Latest news with #BrunelUniversityofLondon
Newsweek
20 hours ago
- Health
- Newsweek
Early Warning Sign for Aggressive Cancers Discovered
Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. A protein found in our cells could act as an early warning sign for aggressive cancers—and a new target for drugs to stop them spreading. This is the discovery of scientists from Brunel University of London, who have shown for the first time that a protein that helps a cell prepare to divide can also trigger metastasis. High levels of 'SAS-6' makes cells grow more and longer cilia—tiny antennae that sense their surroundings. These cilia activate a pathway known as YAP/TAZ, which controls genes that help tumors grow and spread to other parts of the body, the researchers explained. The SAS-6 protein plays a role in building tiny hair-like structures on the cell's surface, which can then activate signals that make cancer cells more aggressive. Illustration representing lungs and cancer spread inside body. Illustration representing lungs and cancer spread inside body. wildpixel/Getty Images "Our data uncover a novel role for the centriolar protein SAS-6 in ciliogenesis [the building of the cell's antennae], YAP activation and cancer cell invasion," said Brunel biomedical scientist Barbara Tanos in a statement. "The main cause of death in cancer patients is metastatic disease, which happens when cancer cells invade tissues far away from the main tumor [spreading to another part of the body]," Dr Tanos explained. "We found that cells with increased SAS-6 levels became more invasive and that this invasion was reverted by removing cilia." The team investigated what happens when cells produce a version of SAS-6 that does not break down. They found the cells not only grew longer cilia but moved more and noticeably changed shape, becoming flatter and more flexible—all signs of an invasive cell. When the scientists blocked the YAP pathway or removed the cilia, however, the cancer invasion "reduced to almost negligible levels". They then found the same pattern in a real lung cancer cell line, which has high levels of SAS-6. Removing the protein in this patient-derived cell line stopped the cancer's ability to spread. Because several human cancers have unusually high levels of SAS-6, it could potentially be used as a marker for metastatic cancer, the scientists said. Research suggests these SAS-6-associated cancers include lung adenocarcinoma, colorectal cancer and breast cancer, among others. Lung adenocarcinoma (a type of non-small cell lung cancer), for example, is the most common type of lung cancer in the U.S., accounting for 45 percent of all lung cancer cases in 2021, according to the Centers for Disease Control and Prevention (CDC). Understanding how SAS-6 and cilia drive cancer cell invasion could also help design novel therapies based on cilia specific signaling pathways, the researchers explained. "We think this gives us a new way to understand how cellular signals control cancer spread," said Tanos. "It could lead to smarter therapies and better ways to predict which cancers will turn aggressive." Newsweek has reached out to the researchers for comment. Do you have a tip on a health story that Newsweek should be covering? Do you have a question about cancer? Let us know via health@ Reference Hargreaves, E., Collinson, R., Jenks, A. D., Staszewski, A., Tsalikis, A., Bodoque, R., Arias-Garcia, M., Abdi, Y., Al-Malki, A., Yuan, Y., Natrajan, R., Haider, S., Iskratsch, T., Wang, W.-J., Godinho, S., Palaskas, N. J., Calvo, F., Vivanco, I., Zech, T., & Tanos, B. E. (2025). Dysregulated SASS6 expression promotes increased ciliogenesis and cell invasion phenotypes. Life Science Alliance, 8(10).
Canada News.Net
09-08-2025
- Health
- Canada News.Net
Chronic fatigue gene study hailed as breakthrough in UK research
LONDON, U.K.: A significant new study from the University of Edinburgh has found genetic differences in people with chronic fatigue syndrome, offering the strongest evidence yet that the condition has a biological basis. The research, part of the DecodeME project, identified eight regions of the genome that differ between individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and those without. The team says the findings help counter long-standing misconceptions that ME/CFS is psychological or caused by laziness. The results offer "the first robust evidence that genes contribute to a person's chance of developing the disease," the researchers said in a statement. ME/CFS affects an estimated 67 million people globally and is characterized by extreme fatigue, cognitive impairment ("brain fog"), and worsening symptoms after even mild physical or mental exertion. There is currently no diagnostic test or cure. The study analyzed DNA samples from 15,579 people who self-reported ME/CFS symptoms and 259,909 people without, all of European ancestry. Researchers found that several gene variants were more common in the ME/CFS group, particularly those linked to the immune and nervous systems. At least two of the regions are tied to the body's response to infection—supporting reports that ME/CFS symptoms often follow an infectious illness. Another region has been linked to chronic pain, which is also common among people with the condition. "These results will not mean that a test or cure will be developed straight away, but they will lead to a greater understanding," said researcher Andy Devereux-Cooke. "They should prove game-changing in the ME/CFS research field." While the study has not yet been peer-reviewed, it has been hailed as a milestone by patients and scientists alike. Some experts noted limitations, particularly the reliance on self-reported cases rather than formal clinical diagnoses. They called for larger follow-up studies to confirm the findings. "This will take considerable investment in academia and by industry," said Dr. Jackie Cliff, an ME/CFS researcher at Brunel University of London, adding that more work is needed to turn the findings into treatments.
Scottish Sun
08-08-2025
- Entertainment
- Scottish Sun
Maths expert reveals the tips to help you win the entire £172m jackpot TONIGHT
We also reveal the psychology behind picking the 'right' numbers and how to make your own lottery number picking game LOTTO CASH Maths expert reveals the top tips to help you win the ENTIRE £172million EuroMillions jackpot tonight Click to share on X/Twitter (Opens in new window) Click to share on Facebook (Opens in new window) QUIT your job, travel round the world, buy a private island... what would you do with £172million? You'd better get planning, because statistics lottery expert Ben Parker has given us the lowdown on top tips to win tonight's monster Euromillions prize tonight. 3 There's a huge jackpot tonight - and you have to be in it to win it Credit: Getty 3 Stats pro Ben Parker is a whizz at crunching probabilities, and his tips could help YOU bag the mega Euromillions prize Ben Parker is a senior lecturer in statistics at Brunel University of London. He's previously crunched the numbers on how you can use maths to win at the hit TV show The Traitors - but now he's given us the inside scoop on tips that many think could increase your chances of winning the entire top prize. Euromillions is one of the most popular lottery games, so you'll need all the help picking the winning numbers in the bi-weekly battle against other players. You pick five numbers from 1-50 and two lucky stars from 1-12, or you can choose a lucky dip - which is when the numbers are randomly selected for you. The jackpot tonight has rolled over to a huge £172 million. Winning the prize would make you instantly richer than the likes of Adele, Dua Lipa and Harry Kane. Of course, the best way to increase your chances of winning is to buy more tickets - but only do that if you can afford it. Make sure you gamble responsibly and only gamble with money you can afford to lose. Set a money limit before playing. If you need advice, visit or Never pick 'right' numbers Statistically, each number has an equal chance of being drawn. That means that there are no numbers which are more likely to help you win. The trick is to pick numbers that players are least likely to pick. You don't want other people picking your numbers, because if you are lucky enough to win in tonight's game, that will mean you have to split the prize with other players. "The odds of winning the Euromillions is 140million to one," said Ben. "It's really unlikely that you will win, but if you do, you'll want to make sure you're the only one getting the prize." One of the main ways that you can avoid picking other people's numbers is to pick numbers on the left of the grid, and avoid those on the right. That's because studies show that people naturally gravitate towards the right-hand side. That's why retailers often place their higher value items to the right of the store, which is something known in the industry as the "invariant right". Should you buy more tickets? YOU'VE got to be in it to win it. Every time you buy a ticket the odds of winning increase. But WARNING - only spend what you can afford. At the end of the day, it's down to luck. This is why some people prefer to be part of a syndicate, where multiple tickets are bought. While this means you'll have to share the pot, the odds become more favourable each ticket you buy. Avoid "smaller" numbers A common tactic players use to choose their lottery numbers is to pick their "favourite" numbers, Ben said. These numbers tend to be lower numbers. He said: "People tend to pick birthdays, or pick 7 if they were born on the seventh month. "They might pick their children's birthday or their mum's birthday, or how old their dog is - people tend to pick these smaller numbers." If you want to increase your chances of winning the entire jackpot then you should avoid these smaller numbers. A good rule of thumb for what counts as a smaller number is one that falls outside birthdays dates, which are 1-31. So, aim for numbers between 32-50, as fewer people will be picking them. 'I went from living in a council house to bagging a mansion after £105million Euromillions win' BUILDER Steve Thompson treated his family to a lavish £4.5million estate after scooping the giant £105million EuroMillions lottery jackpot. Steve bagged the huge win back in 2019, making him richer than Harry Kane and Cheryl Cole. Neighbours near his imposing 7,000 sq ft farmhouse in Kent include Hollywood actors, rockstars and an IT tycoon. Steve wanted his kids to have their own rooms because they had to share in their previous three-bed council house. The dad-of-three and wife Lenka donated £200,000 in a bid to support their hometown, Selsey, in West Sussex.]The huge cricket fan also gave a whopping £100k to the local club for a new pavilion. Steve also invested a chunk of his win with the late Queen's bank, Coutts & Co. They reportedly put 'tens of millions' into a trust and could be set for another huge windfall in years to come. Steve said: "The kids have finally got their own bedrooms. It's a simple thing but it was all they ever wished for. 'I still haven't got over what happened to us and am honestly still trying to process it still. "It feels like yesterday we were in our old lives — it will take a little while to adjust." The phone book trick When it comes to picking numbers, it is better choose those that are totally random to increase your chances of being the only player with those numbers, Ben said. That's because humans are really good at picking numbers based on a pattern - even if you don't realise you're doing it. So it's better to find another way to do it. Of course, you can pick a lucky dip to do this for you. But there are more fun ways to pick random numbers. Ben suggests picking a random numbers in your contacts list stored in your phone. "Pick random phone numbers in your phone book, and look at the last two digits. "If those two digits are between 32 and 50, then keep it, otherwise pick another random phone number. 3 Make picking your numbers a game Make a game out of picking your numbers randomly - get the kids involved too, as it could be a fun family activity. Balls with numbers printed on them are drawn randomly from a machine to pick the Euromillions numbers. Why not create your own random lottery machine? "You could get a load of ping pong balls, number them, then pick them at random," he said. "If you're worried about the low numbers, don't include those." If you don't have ping pong balls hanging around the house, why not draw numbers from a hat? This won't increase your chances of winning - but it does increase the likelihood of picking random numbers and if you win, you could keep the entire pot. Never use ChatGPT Everyone is using ChatGPT these days - but should you use it to help pick your lottery numbers? You might think that using the handy AI tool is a good way of picking random numbers, but Ben warned against it. He said: "Chat GPT is terrible at maths," he said. "It would just pick random numbers that have been seen elsewhere on the internet. "It would probably pick last week's lucky numbers because it knows those were good - and it will try to please you in some ways."
Time of India
07-08-2025
- Health
- Time of India
UK scientists find genes linked with chronic fatigue syndrome
London: Researchers at the University of Edinburgh said on Wednesday they have discovered differences in the DNA of people with chronic fatigue syndrome that should help dispel the notion that the debilitating condition is psychological or driven by laziness. Their study found eight areas of genetic code that are different in people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) than in healthy volunteers. The finding provides "the first robust evidence that genes contribute to a person's chance of developing the disease," the researchers said in a statement. The key features of the condition include worsening of fatigue, pain and brain fog after even minor physical or mental activity. Very little has been known about the causes of ME/CFS, and there is no diagnostic test or cure. The condition is believed to affect around 67 million people worldwide, the researchers said. The DecodeME study analyzed DNA samples from 15,579 people who reported having chronic fatigue on a questionnaire and 259,909 people without it, all of European descent. Gene variants that were more common in people reporting ME/CFS were linked to the immune and nervous systems, according to a report of the study that has not yet been peer-reviewed. At least two of the gene regions relate to how the body responds to infection, which aligns with reports that the symptoms often start after an infectious illness, the researchers said. Another gene region has previously been identified in people with chronic pain, another common symptom of the condition. The findings "align with decades of patients reporting on their experiences," researcher Andy Devereux-Cooke said in a statement, adding that they "should prove game changing in the ME/CFS research field." "These results will not mean that a test or cure will be developed straight away, but they will lead to a greater understanding," he said. Scientists who were not involved in the study said using volunteers who self-reported chronic fatigue syndrome rather than restricting participation to those with a diagnosis from a medical professional somewhat weakened its conclusions. They called for larger studies to replicate the results. Substantial work will be necessary "to translate these findings into new treatments," said Dr. Jackie Cliff, who studies infection and immunity in ME/CFS at Brunel University of London. "This will take considerable investment in academia and by industry."
GMA Network
06-08-2025
- Health
- GMA Network
UK scientists find genes linked with chronic fatigue syndrome
Researchers at the University of Edinburgh said on Wednesday they have discovered differences in the DNA of people with chronic fatigue syndrome that should help dispel the notion that the debilitating condition is psychological or driven by laziness. Their study found eight areas of genetic code that are different in people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) than in healthy volunteers. The finding provides 'the first robust evidence that genes contribute to a person's chance of developing the disease,' the researchers said in a statement. The key features of the condition include worsening of fatigue, pain and brain fog after even minor physical or mental activity. Very little has been known about the causes of ME/CFS, and there is no diagnostic test or cure. The condition is believed to affect around 67 million people worldwide, the researchers said. The DecodeME study analyzed DNA samples from 15,579 people who reported having chronic fatigue on a questionnaire and 259,909 people without it, all of European descent. Gene variants that were more common in people reporting ME/CFS were linked to the immune and nervous systems, according to a report of the study that has not yet been peer-reviewed. At least two of the gene regions relate to how the body responds to infection, which aligns with reports that the symptoms often start after an infectious illness, the researchers said. Another gene region has previously been identified in people with chronic pain, another common symptom of the condition. The findings 'align with decades of patients reporting on their experiences,' researcher Andy Devereux-Cooke said in a statement, adding that they "should prove game changing in the ME/CFS research field.' 'These results will not mean that a test or cure will be developed straight away, but they will lead to a greater understanding," he said. Scientists who were not involved in the study said using volunteers who self-reported chronic fatigue syndrome rather than restricting participation to those with a diagnosis from a medical professional somewhat weakened its conclusions. They called for larger studies to replicate the results. Substantial work will be necessary 'to translate these findings into new treatments," said Dr. Jackie Cliff, who studies infection and immunity in ME/CFS at Brunel University of London. "This will take considerable investment in academia and by industry.' —Reuters
