Cell Cycle Length Emerges as a Critical Cancer Driver
Research By: Kathryn Wikenheiser-Brokamp, MD, PhD
Post Date: April 30, 2025 | Publish Date: April 30, 2025
Experiments in mice developed at Cincinnati Children’s to model human lung cancer play major role in study published in Nature
The ability of gene mutations to cause cancer depends on how fast they force cells to divide, according to a multi-center study published today in Nature.
This finding, researchers say, suggests that developing new therapies targeting cell cycle length could become a way of preventing a smoldering risk of cancer from igniting in high-risk individuals.
The study was led by Rod Bremner, PhD, and colleagues at the Lunenfeld-Tanenbaum Research Institute, a part of the Sinai Health System in Canada. Co-authors included experts from the University of Toronto, Albert Einstein College of Medicine, University of Salamanca, Spain’s National Cancer Research Center (CINO), and Cincinnati Children’s.
Cell division pace as an independent factor
Not all cells that carry mutations will turn into cancer. The body has evolved protective mechanisms to prevent cancer from forming, including programmed cell death, clearance by the immune system, and others.
The research team found that shorter cell cycle length – the time it takes one cell to divide into two daughter cells – makes mutated cells more prone to becoming cancers. In contrast, cells with longer cell cycles exhibit resistance.
In this study, cell cycle length emerged as a hallmark of cancer susceptibility regardless of organ, cancer type, cancer-driving mutation, or timing within the lifespan when the mutation occurred. Further, cell cycle length consistently predicted the cancer cell-of-origin across different cancer types and in different organs.
“Our work suggests that we might be able to intervene in cancer-prone cells to slow them down a little bit with the right therapeutic agents,” Bremner says. “But first, we need to understand the mechanisms governing cell cycle rate in different cell types. There’s definitely a lot to be learned from the trillions of cells that are resistant to cancer, and we have only just got started.”
Mouse model helps make discoveries
A vital part of the study involved experiments performed in mice genetically engineered to model human small-cell lung cancer. The model was developed, and the studies were performed by Nagako Akeno Stuart, PhD, in the laboratory of Kathryn Wikenheiser-Brokamp, MD, PhD, a physician-scientist with the divisions of Pathology and Laboratory Medicine and Pulmonary Biology at Cincinnati Children’s.
“The mouse model we generated and the studies we performed helped demonstrate that the hallmark of shortened cell cycle length consistently predicted the distinct cancer cell-of-origin independent of the organ in which the cancer arose or when the mutation occurred during the life span,” Wikenheiser-Brokamp says.
Together, these studies demonstrate that cell cycle length differentiates the cancer cell-of-origin from cancer resistant cell lineages irrespective of organ or cancer type.
About the study
Funding for this study included grants from the Canadian Institutes of Health Research and the Krembil Foundation to Bremner; a Rankine Family fellowship to co-author Danian Chen, MD, PhD; and grants from the National Heart, Lung and Blood Institute and the American Cancer Society to Wikenheiser-Brokamp.
Read more in an announcement from Sinai Health
Don’t Miss a Post:
- Subscribe to the Research Horizons Newsletter
- Follow Cincinnati Children’s Research Foundation on Bluesky: @cincyresearch
| Original title: | Cell cycle duration determines oncogenic transformation capacity |
| Published in: | Nature |
| Publish date: | April 30, 2025 |
Research By
I work to identify critical factors that control lung development and drive lung disease.
Latest Posts
About this blog
The Research Horizons blog features news and insights about the latest discoveries and innovations developed by the scientists of Cincinnati Children's. This blog does not provide medical advice, diagnosis, or treatment.
Subscribe to Our Newsletter