Up to four in ten cancer cases worldwide could be prevented, a new global analysis has found.

The study examines 30 preventable causes, including tobacco, alcohol, high body mass index, physical inactivity, air pollution, ultraviolet radiation and, for the first time, nine infections that can cause the disease.

Released ahead of World Cancer Day on 4 February, the analysis from the World Health Organization (WHO) and its International Agency for Research on Cancer (IARC) estimates that 37 per cent of all new cancer cases in 2022, around 7.1 million cases, were linked to preventable causes.

Drawing on data from 185 countries and 36 cancer types, the study identifies tobacco as the leading preventable cause of cancer, globally responsible for 15 per cent of all new cancer cases, followed by infections (10 per cent) and alcohol consumption (3 per cent).

Three cancer types, lung, stomach and cervical cancer, accounted for nearly half of all preventable cancer cases in both men and women globally.

Lung cancer was primarily linked to smoking and air pollution, stomach cancer was largely attributable to Helicobacter pylori infection (a bacterial infection of the stomach lining), and cervical cancer was overwhelmingly caused by human papillomavirus (HPV).

Dr André Ilbawi, team lead for cancer control at WHO and author of the study, said: “This is the first global analysis to show how much cancer risk comes from causes we can prevent.

“By examining patterns across countries and population groups, we can provide governments and individuals with more specific information to help prevent many cancer cases before they start.”

The burden of preventable cancer was substantially higher in men than in women, with 45 per cent of new cancer cases in men compared with 30 per cent in women.

In men, smoking accounted for an estimated 23 per cent of all new cancer cases, followed by infections at 9 per cent and alcohol at 4 per cent.

Among women globally, infections accounted for 11 per cent of all new cancer cases, followed by smoking at 6 per cent and high body mass index at 3 per cent.

Dr Isabelle Soerjomataram, deputy head of the IARC Cancer Surveillance Unit and senior author of the study, said: “This landmark study is a comprehensive assessment of preventable cancer worldwide, incorporating for the first time infectious causes of cancer alongside behavioural, environmental and occupational risks.

“Addressing these preventable causes represents one of the most powerful opportunities to reduce the global cancer burden.”

Preventable cancer varied widely between regions.

Among women, preventable cancers ranged from 24 per cent in North Africa and West Asia to 38 per cent in sub-Saharan Africa.

Among men, the highest burden was observed in East Asia at 57 per cent, and the lowest in Latin America and the Caribbean at 28 per cent.

These differences reflect varying exposure to behavioural, environmental, occupational and infectious risk factors, as well as differences in socioeconomic development, national prevention policies and health system capacity.

Memory problems in Alzheimer’s may be linked to disrupted brain replay during rest, new research suggests.

The study, conducted in mice, points to a disrupted brain process that normally helps strengthen and preserve memories.

Researchers say the findings could inform future drugs that target this malfunctioning process and guide tools for earlier detection.

Scientists at University College London (UCL) found that replay events occurred as often in mice with amyloid plaques (protein deposits linked to Alzheimer’s) as in healthy mice, but the underlying patterns were no longer organised.

Instead of reinforcing memories, the coordinated activity of place cells became scrambled.

Dr Sarah Shipley, co-lead author from UCL Cell and Developmental Biology, said: “Alzheimer’s disease is caused by the build-up of harmful proteins and plaques in the brain, leading to symptoms such as memory loss and impaired navigation, but it’s not well understood exactly how these plaques disrupt normal brain processes.

“We wanted to understand how the function of brain cells changes as the disease develops, to identify what’s driving these symptoms.

“When we rest, our brains normally replay recent experiences, this is thought to be key to how memories are formed and maintained.

“We found this replay process is disrupted in mice engineered to develop the amyloid plaques characteristic of Alzheimer’s, and this disruption is associated with how badly animals perform on memory tasks.”

This replay activity takes place in the hippocampus, a region essential for learning and memory. During rest, specific neurons known as place cells activate in rapid sequences that mirror recent experiences.

Place cells, discovered by Nobel Prize-winning UCL neuroscientist Professor John O’Keefe, are neurons that correspond to particular locations.

As a person or animal moves through a space, different place cells fire in sequence. Later, during rest, those same cells typically reactivate in the same order, helping the brain store the experience as a memory.

To study this process, researchers tested how mice performed in a simple maze while recording brain activity at the same time.

Using specialised electrodes, they monitored roughly 100 individual place cells simultaneously as the animals explored and then rested.

This approach allowed the team to compare normal replay patterns with those seen in mice that had developed amyloid pathology associated with Alzheimer’s disease.

The researchers also observed that place cells in affected mice grew less stable over time. Individual neurons stopped reliably representing the same locations, especially after rest periods, which are normally when replay should strengthen memory signals.

These changes had clear behavioural effects.

Mice with disrupted replay performed worse in the maze, frequently revisiting paths they had already explored and appearing unable to remember where they had been.

Professor Caswell Barry, co-lead author from UCL Cell and Developmental Biology, said: “We’ve uncovered a breakdown in how the brain consolidates memories, visible at the level of individual neurons.

“What’s striking is that replay events still occur, but they’ve lost their normal structure. It’s not that the brain stops trying to consolidate memories, the process itself has gone wrong.”

Professor Barry added that the findings may help researchers identify Alzheimer’s earlier or develop treatments that focus on restoring normal replay activity.

Scientists have developed a pancreatic cancer blood test that could detect disease earlier, potentially improving survival if validated in larger studies.

Around 10,500 people are diagnosed with the disease in the UK each year, but it is hard to treat and diagnose.

Because it is often found late, only 10 per cent live longer than five years after diagnosis, with more than half dying within three months of diagnosis.

Researchers from the University of Pennsylvania and the Mayo Clinic say the test could detect pancreatic ductal adenocarcinoma, the most common and one of the most aggressive forms of the disease, in its earliest stages, giving doctors time to treat it and increase patients’ chance of survival.

The team tested stored blood samples from people with pancreatic cancer and from people without it.

They examined two markers already used in medicine, CA19-9 and THBS2.

On their own these are not accurate enough for screening, as CA19-9 can be high in non-cancer conditions such as pancreatitis (inflammation of the pancreas) or bile duct problems, and some people do not produce it because of their genes. THBS2 is a protein linked with tissue changes around tumours.

The researchers discovered two additional proteins in the blood, ANPEP and PIGR, that were higher in people with early pancreatic cancer than in healthy volunteers.

When the team combined all four markers into one test, it correctly identified pancreatic cancer about 92 per cent of the time, at a 5 per cent false-positive rate.

For early-stage cancer, it picked up nearly 8 per cent of cases.

The researchers say the test could be used to screen people at higher risk, such as those with a family history, certain genetic risks, pancreatic cysts or long-term pancreatitis. It also distinguished cancer from non-cancerous conditions like pancreatitis, a key limitation of previous models.

Kenneth Zaret, the study’s lead investigator from the University of Pennsylvania’s Perelman School of Medicine, said: “By adding ANPEP and PIGR to the existing markers, we’ve significantly improved our ability to detect this cancer when it’s most treatable.

“Our retrospective study findings warrant further testing in larger populations, particularly in people before they show symptoms.

“Such ‘prediagnostic’ studies would help determine if the test could be used as a screening tool for people at high risk of developing the disease based on family history, genetic screening results or personal history of pancreatic cysts or pancreatitis.”

However, it could take years before the new blood test has completed the trials and regulatory steps needed for mainstream use.

At present, pancreatic cancer is incurable, with life expectancy just five years from initial diagnosis.

It kills because it aggressively invades nearby organs, blocks the bile and intestinal ducts, and spreads via the blood and lymphatic system to the liver, lungs and abdomen, eventually triggering organ failure.

The pancreas aids digestion and produces hormones, such as insulin and glucagon, which help convert sugar from food into energy. Pancreatic cancer can reduce the gland’s ability to make these hormones, which can lead to unstable blood sugar levels.

Common symptoms include jaundice (yellowing of the skin and eyes), loss of appetite, weight loss, fatigue, a high temperature, feeling or being sick, diarrhoea and constipation.

Research published last year suggested that more than half of patients diagnosed with the six least curable cancers, including lung, liver, brain, oesophageal, stomach and pancreatic, die within a year of diagnosis.

More than 90,000 people are diagnosed with one of these cancers in the UK every year, accounting for nearly half of all common cancer deaths, according to Cancer Research UK.

There are currently no early detection tests and about 80 per cent of people are not diagnosed until the cancer has spread, meaning life-saving treatment is no longer possible.

Last week, Spanish researchers revealed a treatment plan that made pancreatic cancer cells shrink in laboratory mice. However, this requires much more robust testing, meaning it could be years before similar treatments are offered to human patients.