April 30, 2026 – Scientists have discovered how cells generate cancer-driving proteins by slicing RNA into shorter, functional fragments, which could influence cancer progression and generate new targeted therapies.

In a study published in Cell Reports, a team led by Dr. Yuval Malka of the Department of Biochemistry and Molecular Biology at the Faculty of Medicine at the Hebrew University of Jerusalem discusses “RNA dicing,” a process that fragments RNA molecules. The study focuses on a gene called JAK1, long known to play a central role in regulating how cells grow, divide, and respond to immune signals. When JAK1 functions normally, it helps maintain balance. But when it goes awry, it can fuel cancer.

What the team discovered is that JAK1 doesn’t just produce one protein, as was previously assumed. Instead, its RNA can be “diced” into a shorter form that generates a stripped-down but still active protein fragment, essentially the engine of the molecule, known as the JH1 kinase domain. This truncated version operates differently from its full-length counterpart and can push cells toward uncontrolled growth.

“We’re seeing that the cell’s protein-making machinery is far more flexible and dynamic than we thought,” the researchers suggest. “RNA isn’t just a passive messenger. It can be reshaped in ways that change what proteins are made and how they behave.”

The implications for cancer are significant.

The study found that the balance between the full-length JAK1 protein and its diced version can influence whether cells remain under control or become tumorigenic. In particular, certain mutations, called nonsense mutations, appear to tilt the balance. These mutations disable the normal, tumor-suppressing form of JAK1 while amplifying the activity of the shorter, cancer-promoting version.

In endometrial cancers, for example, this imbalance may help explain why some tumors behave more aggressively.

Patients whose tumors carry these mutations, and therefore rely more heavily on the diced JAK1 form, may be especially sensitive to momelotinib, a drug that targets JAK1 activity. This points to more precise treatment strategies, in which patients are matched to therapies based not just on which genes are mutated, but on how those genes are processed at the RNA level.

Mechanisms like RNA dicing also address one of the most puzzling questions in cancer research: how the same gene can play opposite roles in disease. In some contexts, a gene acts as a tumor suppressor; in others, it promotes tumor growth as an oncogene. By processing mRNA in different ways, the cell can effectively shift a gene’s function from harmful to protective.

The researchers have filed a patent for this novel therapeutic approach based on RNA dicing, and a new company, Molecular Therapeutics, has been formed to advance development and clinical trials.

The research paper titled “RNA dicing promotes the expression of an oncogenic JAK1 isoform” is now available in Cell Reports and can be accessed here.

Researchers:

Rob van der Kammen¹ ∙ Or Yakov² ∙ Shinyeong Ju³ ∙ Ferhat Alkan¹ ∙ Onno B. Bleijerveld⁴ ∙ Cheolju Lee^3,5 ∙ William James Faller^1,6 ∙ Yuval Malka^2,7