Cancer – latest in science and technology | èƵ /subject/cancer/ Science news and science articles from èƵ Mon, 13 Jul 2026 11:19:04 +0000 en-US hourly 1 https://wordpress.org/?v=7.0.1 242057827 Four children with terminal brain cancer saved by new cell therapy /article/2533638-four-children-with-terminal-brain-cancer-saved-by-new-cell-therapy/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Mon, 13 Jul 2026 11:00:28 +0000 /?post_type=article&p=2533638 2533638 5 things to know about sunscreen, according to a skin cancer expert /article/2532744-5-things-to-know-about-sunscreen-according-to-a-skin-cancer-expert/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Mon, 06 Jul 2026 13:00:27 +0000 /?post_type=article&p=2532744
Sunscreen protects your skin, but just how much do you need?
Shutterstock

When the sun is out, many of us reach for sunscreen, but myths and misinformation have left some people confused about when and how to use it, and how to ensure we still get enough vitamin D. , a skin cancer expert at QIMR Berghofer Medical Research Institute in Australia, has led clinical trials looking at the link between sun exposure and skin cancer, and sunscreen use and vitamin D. She also recently led the development of a new that considers how to balance the risks and benefits of sun exposure. Here, she lists five things that everyone should know about sunscreen.

Sunscreen should be used as a last line of defence

Many people think it’s OK to lie on the beach all day in a tiny bikini as long as they rub sunscreen all over their exposed skin and reapply it every 2 hours. They think sunscreen makes them bulletproof. But even if you apply the best sunscreen perfectly, it still lets some ultraviolet (UV) radiation through. If you’re out in the sun for hours, that gradually adds up to a dose that is big enough to cause skin damage. At that point, it doesn’t matter if you apply more sunscreen; the damage is already done.

People often assume that if they reapply sunscreen every 2 hours, they’re sort of starting the protection again, but that’s not how it works. You also need to protect yourself with a hat, sunglasses, rash shirt or other protective clothing, and stay in the shade in the middle of the day. Sunscreen should be considered a last line of defence for the parts of your skin that you can’t easily cover while you’re outdoors, like your hands and neck.

There is good evidence that sunscreen protects against skin cancer and wrinkles

The largest, longest-running study of sunscreen was conducted in the Australian town of Nambour. In 1992, 1600 people in the town were randomised to apply daily sunscreen or continue with their normal sunscreen use, which tended to be minimal. It found that those who applied the daily sunscreen were years down the track.

The researchers also created moulds of the backs of the study participants’ hands to look at damage to the surface of the skin. Those in the daily sunscreen group had compared with those who didn’t. When they were followed up on in 2014, they also had .

The sunscreen to choose is the one you like wearing

It’s no good having sunscreen that sits in your cupboard and doesn’t end up on your skin because you don’t like the feel of it. If you’re going on a hike and you’re going to be out all day, it’s better to wear sunscreen with a high sun protection factor (SPF) of 50+. But it’s harder to get a high-SPF sunscreen that feels really nice, so if you’ll be popping out for only short periods throughout the day, you can choose an SPF 15 or 30 sunscreen. Tinted sunscreens can offer the same protection as normal sunscreens, but only if you apply them thickly. But because these often make the skin look overly tinted, people tend to apply them too thinly. One option is to first put on a thick layer of normal sunscreen, then apply the tinted sunscreen on top of it.

Chemical sunscreens, meaning those that contain organic ingredients such as octocrylene and avobenzone, work by absorbing UV radiation from the sun and converting it to harmless heat. Inorganic sunscreens, also known as mineral or physical sunscreens, contain zinc oxide or titanium dioxide particles. They are often reported to work by reflecting or scattering UV radiation, but they actually , like chemical sunscreens.

Wearing two layers of sunscreen helps to achieve adequate coverage

You get the SPF listed on the bottle only if you apply 2 milligrams of sunscreen per square centimetre of skin, which is around in an average adult. But it’s really hard to apply this amount of sunscreen in one go. One day, I decided to measure it out exactly, and I couldn’t rub it all on; it was too much. So now, I apply one layer, let it sink in while I brush my teeth and do other things, and then a second layer, so I can apply the full recommended amount.

I was born in Armidale, Australia, in the late 1960s and didn’t wear sunscreen as a child, despite my pale skin. I’ve since had three skin cancers removed, the first of which appeared when I was just 29. So now, I am careful to protect my skin.

If you’re diligent with sunscreen, you might need to take a vitamin D supplement

We recently conducted a trial called the Sun-D Study to see whether applying SPF 50+ sunscreen every day affects people’s vitamin D levels. We randomly assigned 639 people to apply SPF 50+ sunscreen as part of their daily morning routine on days when the UV index was forecast to reach 3 or higher, or to use it at their own discretion. After about a year, a – about 46 per cent compared with 37 per cent in the control group. If you wear sunscreen every day, I would advise taking a vitamin D supplement so that you don’t become deficient, especially in winter. I take one myself – they are cheap, safe and effective.

People with dark-coloured skin are at greater risk of developing a vitamin D deficiency. I recently led the development of a new that looked at how to balance the various risks and benefits of sun exposure. It brought together experts from many Australian universities and medical organisations, and it concluded that people with dark-coloured skin need to put on sunscreen only if they plan to spend more than 2 hours outdoors on days with high UV radiation levels. This is in recognition of the fact that melanoma incidence is 30 times lower in people with dark-coloured skin than in those with light-coloured skin, and that vitamin D deficiency poses a greater risk.

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I’m the first person whose life was saved by CRISPR base editing /article/2532296-im-the-first-person-whose-life-was-saved-by-crispr-base-editing/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Tue, 30 Jun 2026 12:00:06 +0000 /?post_type=article&p=2532296
Alyssa Tapley received life-saving CRISPR treatment
Alyssa Tapley
When the bone marrow transplant failed to treat my leukaemia, it was like: this is it, there’s nothing else now. The doctors were telling my parents it was a matter of weeks. Not years, not months, but weeks. I’d just turned 13, and I was thinking: “Oh my gosh, this is my last birthday. I’m never gonna grow up and have a family and do all the things that normal people are completely used to, like those normal, everyday things.” But then we heard about the trial and went down to Great Ormond Street Hospital in London. It was like sci-fi. They were like: “Oh, we’re gonna put some CAR Ts in, and they’re gonna multiply and multiply some more, and go around and fight and kill your all your cancer cells.” It all started after Easter in 2021. When I went back to school after the coronavirus lockdown ended, I was really tired. I found it hard to walk home from school; I was falling asleep during breaks and lunches. Eventually, I was too sick to go to school. Really early one morning, my dad noticed my breathing didn’t sound good, and we ended up in A&E. When they put the monitor on me, they started shouting for help. I was in intensive care with double pneumonia for days, and when I woke up, I found out I’d already been put on chemotherapy for leukaemia – that’s when the immune cells in your blood turn cancerous. Mum and Dad say it took the doctors a few days to work out what was wrong. That might be because I had T-cell leukaemia, which is less common than B-cell leukaemia.
Then it all moved really quickly. I had a month of chemo at Leicester Royal Infirmary. It wasn’t working, so I was put on more intense chemo, but that didn’t work either. So at the end of October, I went to Sheffield Children’s Hospital for a bone marrow transplant. The idea is, you kill off the blood stem cells, including the cancerous ones, and then you replace them with the transplant. I was there for five and a half weeks, and I was like, I’m not spending Christmas in hospital, no. And I did get home for Christmas, but afterwards I got a fever and had to go back to Sheffield. That’s when we found out that the transplant hadn’t worked. There was nothing else the doctors could do. For me, I don’t think it really sunk in at the time. But for Mum and Dad, it was hard. Mum says nothing was harder than not having hope. She and Dad started looking everywhere, trying to find out if there was anything at all that could work, if we could go to other countries. They were looking at remortgaging the house and things. And they kept on hearing about CAR Ts – that’s when you change T-cells so they kill cancerous cells – and how they can work when bone marrow transplants fail. But they soon realised it only works for B-cell leukaemia, because if you make T-cells attack T-cells, they just kill each other. Then my consultant from Sheffield heard about a trial Professor was organising. He was using CRISPR base editing to change the CAR T-cells so they don’t look like T cells anymore and so don’t kill each other. And my consultant was like, my patient might be a really good fit. That’s when we went down to Great Ormond Street to meet Professor Waseem and Doctor , who ran the trial. Mum and Dad weren’t sure about me doing the trial. They were worried it wouldn’t work and I’d spent my last weeks in hospital in pain, when we could do stuff like going to Disneyland instead. But they let me make the decision. I was like, I’m doing it. If it’s not gonna help me, it’s gonna help someone else. I was 13 then, I hadn’t really had a chance to do anything, I wasn’t leaving behind anything, I’d had no impact. So it was a way for me to take control of something that I hadn’t been in control of for such a long time, and to try to make a difference for someone else, even if it didn’t work for me. I had two weeks of conditioning in hospital before I had the CAR T-cells. We had some camera crews film it; it was really amazing. A week later, Dr Chiesa told us they’d multiplied. It was the first sign it was working. Everybody at Great Ormond Street was so great. I made a friend even though we didn’t meet each other for two months, we just texted, and got the nurses and the play specialists to put stuff on each other’s windows. And I had another friend who was next door to me, but unfortunately she wasn’t able to have a bone marrow transplant, so she passed away. After four weeks, they tested my bone marrow, and there was nothing there. There were no blood cells to detect. Two weeks later, there was still nothing there, so we went ahead and did my second bone marrow transplant, to replace the blood stem cells. The hardest part was going home. In the hospital, there was almost always someone around that you could talk to. But then when I went home, I wasn’t allowed out of the house in case I caught something, and I wasn’t allowed to see any of my friends. Mum started going back to work, so it was just me and my dog Holly for almost a year. I’m still in remission, but not everything is resolved. My thyroid is underactive, but that’s because of all the chemo, not because of the CAR Ts. This is why it’s so important to keep pushing it, so maybe someday people won’t have to have this intensive chemo and can go straight on to have CAR Ts. I turned 17 in January. I’m doing my A-levels and learning to drive now, which is a bit scary. I want to get a degree apprenticeship in biomedical science. If I can do half as much for someone as the treatment did for me, it would be amazing. I also get to go to conferences to talk about my experience. At one of them, we met Professor David Liu, who developed base editing. I actually cried when I met him. The video’s quite embarrassing. I’m so pleased and privileged to have the opportunity to go and do these things, and talk about why science is so important, and why research is so important. Without it, I wouldn’t be here. As told to Michael Le Page ]]>
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I have a 100 per cent chance of getting cancer due to a rare gene /article/2532073-i-have-a-100-per-cent-chance-of-getting-cancer-due-to-a-rare-gene/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Fri, 26 Jun 2026 14:00:34 +0000 /?post_type=article&p=2532073

Tracy Hutchinson has a rare mutation of the TP53 gene
Tracy Hutchinson

I started to wonder if something funky was going on when multiple people in my family got cancer around the same time. In 1990, my older sister Rebecca was diagnosed with acute lymphoblastic leukaemia, when she was 21 and I was 14. While she was undergoing rigorous chemo, my mum was diagnosed with breast cancer.

Rebecca passed away in 1994 and then, a couple of years after that, my dad got bowel cancer. While he was undergoing treatment, my mum got cancer in her other breast. She survived that, but then she was diagnosed with oesophageal cancer in 2009. She had major surgery, but it came back and she died six weeks later.

In 2020, my other sister was diagnosed with fast-growing triple-negative breast cancer and I thought, oh my god, there’s something going on here. My sister was tested for the BRCA mutations, variants of the BRCA1 and BRCA2 genes that increase breast cancer risk, and it came back negative.

So then she was tested for a different mutation in a gene called TP53, which is much rarer but even worse. Women with this mutation have , with a 50 per cent chance before the age of 30. It’s called Li-Fraumeni syndrome and it basically means your TP53 gene, which normally functions as a cancer-suppressing gene, is a dud.

When my sister was offered the test, I was like: “What’s Li-Fraumeni syndrome?” It’s not something you ever hear about. The test came back positive and she was extremely distraught. Since it can run in families, I was then offered the test too. I decided to do it because I didn’t want my sister to go through this journey on her own.

I had the test in 2022, when I was 47, and it came back positive. I actually felt at peace with it, which a lot of people find surprising, but it was because I finally felt like I had answers for all the troubles my family has been through. It’s a personal thing, though – my brother, for example, has chosen not to get tested.

After getting the diagnosis, my life changed forever. When you have Li-Fraumeni syndrome, there isn’t an hour where you don’t think about it. It’s always on your mind. Within months of finding out I had the gene, I had a double mastectomy as a preventative measure. They found two ductal carcinomas in situ, early forms of cancer, in my left breast after it was removed.

I live in Sydney, so I was able to join an that is investigating annual whole-body MRI as a way to spot tumours in any location in people with mutations in TP53 or other genes that can cause cancer in multiple organs. I had my first one in 2022 and I was very nervous because I didn’t know if they’d find anything. It was normal, but in the second year, they found a 9-millimetre meningioma – a tumour in the meninges, the layers of tissue covering the brain. Fortunately, it’s benign, but I was very freaked out about it. It was a bit of a gamechanger for me.

I have my annual whole-body MRI every November and my “scanxiety” starts building from around July. I start thinking, is this going to be the year when everything changes? But being part of the study also gives me a sense of reassurance, because it’s designed to pick up cancers at an early stage when they are hopefully still treatable. My sister, who survived her breast cancer, now has annual MRIs too.

In addition to whole-body MRI, I have yearly skin checks with a dermatologist and an annual blood test. Every two years, I also have an endoscopy and colonoscopy. They’ve found polyps, abnormal cell growths that can develop into cancer, in my bowel, which were removed, plus some atypical cells in my oesophagus, which they’re keeping an eye on. I’m also on constant alert for anything unusual in my body. I’ll have a sore shoulder and get nervous because I’ll wonder, is this going to be something?

My geneticist thinks my mum might have had a de novo mutation, a mutation that arises spontaneously in an individual rather than being inherited, in her TP53 gene, which was passed down to me and my sisters. We don’t have children, so there isn’t a risk of us passing it on further.

My partner has been really supportive. After I found out I had the syndrome, he said: “You’ve just got to do what you’ve got to do.” When I had my double mastectomy, I didn’t go down the path of having a breast reconstruction and I was worried I looked like a freak, but he said: “Not at all. Your scars tell your battle.”

I try to stay positive because I figure that everyone has something they’re dealing with, be it a chronic disease or an injury or depression, and this is just my thing to bear. My sister-in-law, for example, recently had a stroke. We all have our things – some are visible and some are not – so we need to be compassionate towards each other. Life isn’t a white picket fence.

As told to Alice Klein

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Phages could enable us to hijack vaccine immunity to kill cancer cells /article/2531700-phages-could-enable-us-to-hijack-vaccine-immunity-to-kill-cancer-cells/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Thu, 25 Jun 2026 09:21:51 +0000 /?post_type=article&p=2531700 2531700 Cervical cancer deaths have plummeted thanks to HPV vaccine /article/2530733-cervical-cancer-deaths-have-plummeted-thanks-to-hpv-vaccine/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Wed, 17 Jun 2026 22:30:22 +0000 /?post_type=article&p=2530733
HPV vaccines have revolutionised cervical-cancer prevention since the first one became available in 2006
Subaas Shrestha/NurPhoto via Getty Images
No women in England aged 20 to 24 died of cervical cancer between 2020 and 2024. This is the first time that zero cervical-cancer deaths have been recorded for this age group, and it’s thanks to the introduction of a vaccine against the human papillomavirus, or HPV. “The results are stunning,” says at Queen Mary University of London. “It’s an awful thing when somebody dies very young from cervical cancer. This is a real triumph for vaccination, a real triumph for science and a real triumph for public health to get that vaccine out there with very high uptake very rapidly.” HPV is spread by several kinds of sexual activity, and many strains genetically modify cells in a way that is extremely likely to cause cancer. Women can get cervical cancer in their twenties because of the virus, and around the world many are still dying because of it. The first HPV vaccine became available in 2006. In the UK, it has been offered to girls aged 12 or 13 since 2008. It’s been offered to boys since 2019, both to protect them from other HPV-triggered cancers – like those affecting the mouth, anus, throat and penis – and to prevent them from infecting others. The study is the first evidence that the HPV vaccine prevents cervical-cancer-related deaths, in addition to dramatically reducing HPV infections and . It may seem obvious that it prevents deaths, but we know that the women who are least likely to get vaccinated are also the least likely to go for screening, says Sasieni. So, there was a worry that the vaccine has mainly been preventing cancers that would have been detected early by screening and successfully treated, but not preventing those that would get missed by screening and therefore be more likely to kill women. Fortunately, . Sasieni and his colleague , also at Queen Mary, have been monitoring cervical-cancer rates and deaths in England, and noticed that between 2020 and 2024 – the most recent data available – there were no deaths among women aged 20 to 24. Based on historical rates, around 23 deaths would be expected. “As far back as I’ve seen data, there’s never been a year with none, and so five years in a row with no deaths is really quite something,” says Sasieni.
The dramatic drop is almost certainly due to the HPV vaccine – around 90 per cent of women in England aged 20 to 24 were vaccinated when they were 12 or 13. “This hugely encouraging news shows the life-saving impact of the HPV vaccine, and it’s incredibly exciting to be able to say to this whole generation: cervical cancer and some other cancers shouldn’t be a risk for you,” says , director of vaccination for the National Health Service (NHS) in England. While this study looked only at cervical cancer, the benefits of this vaccine also apply to other HPV-related cancers. It should also protect against warts on the skin and genital and anal areas in both sexes. Sasieni and Falcaro note that there were some deaths among women aged 25 to 29, but far fewer than would be expected. Altogether, they estimate around 200 lives have already been saved, and this is just the start. “The 200 which we’ve estimated in the paper is really just the tip of the iceberg, because it looks like there’s long-term protection against infection,” says Sasieni. “In the future, 18,000 deaths might be a rough estimate of what we’re preventing so far.” Worldwide, however, uptake of the HPV vaccine is low and the rate of cervical cancer is still rising. Death rates may also rise in the UK because fewer teenagers are getting vaccinated. “The bad news is that the vaccine uptake has fallen quite dramatically since covid,” says Sasieni. “Alongside cervical screening, HPV vaccination is central to the NHS ambition to eliminate cervical cancer by 2040,” says Temmink. “It’s a safe and effective vaccine and we urge everyone eligible to take up the offer when invited.”
Journal reference:

The Lancet

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Vaping after quitting smoking is linked to lung cancer /article/2529853-vaping-after-quitting-smoking-is-linked-to-lung-cancer/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Thu, 11 Jun 2026 09:00:47 +0000 /?post_type=article&p=2529853 2529853 ‘Transformative’ pancreatic cancer drug doubles survival time /article/2528738-transformative-pancreatic-cancer-drug-doubles-survival-time/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Mon, 01 Jun 2026 17:11:12 +0000 /?post_type=article&p=2528738
Menta "Steve" Wallace shows a bottle of daraxonrasib, Revolution Medicine??s pancreatic cancer drug, at his home in The Woodlands, Texas, U.S., May 29, 2026. REUTERS/Danielle Villasana
The drug daraxonrasib is being put forward to treat people with advanced pancreatic cancer in clinics
REUTERS/Danielle Villasana

A daily pill doubles the survival time of people with pancreatic cancer, one of the most aggressive and difficult-to-treat forms of the condition, even after they have stopped responding to chemotherapy. What’s more, the convenient pill has fewer side effects than standard chemotherapy.

“It’s a transformative treatment,” says at University College London, who wasn’t involved in the research. “For decades, [survival outcomes] haven’t changed for pancreatic cancer. [The new treatment] gives you double the amount of time to enjoy your life, be with your family and do things that you would like to do.”

About 70 per cent of people with pancreatic cancer . A combination of no routine screening and vague symptoms, like a sore back, means that the condition is usually spotted when it has spread elsewhere. Standard treatment involves chemotherapy, but even then, most people only survive for about , on average. “The disease is really aggressive and difficult to treat,” says Acedo.

More than 90 per cent of pancreatic cancers are driven by mutations in the KRAS gene, which encodes for a protein known as K-Ras. When the gene is mutated, K-Ras gets stuck in a state that drives cancer cells to divide uncontrollably.

at Memorial Sloan Kettering Cancer Center in New York and her colleagues wondered if a drug called daraxonrasib, which binds to the protein, could dampen its signals and slow the growth of cancer cells.

So the team recruited 500 people with metastatic pancreatic cancer from the US, Europe and Asia, all of whom had stopped responding to an initial round of chemotherapy. They were assigned to two groups: the first took daraxonrasib every day and the second continued to receive standard chemotherapy infusions.

The researchers – who presented at the American Society of Clinical Oncology meeting in Chicago on 31 May – found that the participants in the daraxonrasib group went on to survive for 13.2 months, on average, compared with 6.7 months in the chemotherapy group. “It’s fantastic news,” says Acedo. The treatment is the first in decades to improve survival outcomes among patients with advanced pancreatic cancer, she says.

What’s more, only 1 per cent of the participants in the daraxonrasib group stopped taking the drug due to side effects, such as rash, whereas 11 per cent stopped chemotherapy due to adverse events like fatigue. “A daily pill is also much easier to take than chemotherapy, which involves frequent hospital visits and is invasive,” says Acedo.

The team has submitted the findings to the US Food and Drug Administration, and hopes to get the drug approved for use in people with metastatic pancreatic cancer who have had chemotherapy in the coming months, says O’Reilly.

But it is still far from a cure, says Acedo. “It’s a few extra months, which is really promising, but it’s still not years and they’re still dying of the disease,” says Acedo. Nevertheless, further studies may reveal that combining daraxonrasib with other experimental drugs or chemotherapy could lead to even better outcomes, she says.

The researchers are exploring this in ongoing trials, says O’Reilly. They are also looking at whether daraxonrasib could be used as a first-line therapy in untreated patients, she says.

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Pancreatic cancer halted by virus injection in three patients /article/2528235-pancreatic-cancer-halted-by-virus-injection-in-three-patients/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Fri, 29 May 2026 08:00:56 +0000 /?post_type=article&p=2528235 2528235 3D-printed lymph nodes could widen access to CAR T-cell therapy /article/2528140-3d-printed-lymph-nodes-could-widen-access-to-car-t-cell-therapy/?utm_campaign=RSS|NSNS&utm_content=cancer&utm_medium=RSS&utm_source=NSNS Thu, 28 May 2026 11:00:29 +0000 /?post_type=article&p=2528140 2528140