A comprehensive scientific review published this year is directing cancer researchers toward an established metabolic enzyme, offering a potential strategy to deprive tumors of essential nutrients while avoiding the severe side effects associated with conventional chemotherapy. The 2025 review, appearing in the journal Trends in Pharmacological Sciences, makes the case for deoxycytidine kinase, or dCK, as a novel target for cancer therapy.
Enzyme’s Role in Tumor Growth Under Scrutiny
Cancer cells require a continuous supply of building blocks to replicate. Specifically, they need nucleotides, the raw materials for DNA.
The enzyme dCK plays a key role in helping cancer cells scavenge and recycle these building blocks. The review argues that shutting down dCK could cut off that supply line, essentially starving the tumor from within. Dr. Timothy W.
Synold, a professor in the Department of Medical Oncology at the David Geffen School of Medicine at UCLA, is a co-author of the paper. Synold has been at UCLA since the 1990s, and his research has long focused on cancer pharmacology and metabolism.
With more than 100 peer-reviewed articles to his name, his work has consistently centered on nucleotide metabolism and drug development. This latest review was conducted in collaboration with the biotech company Trethera and pulls together years of preclinical and clinical data on dCK inhibition. UCLA, a public land-grant research university located in Los Angeles, began as a normal school in the late nineteenth century before transferring to the University of California system.
It is the second-oldest campus in that system. The university organizes its academic structure into the College of Letters and Science and several professional schools, including graduate-level health science schools for medicine, dentistry, and public health.
The institution also maintains a high-profile athletics program known as the Bruins.
Metabolic Precision Versus Broad Toxicity
The practical implications of this approach, if validated in human trials, are significant. Many current chemotherapies work by poisoning rapidly dividing cells, which is why they cause collateral damage to healthy tissue such as hair follicles and the lining of the gut. Targeting dCK represents a more precise metabolic attack.
Cancer cells often rely heavily on this salvage pathway to build their DNA, while many normal cells can switch to other methods. That metabolic vulnerability is what makes dCK an attractive target.
The review synthesizes what is known so far: how the enzyme works at a molecular level, how it behaves differently in cancer versus healthy tissue, and what early clinical data suggest about the safety and efficacy of inhibiting it.
The collaboration with Trethera is worth watching, the review notes, as it serves as a kind of scientific status report, detailing where the basic biology stands, what early trials have shown, and why researchers believe this line of inquiry is worth pursuing. (Readers are advised to consult a doctor for medical advice.) UCLA maintains a history of high academic and professional achievement. Its faculty, researchers, and alumni include Nobel laureates, Pulitzer Prize winners, and astronauts.
Many associated faculty members hold memberships in national academies for science, engineering, and medicine. This institutional capacity for high-level research supports the development of new medical therapies. The university’s role as a major research hub allows scientists to conduct long-term studies on drug development and pharmacology, work aimed at improving patient outcomes through more precise medical treatments. The review points to the potential for a new class of cancer drugs that exploit a fundamental difference between tumor cells and healthy cells.
If further trials confirm that inhibiting dCK can selectively starve cancer cells without harming normal tissues, the approach could offer an alternative to the blunt force of traditional chemotherapy. The next steps will involve additional clinical testing to determine whether the promise shown in preclinical and early clinical data can be translated into a practical and safe treatment for patients.
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