Finnish Drug Discovery Center and the University of Turku have launched a joint drug discovery project targeting one of oncology’s most stubborn challenges — cancer drug resistance.
Imagine a drug that works. A cancer that responds, a tumor that shrinks, a patient who begins to hope. Then, months or years later, the cancer grows back — smarter, more resilient, unmoved by the very therapy that once held it at bay.
This is cancer drug resistance. And according to Professor Klaus Elenius and Principal Investigator Kari Kurppa from the University of Turku, it is one of the most pressing unsolved problems in modern oncology.
A problem that affects virtually every patient with advanced cancer
Drug resistance is not a rare edge case. It is the rule.
“It affects, I could say, almost all patients with advanced cancer,” says Elenius, who has spent decades studying the molecular mechanisms behind cancer cell survival. When cancer cannot be eradicated through surgery or radiotherapy — when it has spread — drugs can shrink tumors and buy time. But the window is often painfully short. “Usually that is working only for months, or if they are successful, some years. But eventually, resistance develops.”
The problem is rooted in cancer cells’ remarkable capacity to adapt. Unlike normal cells, which follow strict biological rules, cancer cells operate with a kind of molecular chaos — dividing rapidly, accumulating genetic mutations, and constantly probing for new ways to survive. “The cancer cells are not restricted by the rules that normal cells have,” Kurppa explains. “It gives them an enormous width of plasticity. They can basically change their phenotype according to their surroundings.”
This plasticity means that even when a drug kills the vast majority of cancer cells, a small subset may already carry or acquire traits that allow them to tolerate the treatment. These cells survive, buy time, and eventually develop new mechanisms to thrive — clinically observed as relapse on therapy.
Resistance can also be present from the very start. Some tumors simply never respond. Others respond well initially, then relapse. Both forms are common, and both are devastating.
The scale of the problem — and why it’s so hard to solve
The scope of this problem is striking. For the class of cancer therapies known as targeted drugs — molecules designed to attack specific oncogenes expressed in cancer cells but not in healthy tissue — drug resistance is an almost universal outcome. “Basically, you cannot cure any of these patients due to drug resistance,” says Kurppa. “Although most patients get an initial response to the drugs.”
This is not for lack of trying. Overcoming drug resistance is one of the most active areas of research in global oncology. But the biology is extremely complex — resistance mechanisms vary depending on cancer type and therapy — and previous attempts to target the key molecular mediators have largely fallen short, often because the proteins involved are technically very difficult to target.
An idea, a decade in the making
The research now being developed in collaboration with the Finnish Drug Discovery Center has its roots in years of fundamental science at the University of Turku. The team’s deep understanding of a particular class of molecules — built up over many years and extending down to the atomic level — eventually pointed toward a specific mechanism that, they believe, plays a central role in enabling resistance across multiple cancer types and therapies.
Kurppa recalls the moment the core idea first took shape. It was at an international cancer research conference. “I have a notepad from the AACR meeting where I first drafted the idea of the mechanism of action we are now pursuing. These moments — you have a boring moment in a seminar and then start to think about things.” The idea lay dormant for years, waiting for the tools and the team to pursue it. When Kurppa returned from his postdoc, he and Elenius began building toward it in earnest.
The target protein they have identified appears to act as a kind of cellular survival shield — activated when cancer cells come under attack from therapy, it helps them withstand the drug long enough to develop full resistance. Their approach to blocking this activation is, by their own account, unlike anything previously attempted. The protein itself is well known in the field. The mechanism is not.
Details of the molecule and the precise mechanism of action remain confidential for now, as the project moves into advances from academic research to drug discovery stages. What can be said is that the target’s disease relevance is clear, the potential patient population is globally significant, and the approach is novel enough to be considered a potential first-in-class therapy.
Why this collaboration — and why now
For Elenius, one of the persistent frustrations in Finnish academic life science has been the gap between discovery and development. “I think we are lacking a little bit of that tradition in Finland — how to do it,” he says, comparing the path from university lab to drug candidate to the more established culture around this transition in the United States. “In Finland, we all too often have to relearn the whole process from scratch.”
That is precisely the gap that Finnish Drug Discovery Center, or the FDDC is designed to close. For both researchers, the collaboration has already changed the pace and the logic of the work.
“The FDDC knows which steps should be taken and in which order,” says Kurppa. “It already feels like we are speeding up our drug discovery considerably.” Elenius adds: “I’m excited about the opportunity that this would speed things up, and that we could do everything at a more professional level — and maybe even reach a goal we might not be able to reach without this help.”
FDDC CEO Maarit Merla describes the project as the organization’s first academic co-development collaboration. “We bring more than capital — we bring strong and diverse expertise from the pharmaceutical industry, and we want to support the later development path toward the founding of a new Finnish startup company.”
The University of Turku’s TTO office is equally committed. “The path from academic laboratory to new treatments for patients is long,” note business development lead Anne Marjamäki and innovation advisor Marjo Pihlavisto. “We believe this collaboration with FDDC will help accelerate that transition. One of our TTO’s key responsibilities is ensuring that research results are effectively leveraged for the benefit of society.”
What success would mean
If the project delivers on its potential, the implications extend well beyond any single cancer type. A drug that targets the core mechanism by which cancer cells survive therapy could, in principle, be used alongside a broad range of existing treatments — amplifying their efficacy in patients who would otherwise relapse.
“The potential is huge,” says Elenius. “There are no drugs that currently address these problems. The opportunities in helping people with advanced cancer are enormous.”