The Institute of Cancer Research study reveals breakthrough approach to treating deadly pancreatic cancer

The Institute of Cancer Research study reveals breakthrough approach to treating deadly pancreatic cancer

(IN BRIEF) The Institute of Cancer Research, London, has uncovered a promising new treatment target for pancreatic cancer, identifying the protein SPP1 as a driver of tumour spread and poor survival. In studies using tumour samples, organoids, and animal models, researchers showed that blocking SPP1 reduced tumour growth, stopped metastasis, and dramatically increased survival. An antibody against SPP1 extended survival in mice by more than threefold. The research also revealed that blocking SPP1 boosts levels of another protein, GREM1, which keeps cancer cells in a less aggressive state. With more than 10,000 diagnoses and 9,000 deaths annually in the UK, pancreatic cancer remains one of the hardest cancers to treat, but this breakthrough opens the door to new antibody and small molecule drugs that could provide life-extending options for patients.

(PRESS RELEASE) LONDON, 25-Sep-2025 — /EuropaWire/ — The Institute of Cancer Research, London, has identified a protein that could transform treatment options for pancreatic cancer, one of the deadliest and most aggressive cancers. In new findings published in Nature, researchers discovered that blocking the protein SPP1 can stop tumours from spreading and significantly extend survival.

Pancreatic cancer remains extremely challenging to treat, with little progress in survival over the past five decades. Each year in the UK, more than 10,000 people are diagnosed, and over 9,000 die from the disease. Only five percent of patients live beyond ten years. Pancreatic ductal adenocarcinoma (PDAC), the most common and aggressive type, makes up around 90 percent of all cases.

The research, supported by The Institute of Cancer Research (ICR) and the charity Breast Cancer Now, showed that levels of the SPP1 protein rise as pancreatic cancer advances. Studying tumour samples from 644 patients, scientists confirmed that those with higher levels of SPP1 had significantly poorer outcomes.

To test how the protein drives tumour growth, researchers created organoids—lab-grown mini tumours that mimic cancer behaviour. They found that disabling the gene producing SPP1 reduced the size and number of tumours and limited the development of the most invasive cells. In animal studies, switching off the gene prevented the cancer from spreading altogether and dramatically increased survival: while untreated mice lived no longer than 50 days, 20 percent of mice without the gene survived for more than 400 days.

The team also tested an antibody designed to block SPP1. Mice treated with the antibody survived far longer—half lived beyond 100 days compared to just 30 days in the untreated group—and their tumours failed to spread to other organs such as the liver or lungs.

Crucially, the research uncovered an important link between SPP1 and another protein, GREM1, which influences how aggressive pancreatic cancer cells become. Blocking SPP1 raised GREM1 levels, preventing cancer cells from changing into a more dangerous and treatment-resistant state.

These findings pave the way for the development of new drugs, such as antibodies or small molecules, designed to target SPP1 and prevent pancreatic cancer progression.

Professor Axel Behrens, Professor of Stem Cell Biology at The Institute of Cancer Research and Scientific Director of the Cancer Research UK Convergence Science Centre, said:
“A few years ago, we uncovered what drives pancreatic cancer cells to become dangerously aggressive. Now we’ve shown that by targeting SPP1, we can stop tumours from spreading and help patients live longer. The next step is to develop a drug that directly blocks this protein.”

Professor Kristian Helin, Chief Executive of The Institute of Cancer Research, London, added:
“Pancreatic cancer is one of the most devastating diagnoses, with its common form spreading quickly and proving hard to treat. This breakthrough provides a clear new target to slow or halt the disease, and it brings us closer to developing much-needed therapies for patients in urgent need.”

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SOURCE: The Institute of Cancer Research