Study Finds Cancer Drug Target in WNT Pathway

Weill Cornell Medicine researchers developed a selective TNKS2 inhibitor that suppressed growth of cancer cells lacking TNKS1 in laboratory tests.

Updated on Nov. 2, 2026 in Cancer

Clear glass culture flasks and a multi-well plate with pale pink liquid sit on a steel laboratory bench beside a pipette under soft light. — Researchers at Weill Cornell Medicine developed a compound that selectively inhibits the TNKS2 enzyme, suppressing growth of cancer cells lacking TNKS1 in laboratory tests. AI Illustration. Upload story photo >

Researchers at Weill Cornell Medicine identified a vulnerability in WNT-driven cancers and developed a compound that selectively inhibits the TNKS2 enzyme. The study, published November 2 in Nature Chemical Biology, was supported by the National Cancer Institute.

Why it matters

WNT pathway hyperactivity is seen in almost all colorectal cancers and in more than half of breast cancers, making it a widely relevant target. A selective approach could aim to harm cancer cells while sparing healthy cells that depend on both TNKS enzymes.

The inhibitor targets TNKS2 roughly 30 times more strongly than TNKS1 in lab dish tests, suppressing cancer cells with reduced TNKS1 while leaving cells with normal TNKS1 unaffected. Whether these selective effects translate beyond laboratory cultures has not yet been established.

The players

Weill Cornell Medicine

A medical school and research institution in New York City that led the study identifying the WNT-pathway vulnerability and developing the TNKS2 inhibitor.

National Cancer Institute

The federal agency within the National Institutes of Health that funds and conducts cancer research and supported this study.

The details

Researchers knocked down TNKS1 and TNKS2 separately to compare their roles, then confirmed the approach with genetic techniques that selectively suppressed TNKS2. One of the most common large-scale DNA deletions in cancer removes the TNKS1 gene, leaving many tumor cells dependent on TNKS2.

Nov. 2, 2026: Study published in Nature Chemical Biology

Health Landscape

WNT signaling has long been studied as a driver of colorectal and breast cancers, and the National Cancer Institute has supported this line of preclinical research. The new TNKS2 inhibitor extends that work by aiming to exploit a specific genetic loss in tumors while sparing normal cells.

At this preclinical stage, the compound is not available to patients, and its benefits remain unknown for people with WNT-driven cancers. The researchers hope to develop a next-generation compound with better drug-like properties and potentially advance it to clinical trials if it performs well in full preclinical tests.

The takeaway

Selectively targeting cancer-specific genetic losses may offer a route to treatments that spare healthy cells. Readers interested in the field can follow ongoing cancer research supported by federal agencies.