Insight
Study links changing population to low London screening rates

London’s shifting population is holding down breast screening uptake, experts have said, with the capital at 62.8 per cent in 2024, below the NHS’s acceptable 70 per cent threshold.
The London Assembly Health Committee recently heard that the capital faces distinct challenges compared with the rest of the country and that these issues must be addressed.
Josephine Ruwende, a cancer screening lead at NHS England, said frequent moves within the rented sector and the cost-of-living crisis pushing people out of London had made it difficult to reach eligible patients, which she described as “population churn”.
She said: “This is people changing addresses and then not updating their GP, this then affects the invitation process because GP details are used to identify individuals who are eligible.
“In boroughs where we have the highest population churn, we see it strongly associated with lower uptake.”
She noted that even in the wealthiest boroughs there can be high levels of movement, with around 40 per cent of residents changing address within a year.
Such areas also tend to have more people who own second homes or spend long periods abroad, making it harder for the NHS to keep contact details up to date.
As a result, screening invitations may be sent to out-of-date addresses or to people who are overseas.
Leeane Graham, advocacy lead at Black Women Rising, which supports women of colour with a cancer diagnosis, said there were cultural barriers, fear and a mistrust of the health service due to previous experience within communities.
She said: “If you’ve never been for a breast screening before, the thought of having a mammogram can be really, really terrifying.”
Helen Dickens, from Breast Cancer Now, said other reasons included a lack of understanding of breast screening, along with concerns about discomfort, trust and practical issues such as travel.
She said: “We have amazing public transport and we feel that we’ve got great accessibility, but we also know that we don’t have screening centres in every borough.
“We know that for some women that barrier of transport and access will still be a really big reason why they’re not attending screenings.”
NHS London launched its first screening campaign last year in response to the figures, aiming to increase detection at an earlier stage.
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Common cancer marker may play active role in preventing the disease, study finds

Ki-67, a protein used to measure tumour growth, may also help prevent chromosome errors that drive cancer, a study suggests.
The findings could change how scientists view Ki-67, a marker commonly used in breast cancer and other tumours to assess how quickly cancer cells are growing.
Researchers found the protein may help preserve genome stability by maintaining the structural integrity of centromeres, key parts of chromosomes that help ensure DNA is shared correctly during cell division.
The research was led by professor Paola Vagnarelli at Brunel University of London in collaboration with scientists at the University of Edinburgh and the Technical University of Berlin.
Professor Vagnarelli said: “Doctors already measure Ki-67 to see how aggressive a cancer might be. But our results suggest it is actually helping maintain genome stability.
“That means it may be more than a marker. It could potentially also be a therapeutic target.”
The study examined three proteins that attach to chromosomes during cell division and help rebuild the molecular system that tells each new cell what kind of cell it is.
Every human cell carries identical DNA. What makes a liver cell different from a brain cell is which genes are switched on and which are kept inactive.
When a cell divides, that entire system of switches must be rebuilt. The three proteins involved in this process were Ki-67, Repo-Man and PNUTS.
Vagnarelli’s team developed a method that individually removes each protein from a living cell at the precise point of division. Older techniques could not isolate that moment cleanly.
They found that cells rely on all three proteins to reset themselves after division, but each failed in a different way when removed.
Without PNUTS, gene activity spiralled out of control and thousands of genes switched on at once.
Without Repo-Man, cells escaped safety checkpoints that usually stop damaged or abnormal cells from continuing to divide.
“What we didn’t expect was how clean the separation was,” said Vagnarelli.
Each protein fails in its own specific way. There is no redundancy, no safety net. Which means there are three separate points at which this process can go wrong.
“When the system breaks down, cells can emerge with the wrong number of chromosomes. That condition, called aneuploidy, is seen in disorders such as Down syndrome and in many cancers.
“We also found that these chromosome errors can trigger inflammatory signals inside the cell.”
Aneuploidy means a cell has too many or too few chromosomes, which can disrupt normal growth and function.
Inflammatory signals are chemical messages that can make a cell behave as if it is responding to injury or infection.
“These cells behave almost as if they are under attack,” said Vagnarelli.
“The immune response switches on because the genome is unstable.
“That link between chromosome imbalance and inflammation could help explain patterns we see in several diseases.”
The researchers said the findings may help cancer scientists better understand how chromosome instability, loss of gene regulation and cells dividing before they are ready contribute to tumour growth.
They said understanding the normal machinery that prevents these errors may help researchers find ways to push cancer cells into making mistakes they cannot survive.
“We now have a clearer map of the machinery that resets the cell after division,” said Vagnarelli.
“That knowledge gives us a starting point for thinking about new therapeutic approaches.”
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