Researchers at the University Hospital Würzburg and the LMU Munich have tested the effectiveness of CDK4/6 inhibitors in colorectal cancer and achieved promising results. The drugs, originally developed for breast cancer, effectively inhibit the growth of colorectal cancer cells, even in therapy-resistant tumors. The protein p16 plays a crucial role: cells with high p16 expression respond less well to treatment. p16 could serve as a biomarker to identify patients who will benefit most from the therapy.

Colorectal cancer is one of the most common types of cancer worldwide and poses considerable challenges for oncology. Many patients develop resistance to chemotherapy, which makes treatment more difficult. CDK4/6 inhibitors have shown potential in preclinical studies and could offer new options.

CDK4 and CDK6 are enzymes that regulate cell division. In cancer, this pathway is often overactive, leading to uncontrolled growth. The inhibitors block these enzymes and stop cell division.

The team tested the substances on cell lines of colorectal, breast and liver cancer, including resistant variants. In most cases, growth was slowed down, but high p16 levels reduced the effect. Analyses of tissue samples from 185 colorectal cancer patients showed that low p16 activity is associated with a better prognosis, while there is no clear predictive value in early stages.

The study, funded by the Wilhelm Sander Foundation, was published in the journal “Cellular Oncology”. It could lead to individualized therapies. Further investigations into the role of p16 in resistance are planned. Combinations with immune or targeted therapies appear promising and could contribute to treatments with fewer side effects.

Original Paper:

Schneider, J.S., Khaled, N.B., Ye, L., et al. Efficacy of CDK4/6 Inhibition in colorectal cancer and the role of p16 expression in predicting drug resistance. Cell Oncol. (2025). doi.org/10.1007/s13402-025-01080-7

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