the neighboring lymph nodes on the way to the rest of the body.

EPFL, in partnership with Forimtech and the CHUV, developed two compact, light and wireless probes that help doctors with both of these tasks. The Gamma probe improves on similar devices already in use in radioguided surgery, while the Beta probe is a totally new type of device able to detect extremely small bits of cancerous tissue.

The two probes, measuring 20 centimeters long and weighing barely 100 grams, are easy to work with and to insert into the surgical wound. The probes guide the surgeon with auditory signals similar to those of a Geiger counter, accurately locating what the human eye often cannot see.

Hunting down malignant cells

The Beta probe is based on a new concept of particle detection. It identifies the presence of even minute quantities of cancer cells from the main tumor. After removing the tumor, the surgeon will use the probe to see if there is any residual cancer tissue.

The probe works by searching for positrons, which are given off by a tracer substance that, once administered to the patient, attaches itself to cancer cells. Positrons can only travel through one millimeter of tissue. When they are found, cancer cells cannot be far away.

The Beta probe reduces the risk of complications and helps prevent the disease from spreading further. Because it pinpoints unhealthy cells, surgeons are able to preserve as much healthy tissue as possible. The device is still in the clinical test phase. A three-year effectiveness study on 60 patients is under way at the CHUV.

Looking for sentinel lymph nodes and metastases

The Gamma probe represents an improvement on an existing technology. It doesn’t detect cancer cells directly, but it finds the sentinel lymph node near the main tumor. This is the lymph node that cancer cells first reach before spreading to the rest of the body. It is removed and examined by doctors to determine the stage of the disease and identify the most appropriate treatment.

“With the Gamma probe, we can remove just the sentinel lymph node. And if it turns out to be free of cancer cells, that means the tumor hasn’t spread,” said Maurice Matter, a surgeon at the CHUV.

The probe that EPFL helped develop is lighter, more accurate and easier to use than competing devices, and it finds the sentinel lymph node more quickly.

Miniaturizing the electronics

In the case of both probes, the role of EPFL’s researchers was to design the device and miniaturize the electronics. “The system has to be solid enough to withstand sterilization,” said Edoardo Charbon, the director of the Advanced Quantum Architecture Lab (AQUA). “The probe has a little window at one end that picks up the gamma rays or positrons given off by the substance injected into the patient. A scintillator converts the energy of the rays into photons, which are then detected by a highly sensitive sensor.”

The probes, which were given the CE mark in March 2015, have already been used in around 30 operations at the CHUV. Starting this year, testing will be rolled out to hospitals across Europe.

—–
The probes were developed as part of a CTI project (Commission for Technology and Innovation) by three partners: Forimtech (whose founders are from CERN), which contributed its expertise in particle detection, the CHUV, which contributed its clinical expertise, and EPFL, which contributed its expertise in microelectronics and VLSI design.

See the full article here .

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EPFL is Europe’s most cosmopolitan technical university with students, professors and staff from over 120 nations. A dynamic environment, open to Switzerland and the world, EPFL is centered on its three missions: teaching, research and technology transfer. EPFL works together with an extensive network of partners including other universities and institutes of technology, developing and emerging countries, secondary schools and colleges, industry and economy, political circles and the general public, to bring about real impact for society.

#applied-research-technology, #cancer, #epfl, #portable-probes-hunt-down-cancer-cells-during-surgery

From HFCC at WCG: “Help Fight Childhood Cancer Project Researchers Publish a Paper”

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WCGLarge

6 Jun 2016

Summary
The Help Fight Childhood Cancer project searched for a cure for a particular childhood brain cancer. The researchers have found that some of the promising compounds they identified also show an antidepressant capability.

Lay Summary:

The Help Fight Childhood Cancer project researchers have published a paper on serendipitous results they found from the drug candidate search run on World Community Grid. The project originally searched for candidate compounds that targeted specific proteins to help cure a childhood brain cancer called neuroblastoma. Some of the targeted proteins are also involved in several psychological disorders. They have found that some of the identified compounds show an antidepressant capability. Furthermore, additional research might lead to potential treatments for Huntington’s disease and Alzheimer’s disease. The paper was published in the journal Neurochemistry International.

Paper title: Effects of novel small compounds targeting TrkB on neuronal cell survival and depression-like behavior

Authors: Mayu Fukuda, Atsushi Takotori, Yohko Nakamura, Akiko Suganami, Tyuji Hoshino, Yutaka Tamura, Akira Nakagawara

See the full article here.

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World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”

WCG projects run on BOINC software from UC Berkeley.

BOINCLarge

BOINC is a leader in the field(s) of Distributed Computing, Grid Computing and Citizen Cyberscience.BOINC is more properly the Berkeley Open Infrastructure for Network Computing.

BOINC WallPaper

CAN ONE PERSON MAKE A DIFFERENCE? YOU BET!!

“Download and install secure, free software that captures your computer’s spare power when it is on, but idle. You will then be a World Community Grid volunteer. It’s that simple!” You can download the software at either WCG or BOINC.

Please visit the project pages-
OpenZika

Rutgers Open Zika
Zika

Help Stop TB
WCG Help Stop TB

Outsmart Ebola together

Outsmart Ebola Together

Mapping Cancer Markers
mappingcancermarkers2

Uncovering Genome Mysteries
Uncovering Genome Mysteries

Say No to Schistosoma

GO Fight Against Malaria

Drug Search for Leishmaniasis

Computing for Clean Water

The Clean Energy Project

Discovering Dengue Drugs – Together

Help Cure Muscular Dystrophy

Help Fight Childhood Cancer

Help Conquer Cancer

Human Proteome Folding

FightAIDS@Home

World Community Grid is a social initiative of IBM Corporation
IBM Corporation
ibm

IBM – Smarter Planet
sp

#applied-research-technology, #cancer, #help-fight-childhood-cancer-project-researchers-publish-a-paper, #wcg

From SA: “Biden Unveils Major Database to Advance Cancer Research”

Scientific American

Scientific American

June 6, 2016
Bill Berkrot

1
VP Joe Biden. Credit: Marc Nozell/Flickr, CC BY 2.0

A new unified system to facilitate sharing of genomic and clinical data among cancer researchers to help promote advances in personalized treatment for the many forms of the disease was launched on Monday, the U.S. National Cancer Institute said.

Details of the project, known as Genomic Data Commons (GDC), were set to be announced by U.S. Vice President Joe Biden at the American Society of Clinical Oncology meeting in Chicago.

GDC, with an operation center at the University of Chicago, will be a key component of President Obama’s “national cancer moonshot” effort to find cures and his Precision Medicine Initiative, NCI said.

The project will receive funding from $70 million allocated to NCI for cancer genomics projects under the precision medicine initiative, which involves efforts to use advanced genetic information to match individual patients with treatments most likely to help their particular type of cancer.

More and more medicines are being developed that address specific genetic mutations associated with a variety of cancers and tumor types.

GDC will centralize, standardize and make accessible data from large-scale NCI programs such as The Cancer Genome Atlas and an equivalent database for childhood cancers, considered among the largest cancer genomics datasets in the world. The information will be made available at no charge to any cancer researcher.

“The GDC will also house data from a number of newer NCI programs that will sequence the DNA of patients enrolled in NCI clinical trials,” Dr. Louis Staudt of NCI said in a statement.

Georgetown University data scientist Subha Madhavan, who was not involved in the GDC, welcomed the project, given the complexity and vast amounts of information involved.

“The irony of individualized treatment for one patient is that we have to manage billions of bits of information from thousands of others,” Madhavan said in a statement.

“The selection of a precise cancer therapy based on a patient’s molecular profile requires computer-assisted analysis of enormous molecular, clinical, patient history, and pharmacological datasets that often come from very disparate and heterogeneous data sources,” she added.

Data in the GDC, representing thousands of cancer patients and tumors, will be harmonized using standardized software algorithms so that they are accessible and broadly useful to researchers, NCI said.

See the full article here .

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Scientific American, the oldest continuously published magazine in the U.S., has been bringing its readers unique insights about developments in science and technology for more than 160 years.

#applied-research-technology, #biden-unveils-major-database-to-advance-cancer-research, #cancer, #genomic-data-commons-gdc, #scientific-american