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Statins may reduce cancer risk through mechanisms separate to cholesterol

Analysis revealed that variants in the HMGCR gene region, which represent proxies for statin treatment, were associated with overall cancer risk, suggesting that statins could lower overall cancer risk.


Cholesterol-lowering drugs called statins may reduce cancer risk in humans through a pathway unrelated to cholesterol, says a study published today in eLife.

Statins reduce levels of LDL-cholesterol, the so-called ‘bad’ cholesterol, by inhibiting an enzyme called HMG-CoA-reductase (HMGCR). Clinical trials have previously demonstrated convincing evidence that statins reduce the risk of heart attacks and other cardiovascular diseases. But evidence for the potential effect of statins to reduce the risk of is less clear.

“Previous laboratory studies have suggested that lipids including cholesterol play a role in the development of cancer, and that statins inhibit cancer development,” explains lead author Paul Carter, Cardiology Academic Clinical Fellow at the Department of Health and Primary Care, University of Cambridge, UK. “However, no trials have been designed to assess the role of statins for in clinical practice. We decided to assess the potential effect of therapy on cancer risk using evidence from human genetics.”

Humans can develop a genetic tolerance for arsenic

There’s no need to fear arsenic poisoning if you grew up in the Argentinian Andes — hundreds of years of drinking arsenic-laced groundwater will have left you with a genetic tolerance for it.

Geneticists from Lund and Uppsala universities had noticed that certain plants and bacteria could live in environments with lots of arsenic, with natural selection favouring a gene known to improve their ability to metabolise the poison. Curious to see if humans could also gain some kind of arsenic immunity, they looked at a group of people who they knew would have been exposed to the poison over many generations — the indigenous peoples of the Argentinian part of the Andes. Sure enough, a higher-than average proportion of people they studied possessed the AS3MT gene, which lets them flush out toxins faster than “normal” people.

The genetic samples tested for the AS3MT gene came from 346 residents of the small, isolated town of San Antonio de los Cobres, located more than 3,700m above sea level in the Andes. Not only does the bedrock in the surrounding area contain a lot of arsenic which gets into the groundwater, but mining operations from the era of Spanish colonisation onwards have released even more arsenic — so both modern people and mummies dating back 7,000 years have had high levels of arsenic found in their hair and internal organs.

Team reprograms CRISPR system in mice to eliminate tumor cells without affecting healthy cells

The CRISPR/Cas9 gene-editing tool is one of the most promising approaches to advancing treatments of genetic diseases—including cancer—an area of research where progress is constantly being made. Now, the Molecular Cytogenetics Unit led by Sandra Rodríguez-Perales at the Spanish National Cancer Research Centre (CNIO) has taken a step forward by effectively applying this technology to eliminate so-called fusion genes, which in the future could open the door to the development of cancer therapies that specifically destroy tumors without affecting healthy cells. The paper is published in Nature Communications.

Fusion genes are the abnormal result of an incorrect joining of DNA fragments that come from two different genes, an event that occurs by accident during the process of cell division. If the cell cannot benefit from this error, it will die and the will be eliminated. But when the error results in a reproductive or survival advantage, the carrier cell will multiply and the genes and the proteins they encode thus become an event triggering tumor formation. “Many and the fusion genes they produce are at the origin of childhood sarcomas and leukaemias,” explains Sandra Rodríguez-Perales, lead co-author of the study now published by the CNIO. Fusion genes are also found in among others prostate, breast, lung and brain tumors: in total, in up to 20% of all cancers.

Because they are only present in tumor cells, fusion genes attract a great deal of interest among the scientific community because they are highly specific therapeutic targets, and attacking them only affects the tumor and has no effect on .

Searching for the Chemistry of Life: Possible New Way to Create DNA Base Pairs

In the search for the chemical origins of life, researchers have found a possible alternative path for the emergence of the characteristic DNA pattern: According to the experiments, the characteristic DNA base pairs can form by dry heating, without water or other solvents. The team led by Ivan Halasz from the Rudjer Boskovic Institute and Ernest Mestrovic from the pharmaceutical company Xellia presents its observations from DESYs X-ray source PETRA III in the journal Chemical Communications.

“One of the most intriguing questions in the search for the origin of life is how the chemical selection occurred and how the first biomolecules formed,” says Tomislav Stolar from the Rudjer Boskovic Institute in Zagreb, the first author on the paper. While living cells control the production of biomolecules with their sophisticated machinery, the first molecular and supramolecular building blocks of life were likely created by pure chemistry and without enzyme catalysis. For their study, the scientists investigated the formation of nucleobase pairs that act as molecular recognition units in the Deoxyribonucleic Acid (DNA).

Our genetic code is stored in the DNA as a specific sequence spelled by the nucleobases adenine (A), cytosine ©, guanine (G) and thymine (T). The code is arranged in two long, complementary strands wound in a double-helix structure. In the strands, each nucleobase pairs with a complementary partner in the other strand: adenine with thymine and cytosine with guanine.

RAADfest 66 minute version for COPL

I will be 49 tomorrow. I always like to find some sort of life extension vid for my birthday. And boy did I hit it. Here comes Bill Faloon to drown you in info. Fruit flies 48% increase at 4:30, George Church at 9:00, C. Elegans 5X increase 15:30, 114 year old blood cells reprogrammed ti pluripotent at 18:40, epigenetics at 22:30, Senile plasma at 24:30, Dr Mike West 4 paragraphs to summarize at 21:00, 44:00 minutes is Vitality in Aging Interventions Trail which anyone can join. Enjoy.

Drones Can Reforest The Planet Faster Than Humans Can

But people need to be kept at the centre of it.


There is more than one reason that we need to reforest Planet Earth. Less than a fifth of Earth’s original forests have survived the rise of humans since the last glaciation, and over half of them are in just five countries (see figure below).

The biggest effect from loss of forests is loss of habitat and the resultant loss of biodiversity, even if you don’t care about climate change. We’re burning billions of acres of pristine Indonesian rain forests to plant palm oil trees (Scientific American) just to get a cooking oil with a better shelf life.

Forest biodiversity encompasses not just trees, but the multitude of plants, animals and microorganisms that inhabit forested areas — and their associated genetic diversity. Over a billion humans depend on dense forests for their survival, although all humans depend on forests in some degree for some aspect of their lives.

Breakthrough discovery in gene causing severe nerve conditions

Researchers have made a breakthrough genetic discovery into the cause of a spectrum of severe neurological conditions.

A research study, led by the Murdoch Children’s Research Institute (MCRI) and gracing the cover of and published in the October edition of Human Mutation, found two new in the KIF1A gene cause rare nerve disorders.

MCRI researcher Dr. Simranpreet Kaur said mutations in the KIF1A gene caused ‘traffic jams’ in , called neurons, triggering a devastating range of progressive brain disorders. KIF1A-Associated Neurological Disorders (KAND) affects about 300 children worldwide.

The world’s first Gattaca baby tests are finally here

Anxious couples are approaching fertility doctors in the US with requests for a hotly debated new genetic test being called “23andMe, but on embryos.”

The baby-picking test is being offered by a New Jersey startup company, Genomic Prediction, whose plans we first reported on two years ago.

The company says it can use DNA measurements to predict which embryos from an IVF procedure are least likely to end up with any of 11 different common diseases. In the next few weeks it’s set to release case studies on its first clients.

Engineers create nanoparticles that deliver gene-editing tools to specific tissues and organs

One of the most remarkable recent advances in biomedical research has been the development of highly targeted gene-editing methods such as CRISPR that can add, remove, or change a gene within a cell with great precision. The method is already being tested or used for the treatment of patients with sickle cell anemia and cancers such as multiple myeloma and liposarcoma, and today, its creators Emmanuelle Charpentier and Jennifer Doudna received the Nobel Prize in chemistry.

While is remarkably precise in finding and altering genes, there is still no way to target treatment to specific locations in the body. The treatments tested so far involve removing or immune system T cells from the body to modify them, and then infusing them back into a patient to repopulate the bloodstream or reconstitute an immune response—an expensive and time-consuming process.

Building on the accomplishments of Charpentier and Doudna, Tufts researchers have for the first time devised a way to directly deliver gene-editing packages efficiently across the and into specific regions of the brain, into immune system cells, or to specific tissues and organs in mouse models. These applications could open up an entirely new line of strategy in the treatment of neurological conditions, as well as cancer, infectious disease, and autoimmune diseases.

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