A cancer drug is not like a pill for a headache. Its effects – and its side effects – can take months or years to reveal themselves.

Originally published in Nepali in Ukaalo on Friday, 6 March 2026 (22 Falgun 2082), as “मुसामा क्यान्सर जितियो, मानिसमा कहिले?”. Translated into English by the author. Read the original: https://www.ukaalo.com/news/32679/

A recent study on pancreatic cancer from Spain’s National Cancer Research Center (CNIO) has excited the medical world. A team of researchers led by Dr. Mariano Barbacid claims to have cured this cancer completely and permanently in laboratory mice.

A cancer that disappears and never comes back is considered the holy grail of any cancer treatment. Achieving that in pancreatic cancer – known as one of the hardest cancers to treat – is being seen as all the more significant.

The finding is, without doubt, an important result for cancer treatment. It may even set cancer therapy on a new course in the future. But when results like these become newspaper headlines, the public naturally begins to hope: “A cure for cancer has been found.” Cancer treatment is not that simple, and to understand it we have to step out of the illusion of “miracles” and face the hard scientific reality.

The Spanish study: laying siege to cancer

Of all the cancers that affect people, pancreatic cancer – pancreatic ductal adenocarcinoma (PDAC) – is said to be among the deadliest and least treatable. That is not only because it spreads quickly, but because it is a shape-shifter that can outmanoeuvre treatment. It adapts to circumstances, switches on backup systems, and escapes smaller attacks through “back doors.” For decades researchers have tried to shut down the main pathways that drive this cancer, but every time one pathway was blocked, the cancer escaped through another and came back even stronger.

The most interesting part of the Spanish study is the strategy the scientists used. Dr. Barbacid’s team thought about treatment differently: a tumour may survive if one or two pathways are blocked, but it cannot survive if many systems are shut down at once. They realised that stopping pancreatic cancer’s main “engine” was not enough – its “ignition switch” and its “escape route” also had to be closed at the same time. This study used a strategy that shut all three.

The main engine of pancreatic cancer is a mutation in the protein KRAS. Most research on treating pancreatic cancer targets it, and its shape-shifting nature is why most treatment strategies fail. EGFR, a protein one step above KRAS, acts as the engine’s ignition switch. Another protein, STAT3, can show cancer cells a back door to survive when other pathways are blocked. Most treatments used for pancreatic cancer so far have targeted just one of these.

Dr. Barbacid’s team used a strategy that targeted all three proteins at once. With all three pillars of pancreatic cancer knocked down together, the cancer was left with no way to adapt or escape. Targeting KRAS, EGFR and STAT3 simultaneously in mice produced astonishing results: the tumours did not merely shrink, they disappeared and did not come back. It is this news – the complete elimination of pancreatic cancer in laboratory mice – that has excited scientists around the world.

Mice: a filter, not the final destination

In other words, the cancer was completely eliminated in laboratory mice when the researchers used genetic methods to shut down the cancer’s engine, its ignition switch and its escape route all at once. Here it is important to understand the gap between our perception and reality. When we hear the news that “cancer has been cured,” we immediately picture patients walking out of hospital healed. When we read about the Spanish study, we first need to understand this: the cancer disappeared in mice. The method has not yet been tried in humans.

Scientists have cured cancer and other diseases in mice thousands of times. Historically, around 90 percent of treatments that succeed in mice fail when tested in humans. That is not a weakness of science but a reflection of the complexity of our bodies. Laboratory mice are genetically uniform; cancer is induced in them in a controlled way and treated at an early stage. Their immune systems have not been shaped by years of smoke, dust, stress or other illnesses, as ours have.

So success in mice in a controlled laboratory environment should be seen not as the final victory but as a successful screen – a filter. The Spanish study has passed that difficult filter, showing that this approach has the power to cure pancreatic cancer.

From genes to medicine: the hard translation from mice to humans

The hardest challenge now is turning a genetic method used in mice into a treatment that humans can tolerate. In the human body, all three of these genes – KRAS, STAT3 and EGFR – are important for other processes. They cannot simply be cut out genetically as they were in mice; doing so could have terrible consequences. Instead, doctors must rely on a cocktail of drugs that block these proteins – an approach that is less precise and more toxic.

Dr. Barbacid’s team has planned the drugs that could be used to test this approach in humans: a cocktail that targets all three proteins at once. It would begin with RMC-6236, a drug designed to recognise and target KRAS’s cancer-causing mutations. Alongside it, the team plans to use afatinib, a drug against EGFR already used in lung cancer, and SD36, which targets STAT3.

Of the three, RMC-6236, designed to block KRAS, is new, while the other two have already been approved for use in other cancers. But even though they have been approved separately, using them together requires going through the entire approval process again.

Shutting down the cancer’s engine, starter and escape route all at once may look like the right move, but biologically it is risky. All three targets – KRAS, EGFR and STAT3 – are also important for our healthy cells to survive and to fight disease. Mice have short lives and can tolerate a few weeks of harsh treatment; humans must tolerate it for months. Blocking EGFR and STAT3 at the same time could seriously affect the skin, the gut or the immune system. The very first barrier is toxicity. If side effects force doctors to stop treatment, the chance is lost – and the likelihood of the cancer returning even stronger only grows.

Success in mice does not guarantee success in humans

History has taught us to be cautious. In 1998, news that drugs like endostatin had cut off the blood supply to tumors in mice astonished the world. The Nobel laureate James Watson was even quoted as predicting that cancer would be cured within two years. But in humans, the tumors proved cleverer; they found other ways to get blood. The trials were halted midway, and the promised “magic” of those drugs never materialized.

A decade later, another approach for pancreatic cancer, targeting the “Hedgehog” pathway, taught an even harsher lesson. In mice, blocking this pathway dissolved the dense tissue around the tumor, letting chemotherapy drugs get in more easily. But when this strategy, so successful in mice, was tested in humans, the result was the opposite. That dense tissue, it turned out, had not only been blocking the drugs – it had also been holding the cancer in, keeping it from spreading. Dissolving it helped the cancer spread faster. Patients taking the new drug began dying sooner than those who did not, and the trial had to be stopped midway.

Clinical trials: the “valley of death” for drugs

The process of turning a successful animal study into a treatment for humans is known in the pharmaceutical industry as the “valley of death,” because most drugs fail, and whether a drug succeeds or fails is known only after long and expensive stages of testing. The CNIO scientists’ results in mice show that the approach is scientifically strong and that it is worth taking the risk of clinical trials – testing in humans.

The immediate next step is not a prescription but toxicity testing. First, researchers must make sure that blocking KRAS, EGFR and STAT3 – which the body needs for other functions – has only a negligible effect on a patient’s healthy cells. Only if the toxicity proves manageable will the drugs move into the different phases of clinical trials. A drug is approved for use only after it passes all three phases in sequence.

The first stage, called Phase 1, is not meant to cure the disease. It may sound strange, but its purpose is simply to find out whether the drug is safe for humans. The three pathways the scientists shut down – KRAS, EGFR and STAT3 – are essential not just for cancer but for the healthy cells of our body.

A chemical that a mouse’s body can handle might cause kidney failure in a human or harm the heart or the brain. So, at this stage the drug is tested on a very small number of volunteers. Doctors adjust the dose and closely monitor the drug’s negative effects on the body. However beneficial a drug may be, if it does not prove safe at this stage, its testing and use are canceled right there.

Once a cancer drug clears this first safety barrier, Phase 2 begins. Here scientists ask: “Does this drug work?” A few hundred patients receive the drug, and scientists monitor whether tumors shrink, or whether the cancer stops growing. Only if this stage signals that the drug is effective can it move forward. But most drugs fail at exactly this stage; a method that worked in mice may not work in the complex human body.

The last and most important stage of a clinical trial is Phase 3. It is like the drug’s final match, involving thousands of patients.

Its main purpose is not just to see whether the new drug works, but to compare: is it better than the drugs already available? If a new drug kills cancer but causes patients far more suffering than current chemotherapy, using or producing it is not worthwhile. At this stage, patients are divided into two groups – one receives the new drug and the other the current standard treatment. Conclusions are drawn only after comparing the two groups over years.

That is why this process cannot be rushed. A cancer drug is not like a pill for a headache. Its effects and side effects can take months or years to appear. There are past examples, like endostatin, of drugs that were rushed forward amid tumors of miracles but later failed in human trials. Rushed approval can put thousands of lives at risk. The long timelines, the paperwork and the strict oversight are not there to torment patients – they are a shield built to protect them.

Conclusion: what does success really look like?

Science moves forward at an uneven pace. It is slow, expensive and risky, and full of dead ends. Even if the approach shown by the Spanish study succeeds in humans – if everything goes well and nothing gets in the way – a straight timeline suggests it would take eight to ten years to become a drug. This is the messy, slow and expensive reality of cancer drug development.

Talking about it without this context is not only a scientific misrepresentation – but it also slowly erodes public trust. When news that “cancer has been cured” keeps coming, but in practice only disappointment follows, people begin to wonder: is a cure being hidden, or are scientists simply incapable?

The reality is less dramatic but far more honest. The Spanish study is not a miracle. It is something better. It has drawn a clear map for treatment. It justifies the risks of the trials to come over the next few years – though it is no guarantee of success.

This is what real progress looks like in the hard reality of cancer science. It has given us hope that a cancer as deadly as pancreatic cancer might be contained by shutting three doors at once. It is news of hope – but it is also a test of patience.