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A study led by the Cell Cycle and Cancer Group at the Vall d'Hebron Institute of Oncology (VHIO) has identified a vulnerability in liver cancer that could guide the development of new therapies. The work, published in Proceedings of the National Academy of Sciences, shows that some tumor cells depend on the combined action of two proteins, CDK16 and CDK18, to repair their DNA and continue multiplying. When both are inactivated, damage accumulates and the cells' ability to survive is impaired.

The research, led by Dr. Marcos Malumbres, ICREA professor, head of VHIO's Cell Cycle and Cancer Group and director of its Systems Oncology Program, focuses on hepatocellular carcinoma, the most common type of primary liver cancer in adults.

"Although treatments are available that can control the disease and prolong survival, advanced forms remain particularly challenging. Identifying new dependencies in tumor cells allows us to explore treatments that target mechanisms different from those addressed by current therapies," says Malumbres.

"To develop new therapies, we need to understand what allows a tumor cell to stay alive despite the damage it accumulates," the researcher continues. "In this work, we have identified two proteins that support each other. By eliminating both, we deprive the tumor of an important means of repairing its genetic material."

Cyclin-dependent kinases (CDKs) are a family of proteins that regulate various cellular activities.

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