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Nice.


Researchers from the Genes and Cancer research group at the Bellvitge Biomedical Research Institute (IDIBELL) have identified inactivating mutations in a number of genes that code for HLA-I histocompatibility complex proteins, which are involved in the immune response and can condition the response of lung cancer patients to immunotherapy. The study is a result of the collaboration between several national and international research centers, and has been published in the journal Clinical Cancer Research.

“Initially, we performed a genetic screening of lung cancer tumors using xenograft models, that is, human tumors that grow in mice, to obtain tumors with a low load of normal human cells,” explains Dr. Montse Sanchez-Cespedes, the last author of the paper. Sequencing of the tumors made it possible to identify several mutated genes, including some oncogenes and known tumor suppressor genes, and others that not previously described. “Among the latter, we were particularly interested in the B2M gene for its involvement in the functioning of the immune system, a target of new therapies developed for this type of cancer.”

The new immunotherapy treatments aim to block the activity of certain proteins that inhibit the immune system. In lung cancer, this therapeutic option has yielded hopeful results in about twenty percent of patients. However, the treatment can only be effective if the tumor cell has a functional HLA-I complex.

Antibiotic-resistant superbugs are now killing more people than breast cancer, according to a new data analysis by the UK Sepsis Trust.

According to the British Department of Health, about 5,000 people die each year from drug-resistant infections. But the UK Sepsis Trust and others have criticized these figures for being based on studies conducted in other countries, many of them with flawed methodology.

For the new analysis, the UK Sepsis Trust looked at the Department of Health’s own data to come up with an estimate of 12,000 killed per year by superbugs — more than twice as high as the current estimate.

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Big deal.


Researchers from the Genes and Cancer research group at the Bellvitge Biomedical Research Institute (IDIBELL) have identified inactivating mutations in a number of genes that code for HLA-I histocompatibility complex proteins, which are involved in the immune response and can condition the tesponse of lung cancer patients to immunotherapy. The study is a result of the collaboration between several national and international research centers, and has been published in the journal Clinical Cancer Research.

“Initially, we performed a genetic screening of lung cancer tumors using xenograft models, that is, human tumors that grow in mice, to obtain tumors with a low load of normal human cells,” explains Dr. Montse Sanchez-Cespedes, the last author of the paper. Sequencing of the tumors made it possible to identify several mutated genes, including some oncogenes and known tumor suppressor genes, and others that not previously described. “Among the latter, we were particularly interested in the B2M gene for its involvement in the functioning of the immune system, a target of new therapies developed for this type of cancer.”

This observation was validated at a later stage using a large panel of lung tumors, determining that the frequency of B2M mutations in lung cancer is 6–8%. At the same time, the researchers demonstrated that de novo reintroduction of this gene into cell lines that were deficient in B2M restored the functioning of the HLA-I complex.

Pretty wild.


Researchers of the German Center for Neurodegenerative Diseases (DZNE) have found that “alpha-synuclein,” a protein involved in a series of neurological disorders including Parkinson’s disease, is capable of travelling from brain to stomach and that it does so following a specific pathway. Donato Di Monte and co-workers report on this in the journal Acta Neuropathologica. Their study, carried out in rats, sheds new light on pathological processes that could underlie disease progression in humans.

Alpha-synuclein occurs naturally in the nervous system, where it plays an important role in synaptic function. However, in Parkinson’s disease, dementia with Lewy bodies and other neurodegenerative diseases termed “synucleinopathies,” this protein is accumulated within neurons, forming pathological aggregates. Distinct areas of the brain become progressively affected by this condition. The specific mechanisms and pathways involved in this widespread distribution of alpha-synuclein pathology remain to be fully elucidated. Clinical and experimental evidence suggests however that alpha-synuclein — or abnormal forms of it — could “jump” from one neuron to another and thus spread between anatomically interconnected regions.

Alpha-synuclein lesions have also been observed within neurons of the peripheral nervous system, such as those in the gastric wall. In some Parkinson’s patients, these lesions were detected at early disease stages. “Based on these intriguing observations, it has been hypothesized that the pathological process underlying Parkinson’s disease may actually start in the gastrointestinal tract and then move toward the brain,” Professor Di Monte says. “Our present approach was to look at this long-distance transmission of alpha-synuclein from the opposite perspective, investigating the possibility that alpha-synuclein may travel from the brain to the gut.”

Pretty soon, your smart watch may know you’re sick before you do, according to US scientists. The researchers made an app which tracked health data — such as heart rate and skin temperature — collected by 60 people’s smart watches for up to two years, and found that people’s stats changed when they were getting sick.

The authors say smart watches could also help detect the risk of type 2 diabetes and low oxygen on planes, and that they even helped detect Lyme disease in one of the scientists behind the study.

Smart watches and similar portable devices are commonly used for measuring steps and physiological parameters, but have not generally been used to detect illness.

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I can say that I have seen it all with this for cancer research.


SALT LAKE CITY – Researchers at Huntsman Cancer Institute have successfully used synthetic elephant genes to battle human cancer cells.

The synthetic elephant genes are still in the early phases of research, according to HCI, but show promise.

The HCI said there are 1.6 million new cancer diagnosis every year in the United States. Many across the globe are racing to find a cure, but researchers at Huntsman said elephants already have it figured out.

Nice.


In research that could one day lead to advances against neurodegenerative diseases like Alzheimer’s and Parkinson’s, University of Michigan engineering researchers have demonstrated a technique for precisely measuring the properties of individual protein molecules floating in a liquid.

Proteins are essential to the function of every cell. Measuring their properties in blood and other body fluids could unlock valuable information, as the molecules are a vital building block in the body. The body manufactures them in a variety of complex shapes that can transmit messages between cells, carry oxygen and perform other important functions.

Sometimes, however, proteins don’t form properly. Scientists believe that some types of these misshapen proteins, called amyloids, can clump together into masses in the brain. The sticky tangles block normal cell function, leading to brain cell degeneration and disease.

A small study conducted by researchers at Washington University School of Medicine in St. Louis, the Kresge Eye Institute at Wayne State University in Detroit, and the L.V. Prasad Eye Institute in India was published in the journal Ophthalmology. The research included 20 patients who had surgery for Terson syndrome, a specific type of hemorrhage caused mostly by traumatic injury, such as vehicular collisions. Some of the patients experienced this hemorrhaging in both eyes, thus allowing for the study of 28 eyes.

The procedure used to restore sight in these patients is known as a vitrectomy. The surgery removes the jellylike tissue behind the lens of the eye and replaces it with a saline solution. The patients were split into groups who had the surgery within three months of the hemorrhage and those who received it after the three month mark.

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— longer synthetic DNA accelerates customer discoveries —

SAN FRANCISCO, Calif. – January 10, 2017 – Twist Bioscience, a company accelerating science and innovation through rapid, high-quality DNA synthesis on silicon, today announced that it is now shipping genes up to 3,200 base pairs (3.2 kilobase or kB) in length to Ginkgo Bioworks under their existing supply agreement.

“Twist Bioscience continues to deliver record volumes of the highest-quality DNA to advance our organism engineering efforts, meeting or exceeding our aggressive timelines,” said Jason Kelly, CEO and co-founder of Ginkgo Bioworks. “With the availability of synthetic genes up to 3.2kB from Twist, we are able to expedite the rapid prototyping of organism designs to generate cosmetics, nutritional ingredients, flavors, fragrances and other important ingredients.”

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