Treating nerves tumors

The international team of researchers analyzed complete screens of genes and genetic material in malignant peripheral nerve sheath tumors (MPNSTs), and discsovered unknown genetic information about the disease. Researchers show a gene called Lats1/2 suppresses cancer, and losing the gene's expression reprograms cells so they rapidly expand and become cancerous.

Loss of Lats1/2 also causes other genes in the HIPPO signaling pathway (which controls tissue growth) to become hyperactive. These hyperactive genes and their associated proteins (TAZ and YAP) then work with the protein TEAD1 to activate molecular cancer programs that form MPNSTs.

When researchers disrupted overactive TAZ-YAP in mice bred to lack Lats1/2, they also blocked signaling from PDGF (platelet-derived growth factor receptor), which supports tissue growth. These steps reduced the size and number of MPNSTs in the mice. They also inhibited the growth of human MPNST cells in laboratory cultures.

MPNST's develop in what are called Schwann cells. These cells form the myelin sheath. The myelin sheath functions as a protective insulation around peripheral nerves, which connect the brain and spinal cord to extremities and organs and promote transmission of nerve impulses. About half of MPNSTs are linked to mutation of the NF1 gene, which causes a condition called Neurofibromatosis 1.

The other half of MPNSTs have no known genetic origins, and a small proportion of cases can be caused by radiotherapy given to people for cancer treatment. The NF1 gene normally helps control a balanced rate of cell growth. When it mutates, it can cause brown spots on a person or benign tumors along peripheral nerves.

In some cases, NF1 mutation can lead to cases of runaway cell growth, creating very large and sometimes medically problematic plexiform tumors which can turn into MPNSTs. MPNSTs are biologically aggressive tumors and resistant to treatments like chemo and radiation therapy. They're also known for high relapse rates and poor prognosis, often leading to death.
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Protein-like virus essential for memory

A protein involved in cognition and storing long-term memories looks and acts like a protein from viruses. The protein, called Arc, has properties similar to those that viruses use for infecting host cells, and originated from a chance evolutionary event that occurred hundreds of millions of years ago.

The prospect that virus-like proteins could be the basis for a novel form of cell-to-cell communication in the brain could change our understanding of how memories are made, according to Jason Shepherd, Ph.D., a neuroscientist at University of Utah Health.

Researchers suspected that something was different about Arc when his colleagues captured an image of the protein showing that Arc was assembling into large structures. With a shape that resembles a capsule from a lunar lander, these structures looked a lot like the retrovirus, HIV. Prior work had shown that mice lacking Arc forgot things they had learned a mere 24 hours earlier. Further, their brains lacked plasticity.

 There is a window of time early in life when the brain is like a sponge, easily soaking up new knowledge and skills. Without Arc, the window never opens. Scientists had never considered that mechanisms responsible for acquiring knowledge could stem from foreign origins.  A protein important for cognition and memory named Arc can encapsulates genetic material (polyhedron enveloping the ribbon-like strands) and delivers it to brain cells in a manner similar to the way in which viruses infect host cells.

Seeing Arc's unusual propensity to form virus-like structures prompted researchers to scrutinize the protein sequence with a new set of eyes. They found that regions of the code were similar to that from viral capsids. An essential tool for viral infection, capsids carry virus' genetic information and deliver it from cell to cell in its victim.

Given that Arc looks like a viral protein, Shepherd and his colleagues designed a set of experiments to test whether it also acts like one. They first determined that several copies of Arc self-assemble into hollow virus-like capsids and stash its own genetic material, in this case mRNA, inside them. When the scientists added the capsids to mouse brain cells, or neurons, growing in a dish, Arc transferred its genetic cargo into the cells.

After viruses invade host cells, they emerge ready to infect once again. It appears that Arc works in a similar way. The scientists gathered Arc that had been released from mouse neurons and determined that the proteins and their cargo could be taken up by another set of neurons. Unlike for viruses, activating neurons mobilizes Arc, triggering the release of capsids.

A protein involved in cognition and storing long-term memories looks and acts like a protein from viruses, according to research by scientists at University of Utah Health. The protein, called Arc, has properties similar to those that viruses use for infecting host cells and could be the basis for a novel form of communication in the brain. An ancestor to retroviruses, called retrotransposons, inserted its genetic material into the animals' DNA, the event led to the mammalian. The significance of such an event is hinted at by the fact that it happened more than once.
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Ebola virus inhibited in cell cultures

When the Ebola virus enters the human cell, its only purpose is to copy itself, fast. First it must copy all its proteins, then its genetic material. But by inhibiting a specific enzyme we rob the Ebola virus of its ability to copy itself. And that may potentially prevent an Ebola infection from spreading.

When Ebola virus ravaged West Africa, where thousands of people died from the extremely infectious Ebola infection. Once you are infected, all you can do is hope that your own immune system is able to kill the infection, because there is no treatment for Ebola presently.

However, the researchers behind the new study have found what is called a new host factor for Ebola virus. It can be described as a small part of the host's-for example the human body's-own cells, which the Ebola virus uses to copy itself and produce more infection. The virus uses the host factor enzyme PP2A-B56 to start producing proteins. So if the researchers switch off PP2A-B56, the virus' ability to copy itself and produce more infection is never 'switched on.

When we inhibit the PP2A-B56 enzyme, we remove the first link in a long process, which ends with Ebola spreading. The Ebola infection in cell cultures where we have inhibited the PP2A-B56 enzyme is 10 times smaller after 24 hours compared to infections where we have not inhibited this enzyme. But because the researchers have so far focused on cell cultures, there is still work to be done before their results can be used to treat people infected with Ebola.

 Initially the researchers hope to be able to test it on animals and, in the long term, develop a drug that inhibits the relevant enzyme.The potential of the new discovery may turn out to work on other viruses too, because the structure of Ebola virus is very similar to the other filoviruses.
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Viruses share gene with some organisms

A new study finds that viruses share some genes exclusively with cells that are not their hosts, viruses swap genes with a variety of cellular organisms and are agents of diversity. The study looked at protein structures in viruses and across all domains of life: from the single-celled microbes known as bacteria and archaea, to eukaryotes, a group that includes animals, plants, fungi and all other living things.

Viruses that infect archaea and bacteria, for example, are not known to infect eukarya. However, they may still interact in non harmful ways with organisms they do not infect. The team used a bioinformatics approach to analyze the genomes of organisms and the viruses that infect them. Rather than focusing on genetic sequences, which can change over the generations, the team examined the functional components of proteins, which they call folds.

 There are more than 1,400 of folds across all domains of life-has a unique 3-D structure that performs a specific operation. Because folds are critical to protein function, they remain stable even as the sequences that code for them change as a result of mutations or other processes.This makes protein folds reliable markers of evolutionary changes over vast time periods, especially for viruses that mutate notoriously fast.

The researchers found hundreds of folds that are present across all domaind of life and in all types of viruses, which suggests that they came from an ancient ancestor of all life forms. Some folds, however, occur only within a single domain and the viruses that infect it, suggesting a transfer of genetic material only between that group of viruses and their hosts. Out of a total of about 2,000 superfamilies of folds, the team found one that was exclusive to archaea and the viruses that infect archaea, 29 shared only by bacteria and the viruses that infect them, and 37 that are exclusive to eukaryotes and their viruses.

The data also point to other, as yet unknown, mechanisms that allow viruses to exchange genetic material with cells, many virus-hallmark genes in cellular organisms those viruses are not known to infect. People tend to think only about viruses that infect and kill their hosts, we have known for decades that a virus will sometimes enter into a cell and incorporate its genetic material into the cell without killing it. In the case of single-celled organisms, those genes are sometimes passed along to future generations. Human DNA, too, contains remnants of viruses.

Some retroelements and transposons are believed to have originated in ancient viruses. Retroelements are sequences copied from RNA viruses into DNA and inserted into the genomes of nonviral organisms. Transposons, also known as "jumping genes," can move from one part of the genome to another.The team also discovered a large subset of virus-specific protein folds that were not present in any cellular genomes. This suggests that viruses can create new genes and, potentially, transfer those genes to cellular organisms.
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Early signs of cancer

Scientists have discovered how damage to the cell's genetic material can trigger inflammation. Cancerous cells are similar to other cells at early stage, so that they can be removed as part of the body's natural surveillance systems before tumours form.

A key molecule called cGAS is known to bind DNA, triggering inflammation.
When damage occurs, fragments of DNA can get separated from the nucleus and form structures micronuclei.

 cGAS can penetrate these micronuclei and bind to DNA, creating mechanisms that lead to inflammation. DNA damage is one of the early steps in the development of cancer.

Detection of micronuclei by cGAS could be an important early signal to the human body to detect and remove potentially cancerous cells.

Autoinflammatory diseases- when the immune system attacks the body's own tissues can also be an early sign of cancer, this could trigger an inflammatory diseases.
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