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GSK ovarian and womb cancer drug shows promise in early trial

GSK said its ovarian cancer drug shrank or cleared tumours in more than 60 per cent of patients in an early trial as CCO Luke Miels pushes faster development.
The company said that in an early-stage trial, Mocertatug Rezetecan, known as Mo-Rez, shrank or eliminated tumours in 62 per cent of patients with ovarian cancer after chemotherapy had failed, and in 67 per cent of those with endometrial cancer.
Hesham Abdullah, GSK’s global head of cancer research and development, said: “Treatment of gynaecological cancers remains a major challenge, with a pressing need for new therapies that offer improved response rates.
“With Mo-Rez we now have compelling evidence of a promising clinical profile.”
GSK acquired the Mo-Rez treatment, an antibody-drug conjugate, from China’s Hansoh Pharma in late 2023 and has trialled it in 224 patients around the world, including the UK, over the past year.
Only a few patients needed to stop treatment because of side effects, the most common being nausea.
It is given every three weeks by intravenous infusion, meaning directly into a vein.
Combined with data from a separate intermediate trial in China, the results have given the British drugmaker the confidence to go straight to late-stage trials, with five clinical studies planned globally in the next few months, including on patients in the UK.
Speaking to journalists before the conference, Abdullah described Mo-Rez as a “key asset” in the company’s growing cancer portfolio.
It is expected to be a blockbuster drug, with peak annual sales of more than £2bn, which GSK hopes will help it achieve its 2031 sales target of £40bn.
A few years ago GSK did not have any cancer drugs on the market, but it now has four approved medicines and 13 in clinical development.
Last year, oncology generated nearly £2bn in sales, up 43 per cent from 2024, with sales of its endometrial cancer drug Jemperli rising 89 per cent.
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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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