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Dubai: Researchers in Spain have achieved something that has never been done before in pancreatic cancer research, completely eliminating tumours in mice without the cancer fighting back. It is early days, but the scientific community is cautiously optimistic.
Why pancreatic cancer is so difficult to treat
No doubt, pancreatic cancer is one of the most devastating diagnoses a person can receive. In Spain alone, more than 10,300 cases are diagnosed every year, and the picture is similarly grim globally. The five-year survival rate, meaning the percentage of patients still alive five years after diagnosis, sits at less than 10%. That figure has barely moved in decades.
The reason survival rates remain so low comes down to two brutal realities. First, the cancer is usually detected very late, when it has already spread. Second, the treatments available tend to stop working within months because the tumour becomes resistant to them, essentially learning how to fight back against the drugs being used.
The KRAS problem
Around 90% of pancreatic cancers are driven by a faulty gene called KRAS. Think of KRAS as a light switch stuck in the “on” position, constantly telling cancer cells to grow and multiply. Scientists developed drugs to block this switch, and these were approved in 2021, marking the first real targeted treatment advance in over 50 years. However, the tumours consistently found ways around these drugs, developing resistance within a matter of months.
The breakthrough: Blocking three points instead of one
A research team led by Dr Mariano Barbacid at Spain’s National Cancer Research Centre (CNIO) decided to tackle the resistance problem differently. Rather than blocking the KRAS pathway at just one point, they blocked it at three simultaneously.
The logic is simple. If you suspend a beam from the ceiling using one rope, it is relatively easy to cut. Fix it at three points and it becomes far harder to bring down. The same principle applies here. By attacking the cancer’s growth pathway at three different points at once, the tumour has far fewer escape routes.
The team used a combination of three treatments together: an experimental KRAS-blocking drug called daraxonrasib, an existing lung cancer drug called afatinib, and a protein degrader called SD36, which essentially destroys the proteins that help cancer cells survive. This triple combination was tested across three different mouse models of pancreatic cancer. In every case, the tumours regressed significantly and permanently, with no meaningful side effects.
What the experts are saying
Dr Pranay Taori, Specialist in Medical Oncology at Aster Hospital in Qusais, welcomed the findings whilst urging measured expectations. “Recent studies in mice have shown promising results by blocking the KRAS pathway at three different points, successfully overcoming resistance and leading to tumour elimination in preclinical models,” he said.
“This research offers renewed hope in a disease that has long been difficult to treat. Although these findings are encouraging, they need confirmation through well-designed human clinical trials.”
Dr Barbacid himself has been equally careful not to overstate what has been achieved. “We are not yet in a position to carry out clinical trials with this triple therapy,” he has stated clearly.
The road from a successful mouse study to an approved human treatment is long and complex. Adapting this triple therapy for use in clinical settings will require significant further research, safety testing and eventually human trials.
However, the researchers believe that if the approach can be validated in humans, it could represent a genuine turning point in how pancreatic cancer is treated, offering patients something that has been in desperately short supply for decades: a realistic reason for hope.
Areeba Hashmi is a trainee at Gulf News.
