Spanish scientists eliminate pancreatic cancer in mice using triple-drug therapy

Spanish scientists have reported that an experimental combination of three drugs eliminated pancreatic cancer tumours in laboratory mice.

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The findings have attracted global attention and been widely reported by international media outlets, including The Times of India and Business Standard.

The research, led by Spanish Biochemist Mariano Barbacid at Spain’s National Cancer Research Centre (CNIO), was published on 27 January in the scientific journal Proceedings of the National Academy of Sciences (PNAS) after about six years of laboratory work.

Scientists involved in the study described the results as a significant advance in pancreatic cancer research but stressed that the therapy has not yet been tested in humans.

Pancreatic cancer is among the deadliest cancers globally, largely because it is difficult to detect early and highly resistant to treatment. Medical data show that fewer than one in ten patients survive five years after diagnosis.

Findings from animal studies

According to reports by The Times of India, the Spanish research team tested a triple-drug therapy on mice with pancreatic ductal adenocarcinoma, the most common and aggressive form of pancreatic cancer.

The drugs used were gemcitabine, all-trans retinoic acid (ATRA) and neratinib. The study found that tumours in the treated mice completely disappeared after therapy.

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Researchers also observed that the cancer did not return even after treatment was stopped, an outcome described as rare in pancreatic cancer models.

The researchers said the therapy showed low toxicity in animals, with the mice tolerating the treatment well. Low toxicity is considered a critical factor in determining whether a treatment can safely advance to human trials.

Why three drugs

Mr Barbacid has previously argued that pancreatic cancer cannot be effectively treated with a single drug because of its ability to adapt and activate alternative growth pathways.

The triple-drug approach was designed to block several survival mechanisms at the same time. Gemcitabine targets rapidly dividing cancer cells, ATRA weakens the dense protective tissue that surrounds pancreatic tumours, while neratinib blocks signals that promote tumour growth.

By attacking the cancer through multiple pathways simultaneously, the researchers said the therapy prevented tumour cells from adapting and escaping treatment.

The study focused on cancers driven by mutations in the KRAS gene, which is found in more than 90 per cent of pancreatic cancer cases and has long been considered difficult to target.

KRAS is a gene that produces a protein responsible for regulating cell growth, division and survival.

Not a cure for humans

Despite the promising results, experts have cautioned against describing the findings as a cure for pancreatic cancer in humans.

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Several reports noted that success in animal models does not always translate to similar outcomes in people, as human cancers are more complex and influenced by additional biological and environmental factors.

Reacting to online claims describing the findings as a cure, a Nigerian medical doctor who posts on X as @Lordkyril said the study represents “very good news” but remains an early scientific step.

He explained that curing cancer in animal models is an important milestone, but it does not mean the disease has been cured in humans.

Another expert, Waqas Ahmed, also clarified that viral discussions around the study were misleading. He said the research showed tumour elimination in mice, not in people, and that human clinical trials have not yet started.

CNIO said the next phase of the research will involve further validation and safety testing. If approvals are granted by regulators, early-stage clinical trials in humans could follow.

Mr Barbacid, who helped identify the first human cancer gene in the 1980s, has spent decades studying KRAS-driven cancers. His sustained focus on pancreatic cancer has added weight to the findings within the global scientific community.