More than half a million people are diagnosed with pancreatic cancer around the world each year. For many, the disease is discovered only after it has moved beyond the pancreas. The timing can make a profound difference. In the latest global estimates from the International Agency for Research on Cancer (IARC), more than 530,000 people developed pancreatic cancer in 2024, while more than 490,000 died from it. Although pancreatic cancer is only the 12th most commonly diagnosed cancer worldwide, it ranks sixth as a cause of cancer death.

It is also largely a disease of older adults. In the US, where detailed cancer surveillance data are available, the median age at diagnosis is 71. About two-thirds of patients are at least 65, according to the American Cancer Society.

But age is only part of the problem. Pancreatic cancer can remain difficult to recognise because early disease often causes no obvious symptoms. The pancreas sits deep inside the abdomen, making early tumours difficult to detect through a routine physical examination. When symptoms such as jaundice, weight loss, abdominal or back pain appear, the cancer may already have grown substantially or spread.

That is why researchers are beginning to pursue an idea that changes where the fight against pancreatic cancer starts. Instead of waiting for a tumour to become invasive, they want to identify the abnormal changes that come before it — and stop the disease there. The strategy is called cancer interception.

Why Catching It Early Matters

The numbers show why researchers are looking further upstream. In the latest US SEER data, only about 15% of pancreatic cancer cases are diagnosed while the cancer is still confined to the pancreas. For these patients, the five-year relative survival rate is 43.6%.

Once the cancer has spread to nearby lymph nodes, five-year survival falls to 17%. For patients whose cancer has already metastasised to distant parts of the body, it is just 3.4%. Overall, the five-year relative survival rate is 13.7%. Those figures are not simply statistics about treatment. They explain the urgency behind early detection. If doctors can find pancreatic cancer before it spreads, patients have a substantially better chance of surviving it.

The difficulty is that there is currently no routine screening test recommended for people at average risk. The American Cancer Society notes that no screening test has yet been shown to reduce deaths from pancreatic cancer in the general population. Surveillance is instead considered for people at particularly high risk, such as those with certain inherited genetic risks or strong family histories. So researchers are looking for people who can be watched closely before cancer appears.

Following People Before Cancer Arrives

One of the largest efforts is PRECEDE, a clinical study led by Diane Simeone, director of the Moores Cancer Center at the University of California San Diego Health. The study aims to follow 20,000 people at increased risk of pancreatic cancer. Participants include people with a family history of the disease, certain abnormalities in the pancreas and genetic factors that raise their risk.

More than 12,000 people had enrolled by the time researchers presented an update at the American Association for Cancer Research conference on pancreatic cancer in September. More than 50 pancreatic cancers had been detected among participants, many at early stages.

That makes the study more than an exercise in surveillance. It is creating a group of people who can be followed closely as their pancreatic tissue changes, potentially allowing researchers to see what happens in the period between an abnormality and full-blown cancer.

The researchers are also collecting biological samples to study experimental blood tests that could detect pancreatic cancer earlier. And there is another tool they hope can help: artificial intelligence. Researchers are examining whether AI can identify subtle abnormalities in pancreatic scans before they become apparent to the human eye.

If these approaches work, the goal would be to move diagnosis forward, from the point at which cancer is already established to a much earlier stage in its development. But early detection creates a new question. If doctors find something that could become cancer, can they stop it?

Can the Drug Work Earlier?

A new targeted drug has given scientists another reason to investigate. In August, the US Food and Drug Administration approved daraxonrasib for certain patients with advanced pancreatic cancer. The drug targets KRAS, a protein involved in signals that can drive cancer growth.

In a randomized clinical trial involving 500 patients with advanced pancreatic cancer, median overall survival was 13.2 months for patients receiving daraxonrasib, compared with 6.7 months for those receiving standard chemotherapy.
But the drug’s approval does not mean it can prevent pancreatic cancer.

It is approved for advanced disease. Researchers are interested in what might happen if drugs that target cancer-driving pathways are used much earlier, perhaps when abnormal pancreatic cells have not yet developed into an invasive tumour. That is the central idea behind interception.

Stopping Cancer Early

Treating someone who already has metastatic cancer and treating someone who has a precancerous pancreatic abnormality are completely different medical decisions. For a patient with advanced cancer, the potential benefits of a powerful treatment may justify significant side effects. For someone who has an abnormality that might never become cancer, the calculation is different.

Researchers therefore need to know which precancerous changes are dangerous enough to treat and whether the treatment itself causes more harm than the disease it is intended to prevent. That is why much of the evidence for pancreatic cancer interception is still coming from laboratory and animal studies.

A clue From Mice

At the September AACR meeting, Ben Stanger, a cancer researcher at the University of Pennsylvania, and his colleagues presented research involving mice carrying mutations in the Kras gene. KRAS mutations can activate proteins that promote cancer development. The researchers waited until the mice developed tiny precancerous growths in the pancreas. They then treated the animals with a drug designed to interfere with KRAS and related cancer-promoting proteins.

The treatment improved survival in the mice. The finding matters because it suggests that cancer-driving pathways may be vulnerable even before a pancreatic tumour becomes invasive. The researchers still need to establish whether the same strategy is safe and effective in humans, which patients should receive it, and how early treatment should begin.

From Treating Cancer to Stopping Its Progression

This is what makes cancer interception such a significant shift in pancreatic cancer research. The traditional approach begins after a tumour has formed. Doctors then try to remove it, shrink it or keep it from spreading. Interception moves the starting line. Researchers want to identify the biological changes that put pancreatic cells on the path toward cancer and intervene before that process becomes difficult to reverse.

Simeone’s team is already considering whether therapies such as daraxonrasib could eventually be studied in people after surgery for precancerous pancreatic growths or in patients with very early-stage disease. Such use would require clinical trials; the drug is currently approved for advanced pancreatic cancer. Simeone has estimated that combining earlier detection with interception could potentially raise five-year survival from 13.7% to 50%.

That figure is a research projection, not a demonstrated result.The immediate challenge is much more basic: scientists need to prove that they can reliably identify dangerous pancreatic changes early enough, and that treating them will actually prevent cancer from progressing.

For a disease in which only about 15% of cases in current US data are found while still localized, even finding that window would change the problem researchers are trying to solve. The hope behind cancer interception is therefore not simply to find a better drug for pancreatic cancer. It is to change the moment at which doctors have to fight it, from after it has spread to before it has a chance to become invasive.

The human brain looks like one organ. Its history may tell a different story. A Stanford Medicine study has found that the front and back of the developing brain arise from two separate populations of brain cells, following different developmental paths from the earliest stages of embryonic development.

The finding challenges a long-standing idea that the entire brain grows from a common pool of progenitor cells. It may also solve a problem that has frustrated researchers for years: why some of the neurons that keep us breathing and swallowing have been so difficult to grow in the laboratory. The study was published in Nature Neuroscience on September 18.

Two paths, One Brain

Long before a brain takes shape, its cells begin making choices about what they will become. The Stanford researchers found that one group of early cells, carrying the Otx2 gene, develops into the forebrain and midbrain. A different group, marked by Gbx2, develops into the hindbrain. The two groups do not merge.

They also carry different arrangements of chromatin, the material that packages DNA. Those differences help keep the cells on separate developmental tracks. The hindbrain is not a minor part of the brain. It contains the brain stem and controls functions that keep the body running without conscious effort — breathing, heartbeat, swallowing and other basic processes.

Its neurons are also involved in moving the muscles of the face, tongue and throat. Yet scientists have struggled to make these cells from human stem cells. The new study suggests they may have been starting from the wrong place.

“People are always focused on creating the final cell type, like the neuron,” said Rayyan Jokhai, a graduate student and co-first author of the study. “But it’s important to begin at the earliest stages of embryonic development.”

Brain Cells: From Stem Cells to Working Neurons

The researchers used what they learned about early development to guide human pluripotent stem cells toward a hindbrain fate. It worked. The resulting neurons produced electrical signals and carried molecular markers associated with hindbrain regions involved in facial movement and swallowing.

For researchers studying brain-stem diseases, having these cells in the laboratory could be valuable. In spinal muscular atrophy, motor neurons progressively deteriorate. ALS can damage motor neurons in both the forebrain and hindbrain. As the disease progresses, patients can lose the ability to swallow and, eventually, breathe.

Scientists cannot simply take brain-stem tissue from living patients and watch these neurons deteriorate. Lab-grown human hindbrain neurons could provide another option: researchers can study the cells, investigate what goes wrong and test possible treatments.

An Ancient Split

The story gets older when the researchers look beyond humans. They found the same two-origin pattern in chickens and zebrafish. They also found it in acorn worms, distant relatives of humans.

The pattern appears to reach back more than 550 million years. That suggests the separation is not a recent feature of the human brain. Instead, it may be a very old arrangement inherited from ancestors that lived hundreds of millions of years ago. The researchers propose that evolution brought two ancient neural systems together, eventually producing the integrated brain seen in vertebrates. In other words, what looks like one organ may have a much more complicated family history.

More than a story about brain evolution The finding could reshape how scientists make specialised brain cells in the laboratory. It may also open another line of research. The hindbrain contains neural circuits involved in hunger and appetite, raising questions about its role in metabolic disorders and treatments such as semaglutide.

For now, the Stanford team wants to trace the developmental origins of the spinal cord and understand how diseases such as SMA and ALS damage hindbrain neurons. The cells that eventually become parts of the human brain appear to make fundamentally different choices before there is anything recognisable as a brain. By the time the brain looks like one organ, its cells may already be carrying the history of two very different beginnings.

A new UN report asks us to rethink youth mental health not simply as a matter of individual symptoms, but as a question of the wider ecosystems in which young people live, learn and work.

There is a sentence in the middle of the United Nations’ new report on youth mental health that I have not been able to set down: “There is no ‘cure’ for being human”. Thriving, its authors write, does not mean the absence of hardship. It is a rare admission for an institution whose native idiom is targets and indicators, and it signals something larger than a change of tone.

Youth Mental Health & Well-being in an Uncertain World: A Global Call to Action, produced by the UN Youth Office and the United Nations University International Institute for Global Health and launched in September’s UN General Assembly, asks governments to stop treating young people’s distress mainly as a matter of individual symptoms. Instead it proposes an ecosystem model of 10 linked domains: governance, education, decent work, housing, climate, digital technology, peace, the arts, sport and spirituality. Each can tend or erode a young person’s life.

Youth Mental Health: The Sobering Global Figures

The figures are sobering. One in seven people aged 10 to 19 lives with a mental health condition, and half of these conditions emerge by 18. Suicide remains among the leading causes of death for the young, and close to three-quarters of the world’s suicides occur in low- and middle-income countries. Yet only 56% of countries have a child and adolescent mental health policy, against 81% with adult policies, and most spend less than 2% of their health budgets on mental health.

More telling than the numbers is the report’s philosophical turn. Drawing on Tyler VanderWeele’s flourishing research at Harvard, it insists that well-being belongs to the person and to her world at once: the tree and the forest must both be doing well. It speaks of relational well-being, of care, connection and community as the ground of collective health, and of each young person as, in some measure, the embodiment of her surroundings.

Flourishing Denied

African readers will recognise this terrain. Umuntu ngumuntu ngabantu; motho ke motho ka batho: a person is a person through other persons. Ubuntu has long held that personhood is not a possession but an achievement of relation, and that no self can flourish in a community that is failing. The report arrives, by way of Harvard, at a truth spoken in isiZulu, isiXhosa and Sesotho for generations. I welcome that convergence, and want to push it further.

In my own work I call this condition flourishing denied: the tearing of the relational webs that hold a life, from the household to the planet. Read this way, much of what we name youth mental illness is not, or not only, a malfunction inside the young person. It is an accurate registration of a world that has come apart around her. The report comes close to saying so. Citing UNICEF, it notes that six in 10 young people faced systemic challenges in the past year, led by economic instability and climate change, and that more than half lack hope for the future. UNESCO, it adds, has found an erosion of young people’s belief in their own futures, rooted in historical injustice. Despair of this kind is not a disorder of perception. It is, very often, perception itself.

This matters because the language of resilience, which the report uses generously, can return the burden to the young. We teach adolescents to regulate their emotions, to breathe, to cope, and then send them out into economies that have no place for them. Resilience is a virtue; it is not a policy. No young person should have to become heroically adaptable to survive conditions a decent society would not impose.

Nowhere is this clearer than at home. In the second quarter of this year Statistics South Africa reported youth unemployment of 47.4% among 15- to 34-year-olds, and more than a third of 15- to 24-year-olds were neither employed nor in education or training. The report cites South African research finding that between 21 and 24.5% of students live with conditions ranging from social anxiety to post-traumatic stress. Set side by side, these figures make the ecosystem model concrete. For many young South Africans, decent work is not one domain among 10; it is the load-bearing wall.

Hope In Its Pages

The report’s most consequential move is to anchor all this in human rights. It recalls the Secretary-General’s insistence that mental health is a right, not a privilege, and General Assembly resolution A/RES/77/300, which defines mental health not by the absence of a condition but by an environment in which dignity is respected. South Africa needs no persuading. Our Constitution guarantees access to health care, adequate housing and a basic education, and an environment not harmful to health or well-being. The report offers a way to read these guarantees together: a student’s panic attack in an overcrowded residence may be a housing question, a safety question and a labour-market question.

There is hope in its pages too. Much of the report’s texture comes from youth-led initiatives, many of them African: peer-support circles, restorative justice networks, arts-based healing, digital helplines. Young people are already building the ecosystems that states have been slow to fund, and the report rightly insists that they be co-authors of the response, not its beneficiaries.

A call to action is only as good as the action it calls forth, and the report is candid that policies on paper have not yet become services on the ground. Its model is a map. What South Africa needs now is the political will to walk it: to budget for mental health, to design labour, housing and education policy with young minds in view, and to resource the young people already doing the work.

There is an isiZulu word I return to often: ngisazophumelela, I will yet succeed; I am still becoming. It is not a statement of certainty but a grammar of persistence, a future tense spoken from inside difficulty. The question the UN has put to us is whether we will build a world in which it can come true.

Disclaimer: Prof Bohler-Muller writes in her personal capacity and does not necessarily represent the views or position of the University of the Free State.