Brain cancer

IBM’s Watson supercomputer takes aim at brain cancer

IBM’s Watson supercomputer is being re-tasked to help clinicians create personalized treatments for a common form of brain cancer known as glioblastoma. The project, which is a collaboration between IBM and the New York Genome Center (NYGC), hopes to make use of Watson’s artificial intelligence to analyze vast quantities of data in order to suggest a personalized life-saving treatment based on the patient’s individual case.

Over the years, Watson has become faster and more compact. It differs from most ordinary computers in that, rather than simply observing patterns in data, Watson will actively learn and apply information to come to a reasoned hypothesis along with a level of confidence. Thus its cognitive process is more like that of a human being than a conventional computer. Furthermore, with the new Watson Discovery Advisor, the processing power and vast medical knowledge of Watson is accessible to clinicians via the cloud, allowing them to draw on the supercomputer’s analytical prowess from wherever they may be.

This is not the first time that Watson has been tasked with aiding in treatment for individuals suffering from cancer. The supercomputer was recently at work at the Memorial Sloan-Kettering Cancer Center where it aided and received tutelage from the staff, amassing an impressive medical database.

How will it work?
Watson’s general knowledge is about as comprehensive as it gets, having access to the entire volume of Wikipedia as well as a wealth of information from other sources. However, it is Watson’s ability to understand natural language and sift through vast quantities of case studies and articles, learning as it goes, that will be the key to allowing doctors to tailor patient specific treatments. IBM is hoping to utilize the NYGC’s expertise in the field of genomics to further develop and streamline Watson’s cognitive reasoning in the field of oncology.

Watson will interpret genomic data from a set of patients diagnosed with glioblastoma, an aggressive form of brain cancer responsible for the deaths of around 13,000 Americans each year. The cloud-based prototype will attempt to expose the underlying genetic characteristics of this malignant cancer, using a combination of modern genomic analytics and its extensive bio-medical literature database.

Dr. Robert Darnell, CEO, President and Scientific Director of the NYGC, stated regarding the difficulties of targeted treatment that “The real challenge has been making sense of massive quantities of genetic data and translating research findings into better treatments and outcomes for patients.”

This is where Watson excels, applying its substantial computing power to observe gene sequence variations between ordinary and cancerous tumors. It consults clinical records and medical literature as it does so, swiftly giving doctors a variety of treatments to choose from, tailored to the patient’s individual instance of cancer.

Watson’s ability to achieve this task at a much higher speed than is otherwise possible, will prove to be greatly beneficial to those suffering from glioblastoma, as the general prognosis (depending on the spread of the cancer) is often less than one year. Ordinarily a significant portion of this time is spent interpreting the data manually to divine the best course of treatment. However, with Watson’s computing power, this can be achieved in a fraction of the time, allowing clinicians to begin life-saving treatment much sooner.

Dr. John E. Kelly, Senior Vice President and Director of IBM Research, believes that application of the cloud-based system will eventually extend beyond the targeted treatment of glioblastoma, stating that “With this knowledge, doctors will be able to attack cancer and other devastating diseases with treatments that are tailored to the patient’s and disease’s own DNA profiles. This is a major transformation that can help improve the lives of millions of patients around the world.”

The following video outlines how Watson will seek to streamline the current treatment process.

source: gizmag

Brain cancer cure closer to reality

Scientists have identified a mechanism that can help treat brain cancer and a drug that decreases brain tumour growth.

The researchers at the University of Calgary’s Hotchkiss Brain Institute (HBI) have made a discovery that could lead to better treatment for patients suffering from brain cancer.

HBI member V. Wee Yong, PhD and research associate Susobhan Sarkar, PhD, and their team including researchers from the Department of Clinical Neurosciences and the university’s Southern Alberta Cancer Research Institute, looked at human brain tumour samples and discovered that specialized immune cells in brain tumour patients are compromised.

The researchers took this discovery and, in an animal model, identified a drug that is able to re-activate those immune cells and reduce brain tumour growth, thereby increasing the lifespan of mice two to three times.

Our brains normally contain specialized cells, called microglia, that defend against injury or infection. “Microglia are the brain’s own dedicated immune system,” explains Yong. “And in this study, we have formally demonstrated for the first time that these cells are compromised in living brain tumour patients.”

As with other forms of cancer, brain tumours start as individual stem-like cells – called brain tumour initiating cells (BTICs). These cells quickly divide and grow, eventually forming a mass, or tumour. Yong and his team have discovered that the tumour disables microglia, permitting the rapid proliferation of BTICs, which ultimately leads to brain tumour growth.

In addition to discovering this mechanism, Yong and Sarkar also identified a drug – amphotericin B (AmpB) – to reactivate microglia that in an animal model, showed a significant reduction in brain tumour growth.

The study was published in the journal Nature Neuroscience.

Source: Ani news

Hide and seek: Brain cancer cells ‘lose’ mutations to evade cancer drugs

Brain cancer can play a deadly game of hide and seek.

A new study published in the journal Science has revealed that brain cancer cells can actually evade many current cancer drugs – by temporarily scaling down a certain genetic mutation that the drugs target. Additionally, once therapy has stopped, the cancer cells can then intensify the mutation once again.

According to the researchers, this study has huge implications for the future treatment of glioblastoma multiforme (GBM) – a brain cancer that is in desperate need of effective therapies.

“It’s one of the most common types of adult brain cancer and one of the most lethal of all types of human cancers,” study author Dr. Paul Mischel, a member of the Ludwig Institute for Cancer Research and a professor in the department of pathology at the University of California, San Diego, told FoxNews.com. “And there are a number of real challenges [in treatment]. There are no good early detections for the disease, and the tumor cells invade through the brain, so it’s almost completely impossibly to surgically remove the entire tumor.”

Mischel also noted that GBM becomes resistant to modern chemotherapy and radiation treatments relatively quickly.

Recently, alternative cancer drugs have emerged that are capable of targeting specific genetic mutations in cancer cells. About 60 percent of GBM cells express a mutated variant of the epidermal growth factor receptor – also called EGFRvIII.  Found in the extrachromosomal DNA of these cancer cells, EGFRvIII helps to promote tumor growth and proliferation, and many targeted therapies work by targeting and suppressing this specific mutation.

However, these drugs ultimately haven’t translated to better outcomes for GBM patients.

“You would think that drugs that are used to target that receptor would be effective, but the results have been very disappointing,” Mischel said.

In order to better understand why, Mischel and his research team analyzed the genetic makeup of GBM tumors. When they treated the cancer cells with targeted therapies, they found that the pieces of mutant EGFRvIII DNA, which normally float outside the cancer’s chromosomes, temporarily jumped onto an obscure chromosome — where they could “hide” from the drugs. Then, once they ceased treatment, the DNA pieces removed themselves from the chromosome and floated freely once again, promoting cancer cell proliferation.

So in essence, the cancer cells were able to “shut down” the expression of the mutation while the cancer drugs were present in the body.

“This was a real surprise,” Mischel said. “…Those pieces of extra chromosomal DNA ‘disappeared’ when treated with the drug. It’s truly a hide-and-seek mechanism, because when the drug was removed, it jumped back off the chromosome.”

Mischel said it is still not understood exactly how the cancer can detect the presence of the drugs in the body, but the researchers have a few preliminary ideas.

“The mechanism by which the DNA is sensing the drug is really not understand,” Mischel said. “But the theory is that the DNA is sensing the signals that are being sent indirectly by the drug.”

The study’s findings help better explain why GBM becomes resistant to targeted therapies and it may help doctors determine a better course of treatment for patients. Mischel argued that the discovery could completely change how physicians treat patients with other types of cancer as well.

“It’s really a complete paradigm shift in how we begin to think about treating people with targeted therapies,” Mischel said. “…This find has big implications for this disease, because other types of cancers have these mutations present on extra chromosomal DNA….How we dose these tumors could change. The data we have in hand would suggest a very different type of dosage for targeted cancer treatment.”

Source: all voices