Scientists discovered a previously unknown mechanism by which cancer cells thrive, linking their ability to evade self-destruction with their altered energy consumption. Researchers at Technische Universität Dresden found that the protein MCL1, long understood to prevent cancer cells from undergoing apoptosis, or programmed cell death, also actively drives cancer metabolism by controlling the mTOR growth pathway. The findings, published Jan. 5, 2026, suggest that survival and energy use in cancer cells are intrinsically connected.

The research team's work sheds light on why drugs targeting MCL1 can be effective cancer treatments, but also explains the associated risk of heart damage. According to the study, MCL1's influence on the mTOR pathway, a critical regulator of cell growth and metabolism, ties directly into the energy production processes within cancer cells. This connection was previously unappreciated, as the processes of apoptosis avoidance and energy alteration were largely studied as separate phenomena.

"We've uncovered a surprising connection between two defining features of cancer," said Dr. Elena Schmidt, lead researcher on the project at Technische Universität Dresden. "This understanding allows us to rethink how we approach cancer therapy, potentially leading to more targeted and safer treatments."

The team identified a specific method to mitigate the risk of heart damage associated with MCL1-targeting drugs. By carefully modulating the drug's effect on the mTOR pathway, they believe it is possible to selectively target cancer cells while minimizing the impact on healthy heart tissue. This approach could unlock the potential for safer and more effective cancer therapies.

The discovery highlights the complex interplay of cellular processes within cancer and underscores the importance of understanding these connections for developing effective treatments. The research suggests that future cancer therapies may benefit from a more holistic approach, targeting multiple pathways simultaneously to disrupt cancer's ability to survive and thrive. Further studies are underway to refine the method for reducing heart damage and to explore the potential of combining MCL1-targeting drugs with other therapies.