Ask the author session

What if the secret to understanding cancer’s aggressiveness lies not just within the tumor itself, but in the environment where it grows?

In a recent “Ask the Author” session, we had the pleasure of hosting Dr. Yiming Peng-Winkler, a researcher from the Laboratory for Tumor Evolution and Metastasis in Leuven, to discuss his team’s groundbreaking study published in Nature: “Steatosis shapes prognosis-defining liver metastasis heterogeneity in Colorectal Cancer”

👉 You can watch the full interview below — don’t miss it.

The Mystery of Metastatic Growth Patterns

Colorectal cancer (CRC) often spreads to the liver, but not all metastases behave the same way. Clinicians have long observed different “histological growth patterns” under the microscope. One specific type, known as the replacement growth pattern, is particularly aggressive and associated with a much poorer prognosis—a 5-year survival rate of less than 44.2%, compared to 73.4% for other types.

Until now, it was unclear what drove this dangerous form of cancer. Dr. Peng-Winkler’s research provides a startling answer: the metabolic state of the liver itself.

Fatty Liver: A Scaffolding for Cancer

The study reveals that steatosis (fatty liver disease) is not just a passive condition. Instead, it actively shapes how cancer cells grow. In both patient cohorts and mouse models, Dr. Peng-Winkler found that a fatty liver causally promotes the replacement growth pattern.

The mechanism is fascinating:

  • Cancer cells in a steatotic liver use available fatty acids to stabilize a notorious oncoprotein called MYC.
  • MYC then triggers the synthesis of proline and collagen.
  • This collagen acts as a physical scaffold, allowing cancer cells to infiltrate and replace healthy liver tissue.

A New Frontier for Precision Oncology

This research has profound implications for clinical practice, especially since steatosis affects roughly 25% of the population. Dr. Peng-Winkler suggests that assessing liver fat could become a vital part of risk stratification for CRC patients. Furthermore, it opens the door to therapies targeting metabolic pathways—like MYC or collagen production—to suppress these aggressive metastases.

As Dr. Peng-Winkler notes, precision oncology must look beyond the tumor and consider the metabolic conditions of the host organ.

Ready to dive deeper into the science? Watch the full video interview to hear Dr. Yiming Peng-Winkler explain the translational design of this study, the experimental models used to prove causality, and his vision for the future of cancer treatment.

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