Could a Leuven discovery open a new route to treating liver metastases?
VIB and KU Leuven researchers have identified a mechanism through which metastatic cancer cells exploit a fatty acid in the liver to weaken immune defences, creating a possible treatment target that remains years from clinical use.
Liver metastases are difficult to treat and are frequently responsible for serious illness in people whose cancer began elsewhere. Identifying a mechanism that makes these tumours less vulnerable to immune attack could eventually support new treatments, although the present evidence remains preclinical.
Researchers at the - Center for Cancer Biology in reported on 5 August that they had identified a mechanism through which breast and colorectal cancer cells use palmitate, a fatty acid available in the liver, to suppress part of the immune response. In experimental models, disrupting that mechanism restored immune-cell activity and reduced the growth of liver metastases, but the team has not yet demonstrated a treatment in patients.
For people receiving cancer care in Belgium, the immediate message is therefore one of scientific progress rather than a change in therapy. The peer-reviewed study, published in , identifies a potential drug target, not an approved medicine or clinical protocol. and explicitly caution that further research is required before the findings can produce a therapy.
The study was led by doctoral researcher Anke Vandekeere and professor Sarah-Maria Fendt. Their team found that metastatic cells use an enzyme called DHHC17 to attach palmitate to laminin-511, a protein involved in the environment surrounding cells. This modification stabilises the protein and enables cancer cells to release it. According to the paper, laminin-511 then reduces the ability of neutrophils—white blood cells that can kill cancer cells—to attack the metastases.
When the researchers reduced DHHC17 activity in mouse models, metastatic growth in the liver declined, provided neutrophils were present. Restoring laminin-511 or blocking neutrophil degranulation reversed that effect, supporting the proposed chain of cause and effect. The experiments covered models of breast and colorectal cancer and distinguished liver metastases from those growing in the lung.
The work also drew on human material. records contributions from ’s UPTIDER tissue-donation programme and from Erasmus MC in Rotterdam, alongside collaborators in Barcelona, Düsseldorf and London. Those samples helped the researchers test whether features observed in laboratory models were relevant to human disease, but they did not amount to a clinical trial showing that DHHC17 inhibition is safe or effective in patients.
That distinction matters because liver metastases are not a single disease. They are secondary tumours originating elsewhere—commonly in organs such as the colon or breast—and treatment depends on the primary cancer, the number and position of lesions, disease elsewhere in the body and the patient’s overall condition. A 2025 review in the describes surgery, thermal ablation and stereotactic radiotherapy as complementary established options for selected patients, generally alongside systemic treatments chosen by multidisciplinary cancer teams.
The result fits a broader shift in oncology. Researchers increasingly study not only mutations inside a tumour but also the tumour microenvironment: the surrounding nutrients, structural proteins and immune cells that can help or hinder cancer. Fendt’s group argues that the liver’s distinctive metabolic and relatively immune-tolerant environment gives metastatic cells opportunities that may not exist in the same form in other organs.
There is a European dimension, although the discovery remains principally a Belgian-led biomedical story. The European Commission’s Cancer Mission makes tumour-host interactions, immune-centred treatments and equitable access to personalised care explicit research priorities. The project also received support from Belgian funders including the Research Foundation , , the Foundation against Cancer, Kom op tegen Kanker, the Baillet Latour Fund and the Francqui Foundation, as well as European and international funding.
The next task is to determine whether DHHC17, laminin-511 or another point in the pathway can be targeted selectively without disrupting essential functions in healthy tissue. Researchers will need suitable drug candidates, toxicity studies and stronger validation in human tumours before clinical trials can be considered. Until those stages are completed, patients should not alter treatment or diet on the basis of this study; the presence of palmitate in the mechanism does not establish that avoiding a particular food will treat existing metastases.
Impact
Regional — The discovery strengthens Leuven and Flanders’ position in cancer-metabolism research and reflects cooperation among VIB, KU Leuven, UZ Leuven and publicly supported research funders.
Local — The work reinforces Leuven’s role as a centre for cancer, metabolism and immunology research. It draws on collaboration involving VIB, KU Leuven and UZ Leuven, connecting laboratory research with human tissue resources and clinical expertise in the city. The immediate impact is therefore on Leuven’s research capacity and international scientific profile, not on local healthcare provision. Patients treated in Leuven or elsewhere in Flanders will not see a change in current cancer care based on this study alone.
What it means for you
Patients and families should not change treatment, medication or diet because of this finding. Palmitate’s role in an experimental tumour pathway does not establish that avoiding particular foods can prevent or treat liver metastases. Anyone receiving cancer care should continue following their oncology team’s advice. There is currently no DHHC17-targeting treatment, patient trial, application deadline or additional healthcare cost linked to the announcement. The next meaningful developments to watch for are independent validation, the identification of a suitable drug candidate and, eventually, an announced clinical trial; no dates were provided.
Opposing perspectives
- VIB-KU Leuven discovery perspective
Anke Vandekeere and Sarah-Maria Fendt frame the pathway as a promising therapeutic opening because interfering with tumour use of the liver environment restored neutrophil activity and slowed metastases in experimental models. Their emphasis is on making metastatic cells vulnerable to immune attack again.
- Clinical-care evidence perspective
Clinical evidence reviewed in the European Journal of Cancer supports surgery, ablation, stereotactic radiotherapy and systemic therapy as current options selected by multidisciplinary teams. From this perspective, the Leuven mechanism is hypothesis-generating and cannot affect patient care until safety and efficacy are demonstrated in clinical trials.
Who, where and what
Key people, places and terms in this story
Flemish city serving as the study’s principal research hub.
Belgian region whose biomedical research capacity and profile are strengthened by the Leuven discovery.
University whose researchers helped identify the metastatic pathway.
University hospital contributing to Leuven’s research and clinical ecosystem.
EU cancer-research initiative included among the article’s contextual sources.
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Flemish city serving as the study’s principal research hub.
Belgian region whose biomedical research capacity and profile are strengthened by the Leuven discovery.
EU cancer-research initiative included among the article’s contextual sources.
University whose researchers helped identify the metastatic pathway.
University hospital contributing to Leuven’s research and clinical ecosystem.
Flemish life-sciences research institute involved in the study.
Peer-reviewed journal that published the study on 5 August 2026.
University whose research portal records the publication.
Journal providing review literature used for broader context.
Biomedical literature database through which the contextual review is available.
Fatty acid in the liver that metastatic cancer cells exploit in the identified pathway.
Cancer-cell enzyme whose reduced activity slowed liver metastases in experimental models when neutrophils were present.
Molecule linking DHHC17 activity to reduced neutrophil killing capacity.
Sources & evidence
- View sourceNature MetabolismPrimaryacademic· nature.com· 5 August 2026Retrieved 25 August 2026· 58 days ago· Dated
- View sourceVIBprimary· press.vib.be· 5 August 2026Retrieved 25 August 2026· 58 days ago· Dated
- View sourceErasmus University Rotterdam research portalcorroborating· pure.eur.nl· 5 August 2026Retrieved 25 August 2026· 58 days ago· Dated
- View sourceEuropean Commission Cancer Missionofficial· research-and-innovation.ec.europa.eu· 30 March 2026Retrieved 25 August 2026· 186 days ago· Dated
Related topics
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This briefing was prepared with AI assistance and reviewed by a Belgium Impulse editor before publication. methodology.