New Blood Test Offers Better or Equal Skin Cancer Detection Rate than a Biopsy

Skin cancer is the most common cancer in the world, and it’s the one that’s most easily treated when caught early. Since the blood test is less invasive than a biopsy, this new advance should be helpful in convincing more people to receive treatment early on.

It’s a world first. A newly developed blood test is capable of the early detection of melanoma, with over 80 percent accuracy.

It could help save thousands of lives, according to the Australian Edith Cowan University Melanoma Research Group scientists who developed the test.

Melanoma is the most deadly form of skin cancer, claiming 59,782 lives around the world in 2015. Australasia, North America and Europe are the regions most susceptible to the disease.

There’s good news. If caught early, the survival rate for melanoma climbs to 95 percent. But if you miss that early window, your chances will plummet to below 50 percent. This is what the blood test is designed to help prevent.

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The blood test, called MelDX, works by detecting the antibodies the body produces as soon as melanoma develops. The team analysed 1,627 different types of antibodies, and narrowed them down to a combination of 10 that indicate the presence of melanoma in the body.

They then took blood from 104 people with melanoma and 105 healthy controls, and found that MelDX was capable of detecting melanoma with 81.5 percent accuracy.

More specifically, it was able to detect the cancer in 79 percent of the patients with melanoma; and has a false positive rate in only 16 percent in healthy patients.

The detection rate may actually be a little higher than the accuracy of skin biopsies, which, according to a 2012 study, was 76 percent in an Australian public hospital.

That’s not a perfect result, but it does provide a starting point before other, more invasive tests are embarked on; in conjunction with current diagnostic techniques, it could improve early diagnosis – and therefore people’s chance of survival.

The next step, the researchers said, will be to take MelDX to clinical trial, which is currently being organised, and which could help refine the test.

“We envision this taking about three years. If this is successful we would hope to be able to have a test ready for use in pathology clinics shortly afterwards,” said Melanoma Research Group head Mel Ziman.

“The ultimate goal is for this blood test to be used to provide greater diagnostic certainty prior to biopsy and for routine screening of people who are at a higher risk of melanoma, such as those with a large number of moles or those with pale skin or a family history of the disease.”

Meanwhile, there are easy ways you can help protect yourself from melanoma and other skin cancers, including wearing sunscreen, staying in the shade during the hottest hours of the day, and avoiding UV tanning beds.

Boosting Serotonin Can Speed Learning

I’m sure this research has more implications than currently realized.

Serotonin is thought to mediate communications between neural cells and play an essential role in functional, and dysfunctional, cognition. For a long time, serotonin has been recognized as a major target of antidepressants (selective-serotonin-reuptake-inhibitor (SSRIs) that are used to treat various psychiatric conditions, such as depression, obsessive-compulsive-disorder and forms of anxiety. However, serotonin in humans, and other animals, is associated with a bewildering variety of aspects of cognition and decision-making, including punishment, reward and patience.

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In the experiments, mice were trained to choose one of the two targets to receive water rewards. Mice continually had to learn which of the targets was more rewarding, as the reward rates changed without warning. Crucially, sometimes serotonin release in the brain was temporarily boosted in mice with genetically modified serotonin neurons by a technique called optogenetics, allowing the effects of serotonin on learning to be assessed.

Iigaya built a computational account of mice behaviour based on reinforcement learning principles, which are widely used in machine-learning and AI. Iigaya found that the learning rate, i.e. how fast the modelled mice learn, was modulated by serotonin stimulation. He compared trials with and without stimulation of serotonin neurons, and observed that the learning rate was significantly faster when stimulation was delivered, meaning that boosting serotonin sped up learning in mice.

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The authors conclude: “Our results suggest that serotonin boosts [brain] plasticity by influencing the rate of learning. This resonates, for instance, with the fact that treatment with an SSRI can be more effective when combined with so-called cognitive behavioral therapy, which encourages the breaking of habits in patients.”

Substantial clinical research shows that SSRI treatment is often most effective if combined with cognitive-behavioural-therapy (CBT). The goal of CBT is to change maladaptive thinking and behaviour actively, through sessions that are designed for patients to (re)learn their way to think and behave. However, scientists have had limited understanding of how and why SSRI and CBT work together for treatments. The new findings point to a possible functional link between the two, with serotonin boosting the learning inherent to CBT, providing clues as to one of the roles that this neuromodulator plays in the treatment of psychiatric disorders.

Some Genetic Links of Psychiatric and Neurological Brain Disorders Found

Research to improve the treatments of the future that also highlights how much there is about the human mind that isn’t yet scientifically known.

Today, we use sophisticated methods, such as DNA tests, AI analyses, and high-tech treatments, to understand brain disorders such as depression, Alzheimer’s, and schizophrenia.

But there’s still a lot of really basic stuff about these conditions that we simply don’t understand. That hinders our ability to effectively treat the hundreds of millions of people suffering from psychiatric and neurological illnesses.

In an effort to improve our understanding of brain disorders, an international team of researchers unified under the name the Brainstorm Consortium set out to determine if there’s a genetic link between different disorders.

They published the results of their study this week in the journal Science.

The first step in the study was gathering a lot of data.

First, the researchers pulled data from various genome-wide association studies (GWASs), which look for tiny variations in the human genome that crop up more frequently in people who have a certain disease or disorder than in those who don’t.

In total, the GWASs that the researchers analyzed included data on 265,218 patients with at least one of 25 brain disorders. Ten disorders were psychiatric (major depressive disorder (MDD), schizophrenia, etc.) and 15 were neurological (Alzheimer’s, epilepsy, etc.).

The GWASs also included 784,643 people not diagnosed with any of those disorders to act as control subjects.

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The point of all this data? To find connections that might give the researchers clues about where else to look for information about these brain conditions, especially what they might have in common.

Once they gathered all this data, the Brainstorm Consortium researchers could start to look for those connections.

They discovered that many psychiatric disorders shared the same genome variants. Schizophrenia in particular overlapped significantly with most of the other psychiatric disorders.

The same was not true for the neurological disorders. The researchers believe this suggests that psychiatric conditions are more closely related, at least genetically, than are neurological disorders, which seem to have more distinct genetic causes.

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Ultimately, better understanding the genetic connection between various disorders could improve how we treat them in the future, Pat Levitt, one of the authors of the Brainstorm Consortium’s paper, noted in a news release.

While the authors assert the need for further studies, their international collaboration puts us one step closer to understanding the human brain.

If we’re lucky, that understanding will improve how we treat disorders to such an extent that today’s “high-tech” treatment options will seem antiquated when compared to the treatments of tomorrow.

Research: Depressive Episodes Can Damage Memory

The extent of the damage depends on the severity and length of the depressive episodes. This new research gives a concrete example of why it is important to improve mental health outcomes — it turns out that depression can have directly negative effects on the brain, and there are plenty of implications for human society based on that.

During a depressive episode the ability of the brain to form new brain cells is reduced. Scientists of the Ruhr-Universität Bochum examined how this affects the memory with a computational model. It was previously known that people in an acute depressive episode were less likely to remember current events. The computational model however suggests that older memories were affected as well. How long the memory deficits reach back depends on how long the depressive episode lasts. The team around the computational neuroscientist Prof Dr Sen Cheng published their findings in the journal PLOS ONE on 7th June 2018.

Computational model simulates a depressive brain

In major depressive disorder patients may suffer from such severe cognitive impairments that, in some cases, are called pseudodementia. Unlike in the classic form of dementia, in pseudodementia memory recovers when the depressive episode ends. To understand this process, the scientists from Bochum developed a computational model that captures the characteristic features of the brain of a patient with depressions. They tested the ability of the model to store and recall new memories.

As is the case in patients, the simulation alternated between depressive episodes and episodes without any symptoms. During a depressive episode, the brain forms fewer new neurons in the model.

Whereas in previous models, memories were represented as static patterns of neural activity, the model developed by Sen Cheng and his colleagues views memories as a sequence of neural activity patterns. “This allows us not only to store events in memory but also their temporal order,” says Sen Cheng.

Impact on brain stronger than thought

The computational model was able to recall memories more accurately, if the responsible brain region was able to form many new neurons, just like the scientists expected. However, if the brain region formed fewer new brain cells, it was harder to distinguish similar memories and to recall them separately.

The computational model not only showed deficits in recalling current events, it also struggled with memories that were collected before the depressive episode. The longer the depressive episode lasted the further the memory problems reached back.

“So far it was assumed that memory deficits only occur during a depressive episode,” says Sen Cheng. “If our model is right, major depressive disorder could have consequences that are more far reaching. Once remote memories have been damaged, they do not recover, even after the depression has subsided.”

Developing Drug Impairs Process Cancer Cells Use for Growth

It looks like this will be useful later on.

A drug discovered and advanced by The University of Texas MD Anderson Cancer Center’s Institute for Applied Cancer Science (IACS) and the Center for Co-Clinical Trials (CCCT) inhibits a vital metabolic process required for cancer cells’ growth and survival.

IACS-10759 is the first small molecule drug to be developed from concept to clinical trial by MD Anderson’s Therapeutics Discovery team, which includes IACS and the CCCT. Therapeutics Discovery is a unique group of clinicians, researchers and drug development experts working collaboratively to create new treatment options, including small molecules, biologics, and cell-based therapies.

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Metabolic reprogramming is an emerging hallmark of tumor biology where cancer cells evolve to rely on two key metabolic processes, glycolysis and oxidative phosphorylation (OXPHOS), to support their growth and survival. Extensive efforts have focused on therapeutic targeting of glycolysis, while OXPHOS has remained largely unexplored, partly due to an incomplete understanding of tumor contexts where OXPHOS is essential.

“Through a comprehensive translational effort enabled by collaboration across MD Anderson, we have identified multiple cancers that are highly dependent on OXPHOS,” said Marszalek.

This effort inspired the discovery and development of IACS-10759, a potent and selective inhibitor of OXPHOS. Its advancement to clinical trials was made possible by a multidisciplinary team of more than 25 scientists across Therapeutics Discovery.

“Through this collaborative, 18-month process, we identified and rapidly advanced IACS-10759 as the molecule for clinical development,” said Di Francesco. “We believe IACS-10759 will provide a promising new therapy for cancer patients.”

Cognitive Impairment in Mice With Dementia Reversed

It’s a significant development for treating that disease and those similar to it.

Reversing memory deficits and impairments in spatial learning is a major goal in the field of dementia research. A lack of knowledge about cellular pathways critical to the development of dementia, however, has stood in the way of significant clinical advance. But now, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) are breaking through that barrier. They show, for the first time in an animal model, that tau pathology — the second-most important lesion in the brain in patients with Alzheimer’s disease — can be reversed by a drug.

“We show that we can intervene after disease is established and pharmacologically rescue mice that have tau-induced memory deficits,” explained senior investigator Domenico Praticò, MD, Scott Richards North Star Foundation Chair for Alzheimer’s Research, Professor in the Departments of Pharmacology and Microbiology, and Director of the Alzheimer’s Center at Temple at LKSOM. The study, published online in the journal Molecular Neurobiology, raises new hope for human patients affected by dementia.

The researchers landed on their breakthrough after discovering that inflammatory molecules known as leukotrienes are deregulated in Alzheimer’s disease and related dementias. In experiments in animals, they found that the leukotriene pathway plays an especially important role in the later stages of disease.

“At the onset of dementia, leukotrienes attempt to protect nerve cells, but over the long term, they cause damage,” Dr. Praticò said. “Having discovered this, we wanted to know whether blocking leukotrienes could reverse the damage, whether we could do something to fix memory and learning impairments in mice having already abundant tau pathology.”

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After 16 weeks of treatment, animals were administered maze tests to assess their working memory and their spatial learning memory. Compared with untreated animals, tau mice that had received zileuton performed significantly better on the tests. Their superior performance suggested a successful reversal of memory deficiency.

To determine why this happened, the researchers first analyzed leukotriene levels. They found that treated tau mice experienced a 90-percent reduction in leukotrienes compared with untreated mice. In addition, levels of phosphorylated and insoluble tau, the form of the protein that is known to directly damage synapses, were 50 percent lower in treated animals. Microscopic examination revealed vast differences in synaptic integrity between the groups of mice. Whereas untreated animals had severe synaptic deterioration, the synapses of treated tau animals were indistinguishable from those of ordinary mice without the disease.

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The study is especially exciting because zileuton is already approved by the Food and Drug Administration for the treatment of asthma. “Leukotrienes are in the lungs and the brain, but we now know that in addition to their functional role in asthma, they also have a functional role in dementia,” Dr. Praticò explained.

“This is an old drug for a new disease,” he added. “The research could soon be translated to the clinic, to human patients with Alzheimer’s disease.”

Article Examining Depression

The article mentions standards such as medication and counseling, but perhaps the best way to reduce high depressive rates in the population is to restructure society to make it much better for most people than it is currently.

Clinical depression has surged to epidemic proportions in recent decades, from little-mentioned misery at the margins of society to a phenomenon that is rarely far from the news. It is widespread in classrooms and boardrooms, refugee camps and inner cities, farms and suburbs.

At any one time it is estimated that more than 300 million people have depression – about 4% of the world’s population when the figures were published by the World Health Organization (WHO) in 2015. Women are more likely to be depressed than men.

Depression is the leading global disability, and unipolar (as opposed to bipolar) depression is the 10th leading cause of early death, it calculates. The link between suicide, the second leading cause of death for young people aged 15-29, and depression is clear, and around the world two people kill themselves every minute.

While rates for depression and other common mental health conditions vary considerably, the US is the “most depressed” country in the world, followed closely by Colombia, Ukraine, the Netherlands and France. At the other end of the scale are Japan, Nigeria and China.

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Things have improved since people with mental illness were believed to be possessed by the devil and cast out of their communities, or hanged as witches. But there remains a widespread misunderstanding of the illness, particularly the persistent trope that people with depression should just “buck up”, or “get out more”.

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The WHO estimates that fewer than half of people with depression are receiving treatment. Many more will be getting inadequate help, often focused on medication, with too little investment in talking therapies, which are regarded as a crucial ally.

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There have been positive experiments with both ketamine and psilocybin, the active ingredient in magic mushrooms. Further hopes for a new generation of treatments have been raised by recent discoveries of 44 gene variants that scientists believe raise the risk of depression. Another controversial area of research is treatment for low immunity and mooted links between depression and inflammation.

Countries are increasingly recognising the need to train more psychologists to replace or complement drug treatments.

And perhaps most importantly, there is a cultural movement to make it easier for people to ask for help and speak out about their illness.