LOS ANGELES — For decades, the enzyme deoxycytidine kinase, or dCK, was known mostly as a backstage player in cellular metabolism, quietly helping activate certain antiviral drugs and the chemotherapy agent gemcitabine. Now, a sweeping new review from researchers at Trethera and UCLA is reframing dCK as a central target in the fight against some of the most aggressive cancers. Published in 2025 in the journal Trends in Pharmacological Sciences, the review synthesizes more than 100 studies to clarify exactly how dCK fuels cancer growth.
The enzyme’s job is to phosphorylate three building blocks — deoxycytidine, deoxyadenosine, and deoxyguanosine — converting them into the nucleotide precursors that DNA replication requires. In healthy cells, this is a routine chore.
In cancer cells, it becomes a lifeline. The enzyme was first characterized in the 1970s, but its role in cancer metabolism has only come into sharper focus in recent years. The review details how dCK is often overexpressed in several major cancers, including acute lymphoblastic leukemia (ALL), non-small cell lung cancer, and pancreatic cancer.
That overexpression gives cancer cells a selective advantage, allowing them to replicate faster by hijacking the salvage pathway of nucleotide synthesis.
A metabolic vulnerability
Here is where the biology gets personal for patients and their families. Normal cells have multiple ways to get the nucleotides they need for DNA replication. Cancer cells, growing at breakneck speed, become heavily dependent on the salvage pathway — and on dCK to run it.
Inhibit dCK, the logic goes, and you starve the cancer of its raw materials while leaving most healthy cells relatively unscathed. The review makes clear that this metabolic vulnerability is not theoretical.
Trethera and UCLA researchers have mapped out how disrupting dCK activity could form the basis for a new class of cancer therapies. Unlike traditional chemotherapy, which attacks all rapidly dividing cells, a dCK-targeted approach would exploit a specific weakness in the tumor’s own biology.
What this means for treatment
For families facing a diagnosis of ALL, non-small cell lung cancer, or pancreatic cancer — all diseases with notoriously limited treatment options — the implications are significant. The review points to dCK as a target that could be hit with small-molecule inhibitors, potentially offering a more precise weapon than the broad-spectrum chemotherapies that have been the mainstay for decades. The research also revisits dCK’s older, better-known role.
The enzyme has long been recognized for its ability to activate certain antiviral drugs and the chemotherapy agent gemcitabine. That dual identity — both an activator of existing drugs and a standalone target for new ones — makes dCK an unusually versatile candidate for drug development.
The review, which draws on over 100 studies, represents one of the most comprehensive efforts to date to untangle dCK’s role in cancer metabolism. It lays out a roadmap for researchers working to design inhibitors that could enter clinical trials.
Looking ahead
The work by Trethera and UCLA is part of a broader shift in cancer research: moving away from one-size-fits-all chemotherapy and toward therapies that exploit the unique metabolic wiring of tumors. For patients with cancers that overexpress dCK, this line of investigation offers a new reason for hope. The next step will be translating these findings from the lab bench to the bedside.
Researchers are now working to develop selective dCK inhibitors that can be tested in human trials. For the families waiting, the science is moving as fast as it can. Consult your doctor for medical advice.
Sources
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