Cancer also knows how to wait: Study uncovers the hidden step between mutation and tumor biomass appearance
· Medical Xpressedited by Lisa Lock, reviewed by Robert Egan
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The development of cancer is not a process triggered immediately by the emergence of an oncogenic mutation. There is growing evidence for the existence of an intermediate phase—hitherto poorly defined—in which mutated cells remain in a latent state, "accumulating the potential needed to grow, like a biological time bomb," explains Antonio Gentilella, a professor at the Faculty of Pharmacy and Food Sciences at the University of Barcelona and head of the Cancer Metabolism Research Group at the Bellvitge Biomedical Research Institute (IDIBELL), part of the Bellvitge Campus.
Now, a study led by Gentilella published in the Proceedings of the National Academy of Sciences analyzes this period in detail and reveals a previously unknown mechanism that temporarily separates the acquisition of the mutation that triggers cancer from the emergence of a clinically detectable tumor. This is the MYC-LARP1-mTOR molecular axis, a key mechanism that links the two processes.
From mutation to tumor, via latency
For decades, the dominant model in cancer biology has argued that mutations in key genes (oncogenes) drive tumor formation more or less directly. But "there is growing evidence that these driver mutations, and those that accumulate later, may be present in apparently healthy tissues for years, even decades, without a clinically detectable tumor appearing," Gentilella explains.
The study conducted by IDIBELL and the UB explains this phenomenon. The researchers demonstrated that the oncogenic mutation (in this case, they studied the one affecting the MYC oncogene, which is involved in 60% of cancers) "primes" the cell for growth but is not capable, on its own, of generating tumor mass. For a tumor to emerge, a second step is required: The cell must have the metabolic resources that enable it to produce biomass, that is, to grow and divide sustainably.
"This finding redefines the origin of the tumor as a process that is not only genetic, but also metabolic and biosynthetic," Gentilella notes.
The MYC-LARP1-mTOR axis: The switch that determines when tumor growth begins
The research team identified a key molecular mechanism, the MYC-LARP1-mTOR axis, connecting these processes, as they have observed in colorectal cancer models.
On the one hand, the MYC oncogene activates a program that sets in motion the cellular machinery necessary for protein production and growth. On the other, the LARP1 protein keeps this program ready but inactive, waiting for a signal. This signal arrives when the environment provides the necessary conditions for growth, allowing the program to be executed through mTOR. Only then does tumor expansion begin. Thus, overall, the MYC-LARP1-mTOR axis acts as a biological switch that temporally separates the preparation and execution of tumor growth.
The work has been carried out in colorectal cancer models. However, its scope could be much greater, since "MYC is altered in more than 60% of human cancers, suggesting that the MYC-LARP1-mTOR axis is likely involved in multiple tumor types," Gentilella details. "We have preliminary experimental evidence that this model also applies to other tumors," he adds.
A window of opportunity to intercept cancer before it appears
Overall, this study proposes a new way of conceptualizing cancer onset as a two-step process. Rather than being the direct consequence of one or more mutations, cancer would emerge after a silent period in which the transformed cells remain waiting for a favorable environment. This opens a very valuable window of opportunity before tumor expansion, suggesting a potential timeframe of intervention to intercept cancer before it develops.
In this context, LARP1 emerges as a key molecular target, as it functionally connects MYC, which prepares the machinery for expansion, and mTOR, which gives the approval signal for expansion. "It is still too early to talk about direct clinical applications, but everything points to the idea that altering LARP1 interferes with this reservoir of latent cells and the cancer initiation process," says Dr. Gentilella.
The team continues to work along these lines—initial results in animal models show that LARP1 is essential for tumor formation. These findings provide a unique tool for studying tumor latency and developing strategies to prevent cancer from manifesting.
Publication details
Pedro Fuentes et al, LARP1 integrates MYC and mTOR signaling to enable anabolic growth during tumor initiation, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2523043123. On bioRxiv: DOI: 10.64898/2025.12.05.689906
Journal information: Proceedings of the National Academy of Sciences , bioRxiv
Key medical concepts
Oncogene, mycMTOR protein, human
Clinical categories
Oncology Provided by University of Barcelona Who's behind this story?
Lisa Lock
BA art history, MA material culture. Former museum editor, paramedic, and transplant coordinator. Editing for Science X since 2021. Full profile →
Robert Egan
Bachelor's in mathematical biology, Master's in creative writing. Well-traveled with unique perspectives on science and language. Full profile →
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