Normal cells help corral tumors (left) and when removed lead to expansion of cancers. Credit: Yale University

Scientists have spent decades studying the nature of tumor cells, but few have looked to see what was happening in the surrounding tissue.

When Yale researchers took a closer look at skin cells, they discovered the unaffected neighbor cells are not helplessly awaiting invasion of cancer cells but acting like cellular police, actively correcting tissue flaws created by their aberrant neighbors, the investigators report Aug. 2 in the journal Nature.

"The normal cells can even corral and escort mutant cells out of the tissue and clean up the mess the mutant cells left behind, in order to keep the tissue healthy and functional," said Samara Brown. She and fellow graduate student Cristiana Pineda are lead authors of the study.

"We found a dynamic, active process of correction conserved across different mutational systems and even a mutation-independent model," Pineda added.

The Yale team studied damaged cells or activated oncogenes in mouse tissue and used new live-imaging technology to study behavior of surrounding cells. They found these wild-type cells were necessary for the elimination of tumors, which progressed dramatically in their absence, and for correcting aberrations caused by damaged cells.

Primary funding for the study was provided by the National Institutes of Health and New York Stem Cell Foundation.

Brown and Pineda work in the lab of senior author Valentina Greco, associate professor of genetics, cell biology, and dermatology.

Explore further: A key link between tumors and healthy tissue identified

More information: Samara Brown et al, Correction of aberrant growth preserves tissue homeostasis, Nature (2017). DOI: 10.1038/nature23304

Journal reference: Nature

Provided by: Yale University

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Good cellular neighbors combat incipient cancers - Medical Xpress - Medical Xpress

Altering human heredity? In a first, researchers safely repaired a disease-causing gene in human embryos, targeting a heart defect best known for killing young athletes a big step toward one day preventing a list of inherited diseases.

In a surprising discovery, a research team led by Oregon Health and & Science University reported Wednesday that embryos can help fix themselves if scientists jump-start the process early enough.

It's laboratory research only, nowhere near ready to be tried in a pregnancy. But it suggests that scientists might alter DNA in a way that protects not just one baby from a disease that runs in the family, but his or her offspring as well. And that raises ethical questions.

"I for one believe, and this paper supports the view, that ultimately gene editing of human embryos can be made safe. Then the question truly becomes, if we can do it, should we do it?" said Dr. George Daley, a stem cell scientist and dean of Harvard Medical School. He wasn't involved in the new research and praised it as "quite remarkable."

"This is definitely a leap forward," agreed developmental geneticist Robin Lovell-Badge of Britain's Francis Crick Institute.

Today, couples seeking to avoid passing on a bad gene sometimes have embryos created in fertility clinics so they can discard those that inherit the disease and attempt pregnancy only with healthy ones, if there are any.

Gene editing in theory could rescue diseased embryos. But so-called "germline" changes altering sperm, eggs or embryos are controversial because they would be permanent, passed down to future generations. Critics worry about attempts at "designer babies" instead of just preventing disease, and a few previous attempts at learning to edit embryos, in China, didn't work well and, more importantly, raised safety concerns.

In a series of laboratory experiments reported in the journal Nature, the Oregon researchers tried a different approach.

They targeted a gene mutation that causes a heart-weakening disease, hypertrophic cardiomyopathy, that affects about 1 in 500 people. Inheriting just one copy of the bad gene can cause it.

The team programmed a gene-editing tool, named CRISPR-Cas9, that acts like a pair of molecular scissors to find that mutation a missing piece of genetic material.

Then came the test. Researchers injected sperm from a patient with the heart condition along with those molecular scissors into healthy donated eggs at the same time. The scissors cut the defective DNA in the sperm.

Normally cells will repair a CRISPR-induced cut in DNA by essentially gluing the ends back together. Or scientists can try delivering the missing DNA in a repair package, like a computer's cut-and-paste program.

Instead, the newly forming embryos made their own perfect fix without that outside help, reported Oregon Health & Science University senior researcher Shoukhrat Mitalipov.

We all inherit two copies of each gene, one from dad and one from mom and those embryos just copied the healthy one from the donated egg.

"The embryos are really looking for the blueprint," Mitalipov, who directs OHSU's Center for Embryonic Cell and Gene Therapy, said in an interview. "We're finding embryos will repair themselves if you have another healthy copy."

It worked 72 percent of the time, in 42 out of 58 embryos. Normally a sick parent has a 50-50 chance of passing on the mutation.

Drew Angerer/Getty Images

Previous embryo-editing attempts in China found not every cell was repaired, a safety concern called mosaicism. Beginning the process before fertilization avoided that problem: Until now, "everybody was injecting too late," Mitalipov said.

Nor did intense testing uncover any "off-target" errors, cuts to DNA in the wrong places, reported the team, which also included researchers from the Salk Institute for Biological Studies in California and South Korea's Institute for Basic Science. None of the embryos was allowed to develop beyond eight cells, a standard for laboratory research.

Genetics and ethics experts not involved in the work say it's a critical first step but just one step toward eventually testing the process in pregnancy, something currently prohibited by U.S. policy.

"This is very elegant lab work," but it's moving so fast that society needs to catch up and debate how far it should go, said Johns Hopkins University bioethicist Jeffrey Kahn.

And lots more research is needed to tell if it's really safe, added Britain's Lovell-Badge.

"What we do not want is for rogue clinicians to start offering treatments" that are unproven like has happened with some other experimental technologies, he stressed.

Among key questions: Would the technique work if mom, not dad, harbored the mutation? Is repair even possible if both parents pass on a bad gene?

Mitalipov is "pushing a frontier," but it's responsible basic research that's critical for understanding embryos and disease inheritance, noted University of Pittsburgh professor Kyle Orwig.

In fact, Mitalipov said the research should offer critics some reassurance: If embryos prefer self-repair, it would be extremely hard to add traits for "designer babies" rather than just eliminate disease.

"All we did is un-modify the already mutated gene."

Published at 1:33 PM EDT on Aug 2, 2017

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Scientists Repair Gene in Human Embryos for First Time - NBC New York

In BriefA team of researchers from New York's Albert Einstein College of Medicine just discovered a breakthrough in anti-aging research. Their findings suggest that the brain's hypothalamus is crucial in keeping aging and age-related diseases in check.

Researchers at the Albert Einstein College of Medicine in New York have successfully tested a new procedure on mice that could help keep age-related diseases, and even aging itself, at bay. Reporting their findings in the journal Nature, the researchers discovered the crucial role the hypothalamusthe region of the brain responsible for the bodys hormonal and metabolic processes plays in aging.Click to View Full Infographic

Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging, led researcher Dongsheng Cai said in a press release. They found, however, that the process isnt irreversible.

In order to figure out if the disappearance of stem cells was caused by (or due to) aging, they injected mice with a toxin that killed 70 percent of their neural stem cells. This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal, Cai explained.

In a second experiment, the researchers implanted stem cells ready tobecomefresh neurons into the brains of older mice. This extended the life of the mice by 10 to 15 percent, and kept them physically and mentally fit for several months.

Previously, other researchers have hinted at the role the hypothalamus has in aging though it has never before beenpinpointed quite so clearly.Cais team seems to have provided the missing link, which could significantly pushed anti-aging research forward. It is a tour de force, David Sinclair at Harvard Medical School told The Guardian. Its a breakthrough. The brain controls how long we live.

Research in the field of aging has increased over the last several yearsas scientists warmup to the idea that aging itself is a disease that can, and should,be cured. Perhaps not surprisingly, a lot of these potential treatments have a basis in some function of the brain. One study examines the mitochondria, while others look at drugs that are already being used to treat the effects of aging. Onestudyis even going so far as to explore the anti-aging potential of transfusions using young blood.

For Cais research, the next step is to test the procedure on humans, and the team wants to begin clinical trials soon. However, that may be a ways off yet.Of course humans are more complex, Cai said, also speaking toThe Guardian. However, if the mechanism is fundamental, you might expect to see effects when an intervention is based on it.

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Scientists Successfully Slow Aging in Mice Using Stem Cells - Futurism

Photo Scientists have discovered that even a decapitated planarian flatworm can detect light before it grows back its head and eyes. Credit Kent Wood/Science Source

The planarian flatworm is a smooshed noodle of an organism that can be found all over the planet. It has a triangular head occupied by a rather primitive version of a brain and two black dots for eyes. You can chop off this head, and it will grow back in about a week eyes, brain and all. And you can hack away at the critter until all thats left is a tiny speck of worm dust and the thing will still grow back.

But now this peculiar creature, famous for its regenerative abilities (like when some grew two heads in space), may have another unforeseen idiosyncrasy: It not only reacts to light after decapitation, but it gradually recoups an ability to see finer aspects of light as its eyes and brain grow back. And despite lacking the machinery to see colors, the worm somehow creates a workaround, essentially converting this rainbow colored world to a grayscale, said Akash Gulyani a multidisciplinary scientist at the Institute for Stem Cell Biology and Regenerative Medicine in Bangalore, India, who led the study.

His teams findings, published last week in Science Advances, could offer new opportunities for studying how animals recover after injuries and reveal additional details about function to the story of how animal eyes evolved.

Planarians, like many other organisms across the animal kingdom, have fairly basic eyes, unable to detect color and lacking a lens to focus. The eyes are shaped like cups and lined with cells that detect the presence of light and the direction from which it comes. They send signals to two blobs of cells that constitute a pretty basic brain (some argue the first one). Their view of the world is probably limited to moving shadows, not the clear picture production of a humans cones, rods and lenses.

In the wild, the worms avoid sunlight and the predators and other dangers lurking within it.

And when scientists shined bright lights on the animals in the lab both UV and white, which contains a rainbow of colors or hues they swim away, flapping the sides of their little noodle bodies like wiggly linguine. When given a choice between hues, the worms preferred green over blue and red over green, the scientists found. They werent detecting wavelengths or truly sensing colors, but perceiving one as darker than another, as if representing a deeper, safer depth in the wild, the scientists reasoned.

But decapitated worms still responded to UV light. You wont believe what happened, Dr. Gulyani recalled some students reporting, the samples ran away from the light even though they didnt have heads.

This reflex-like response had been observed by other scientists, but not fully explained. It made sense, because the worms split in half to reproduce, and a blind, brainless tailpiece is vulnerable as its body develops. But as the body parts regenerated, function gradually recovered. With eyes, the worms could detect white light again. And after the brain was fully developed and the connections became strong, the worms regained their fine-tuning abilities. But just how they do this and why they developed the greater complexity is still a mystery.

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Chop Off This Worm's Head and It Can Still Detect Light - New York Times

New York, Aug 3 (IANS) In a discovery that could improve treatments for autoimmune diseases and cancer, researchers have found a way to turn pro-inflammatory cells that boost the immune system into anti-inflammatory cells that suppress it, and vice versa.

When the immune system is imbalanced, either due to overly-active cells or cells that suppress its function, it causes a wide range of diseases, from psoriasis to cancer.

By manipulating the function of certain immune cells, called T cells, researchers could help restore the systems balance and create new treatments to target these diseases.

The new method to reprogramme specific T cells, revealed by scientists at Gladstone Institutes in San Francisco, is a step in that direction.

Our findings could have a significant impact on the treatment of autoimmune diseases, as well as on stem cell and immuno-oncology therapies, said Gladstone Senior Investigator Sheng Ding, who is also a professor at the University of California, San Francisco.

The researchers studied two types of cells called effector T cells, which activate the immune system to defend our body against different pathogens, and regulatory T cells, which help control the immune system and prevent it from attacking healthy parts of its environment.

By drawing on their expertise in drug discovery, Dings team identified a small-molecule drug that can successfully reprogramme effector T cells into regulatory T cells.

The study, published in the journal Nature, describes in detail a metabolic mechanism that helps convert one cell type into another.

This new approach to reprogram T cells could have several medical applications.

For instance, in autoimmune disease, effector T cells are overly activated and cause damage to body.

Converting these cells into regulatory T cells could help reduce the hyperactivity and return balance to the immune system, thus treating the root of the disease.

Our work could also contribute to ongoing efforts in immuno-oncology and the treatment of cancer, explained Tao Xu, postdoctoral scholar in Dings laboratory and first author of the study.

This type of therapy doesnt target the cancer directly, but rather works on activating the immune system so it can recognise cancer cells and attack them, Xu added.

Many cancers take control of regulatory T cells to suppress the immune system, creating an environment where tumours can grow without being detected.

In such cases, the teams findings could be used to transform regulatory T cells into effector T cells to strengthen the immune system so it can better recognise and destroy cancer cells.

This is published unedited from the IANS feed.

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Researchers find how to reprogramme cells in immune system - India.com

Sometimes it baffles scientists how steadily our bodies age throughout the passage of time. It occurs way faster we might expect sometimes. There might be various reasons for the slowing down or becoming fast of the raging process.

So, we often do our best to try to slow down or cheat the aging process using a relatively wider range of therapies, from refining our dietary habits to enduring plastic surgery.

Stem cells are found in a place in our brains called hypothalamus and they might play a vital role in how fast and slow we age.

Dr. Dongsheng Cai, from the Albert Einstein College of Medicine, in New York City, NY, with his team of specialists, has discovered that adding fresh stem cells to the hypothalamus might be effective if you want to delay aging.The results of this study are published in the current issue of Nature.

Previous research conducted at the Albert Einstein College of Medicine had already indicated that the hypothalamus plays a critical role in controlling the aging process.Dr. Cai and his team are now able to find the specific cells that are conscientious for the aging process: neural stem cells also involved in neurogenesis that is, the formation of brand new brain neurons.

The researchers distinguished that the quantity of brain stem cells in the hypothalamus progressively declines with time, and this influences the rapidity at which the aging process proceeds. However, they add that their study has shown that the speed of process can be reduced.

Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging. But we also found that [] [b]y replenishing these stem cells or the molecules they produce, its possible to slow and even reverse various aspects of aging throughout the body.

In their study, the researchers experimented on mice to test the function of neural stem cells. They observed that the quantity of stem cells in mices hypothalamus began to decay at around 10 months old, which, rendering to the scientists, is long before aging becomes evident.

By old age about 2 years of age in mice most of those [stem] cells were gone, notes Dr. Cai.

The subsequent step in the analysis was to experiment for the cause of aging, rather than just correlation, between declining numbers of neural stem cells and the inception of the aging process.To do this, the scientists selectively disordered the related stem cells in middle-aged mice. They detected that, in these mice, onset of aging was much faster than in the controlled specimens, whose neural stem cells were not manipulated.

This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal, says Dr. Cai.

Finally, the researchers wanted to figure out whether introducing a fresh supply of stem cells to the hypothalamus could slow down the aging progression.They introduced brand new stem cells both into the hypothalami of the mice whose stem cells had been disordered, and into those of regular, well middle-aged mice.Dr. Cai and his coworkers established that this action was quite fruitful: in all the mice, the aging procedure was either reduced down, or different aspects of aging were countered altogether.What happens, the researchers concluded, is that the stem cells discharge microRNAs (miRNAs), which are a type of particle(molecule) convoluted in the directive of gene expression.

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Do Stem Cells have the ability to reverse aging process? - Fox Weekly