NTRK fusion tests detect whether a tumor contains gene fusions that join an NTRK gene (NTRK1, NTRK2, or NTRK3) to another gene, producing an abnormal TRK fusion protein whose constitutive kinase activity can drive cancer growth.

These tests measure the fusion at the DNA, RNA, or protein level (methods include NGS, RT‑PCR, RNA sequencing, FISH, or IHC) and serve as a predictive biomarker to identify patients who may benefit from TRK inhibitor therapies and to guide treatment decisions.

Samples for NTRK fusion testing are most commonly taken from tumor tissue collected during a biopsy or surgical resection — the specimen is typically fixed (formalin‑fixed, paraffin‑embedded, FFPE) or sometimes frozen and then sent to the testing laboratory. Cytology specimens or fine‑needle aspirates prepared as cell blocks can also be used. Some laboratories offer a blood-based “liquid biopsy” option that detects NTRK fusions in circulating tumor DNA (ctDNA) from a plasma sample collected by standard venipuncture into a cell‑free DNA preservation tube.

Collection is performed by a clinician or trained phlebotomist according to the laboratory’s instructions: tissue should be adequately sampled with sufficient tumor content and promptly preserved (avoiding over‑fixation), and blood should be drawn into the specified tube and shipped under recommended conditions. Proper labeling and submission of relevant clinical information help ensure the lab can process the sample and generate the most reliable result.

A positive NTRK fusion result for your sample means a tumor cell in the tested tissue contains a fusion of an NTRK gene with another gene; that finding describes the tumor’s biology rather than your overall lifetime cancer risk. In many cancers a detected NTRK fusion indicates the tumor may be driven by abnormal TRK protein activity and could make the tumor eligible for TRK inhibitor therapies, but it does not mean you have an inherited predisposition to cancer—most NTRK fusions are somatic (acquired) changes in the tumor itself.

A negative result means no NTRK fusion was detected in the tested sample but does not rule out cancer or other actionable changes; absence of an NTRK fusion simply means this particular target is not present to guide TRK-directed therapy. Interpret results with your oncology team, who can explain how the finding applies to your specific diagnosis, treatment options, and whether additional genetic or tumor testing is recommended.

NTRK fusion testing is generally reliable when using validated, appropriate methods, but accuracy depends on the assay type, specimen quality, and laboratory validation. RNA-based next‑generation sequencing (NGS) is considered the most sensitive and specific approach for detecting a wide range of fusion partners because it reads expressed fusion transcripts; DNA‑based NGS can detect many fusions but may miss events that span large or complex introns. Immunohistochemistry (IHC) is a useful, rapid screening tool with variable sensitivity (especially lower for some NTRK3 fusions) and occasional false positives in certain tumor types, so positive IHC is usually confirmed by molecular testing. FISH and RT‑PCR can be accurate for known rearrangements but may miss novel partners or complex fusions and typically do not identify the fusion partner (FISH) unless probes are designed specifically.

In clinical practice, accuracy is maximized by using orthogonal testing (e.g., confirmatory RNA‑NGS after positive IHC), sending adequate, well‑preserved tissue (or high‑quality RNA), and using an accredited laboratory with validated assays. Because NTRK fusions are rare in most cancers, pretest probability affects positive predictive value—screening strategies and reflex confirmatory testing are important to avoid false positives or negatives that would affect treatment decisions. Overall, when performed and interpreted appropriately, NTRK fusion testing is reliable for guiding targeted therapy selection, but method choice and laboratory quality are critical.

Test for NTRK fusions at initial diagnosis (or when considering targeted therapy) and whenever disease biology may have changed — for example at progression, relapse, before starting a new line of therapy, or if a new metastatic site is biopsied. Use validated tissue NGS or a liquid biopsy based on tumor accessibility and clinical context.

When using circulating tumor DNA for on‑treatment monitoring, testing intervals vary by clinical protocol; many centers align ctDNA checks with imaging/clinic visits (commonly every 4–12 weeks during active therapy) and reduce frequency during surveillance. Individual timing should be guided by your oncologist, treatment plan and the laboratory assay’s characteristics.

No, NTRK fusion test results highlight patterns of imbalance or resilience—not medical diagnoses. They should be interpreted alongside symptoms, medical history, and other lab or biomarker data by a qualified clinician.

NTRK fusions are genetic changes in the tumor, so you cannot change the fusion itself with lifestyle measures; “improving” levels usually means treating the tumor that harbors the fusion. The main clinical approach is to discuss targeted therapy (TRK inhibitors), clinical trials, or other systemic treatments with your oncologist — many patients with confirmed NTRK fusions are considered for TRK inhibitors when appropriate. Decisions should be made by your treating team or a molecular tumor board, and any treatment plan requires specialist guidance and monitoring.

Also consider confirming the result and ensuring the best test method: RNA‑based NGS or validated fusion assays detect NTRK fusions more reliably than some DNA panels, and repeat testing or a liquid biopsy may be useful if initial tissue was limited. If you have questions about test accuracy, treatment options, clinical trials, or monitoring strategies (imaging and biomarkers), ask your oncologist or seek a second opinion from a genomic‑medicine specialist.