MET gene mutation tests measure genetic and molecular alterations that activate the MET receptor tyrosine kinase in tumors — most commonly point mutations (including exon 14 skipping alterations), gene amplifications (increased copy number), gene fusions/rearrangements, and sometimes protein overexpression. These changes indicate oncogenic MET signaling that can drive tumor growth and influence prognosis.

Clinically, detecting these MET alterations (by DNA/RNA sequencing, FISH for amplification, or IHC for protein) helps identify patients who may benefit from MET-targeted therapies and informs treatment selection and eligibility for clinical trials.

Samples for MET gene mutation testing are most commonly collected from either tumor tissue or blood. Tumor tissue is obtained during a diagnostic biopsy or surgery (core needle, excisional, or fine‑needle aspirate) and is usually submitted as a formalin‑fixed, paraffin‑embedded (FFPE) block or unstained slides. A blood sample is collected by venipuncture into specialized tubes for plasma; the lab isolates circulating tumor DNA (ctDNA) from plasma for noninvasive detection of somatic MET mutations. Some tests also accept saliva or buccal swabs when assessing germline (inherited) MET variants, though saliva is not typically used to identify tumor‑specific changes.

The choice of sample depends on the test purpose: tissue sequencing is the gold standard for profiling tumor‑specific MET alterations, plasma ctDNA is used when tissue is unavailable or for monitoring over time, and saliva/buccal swab is for germline testing. Collection kits and specific handling instructions are provided by the testing laboratory to preserve DNA quality. Test results are informational about MET mutation status and should be reviewed with a healthcare professional—these services are not a substitute for medical diagnosis or treatment decisions.

A MET gene mutation test can detect changes in the MET gene either in your normal (germline) DNA or in tumor tissue (somatic). Germline pathogenic MET variants are rare but can raise your inherited risk for specific cancers—most notably hereditary papillary renal cell carcinoma—so a positive germline result may indicate increased lifetime risk for those cancers. Somatic MET alterations (for example exon 14 skipping, amplifications, or certain point mutations) found in a tumor do not indicate inherited risk but can show that MET is driving that particular cancer and may make the tumor eligible for MET-targeted therapies or clinical trials.

Interpretation matters: a clearly pathogenic or likely pathogenic result has clinical implications, a variant of uncertain significance (VUS) is inconclusive, and a negative result does not guarantee no increased cancer risk from other genes or non-genetic factors. Tests have technical and biological limits (sampling, tumor heterogeneity, assay sensitivity). Discuss results with a medical geneticist or oncologist to understand what the specific finding means for your cancer risk, surveillance, treatment options, and whether family testing is appropriate.

MET mutation testing is generally reliable when performed by validated, accredited laboratories using appropriate methods, but accuracy depends on the specific assay and sample. DNA-based next‑generation sequencing (NGS), targeted PCR, FISH (for amplification), and RNA assays (for exon‑14 skipping/fusions) each have strengths and limits: RNA assays detect splice variants better, FISH and validated copy‑number NGS better assess amplification, and high‑quality tissue NGS typically has higher sensitivity than cell‑free (plasma) testing. Sensitivity, specificity and the limit of detection vary by platform, sample quality, tumor fraction and allele frequency, so low‑frequency variants or heterogeneous tumors can yield false negatives and sequencing artifacts or clonal hematopoiesis can cause false positives.

Because results directly affect treatment, clinicians should use tests from CLIA/CAP‑accredited labs (or equivalent), review the assay’s limit‑of‑detection and reporting metrics, and consider orthogonal confirmation (different method or specimen) for critical findings. Plasma (ctDNA) testing is useful for less invasive screening and monitoring but may miss alterations present in tissue; when a MET alteration is suspected or would change therapy, tissue testing or reflex RNA/FISH confirmation improves reliability. Interpretation in the clinical context by the treating team is essential.

How often you should test MET mutation levels depends on your cancer type, stage, current treatment and whether you’re using tissue or plasma (liquid) testing — there’s no one-size-fits-all interval. Common practice is to establish a baseline at diagnosis, re-test if the disease progresses or if you change therapies, and perform targeted monitoring during therapy when clinicians need to detect emerging resistance or confirm response.

Follow the schedule your oncologist recommends (they’ll coordinate mutation testing with imaging, treatment cycles and symptoms); testing may be done sooner if new symptoms arise, if treatment response is unclear, or if trial/insurance requirements dictate different timing.

No — MET gene mutation test results are not by themselves diagnostic. They identify patterns of imbalance or resilience in the MET signaling pathway that may inform risk, prognosis, or treatment options, but they do not constitute a medical diagnosis.

Results must be interpreted in the context of clinical symptoms, medical history, imaging, and other laboratory or biomarker data by a qualified clinician who can integrate all information and determine appropriate next steps.

You generally cannot “fix” or reverse a MET gene mutation yourself — management is clinical. If the MET alteration is driving a cancer, treatment is aimed at controlling the tumor (for example with MET-targeted drugs when appropriate, chemotherapy, immunotherapy, surgery or radiation) and may include enrollment in clinical trials; your oncology team will decide the best approach. Doctors commonly use repeat molecular testing (tumor biopsy or circulating tumor DNA/plasma tests) to monitor mutation levels or variant allele fraction and to assess response or resistance to therapy.

Lifestyle changes or supplements do not change the underlying mutation, though maintaining good nutrition, exercise, and adherence to prescribed treatment can help you tolerate therapy. Ask your oncologist about targeted treatment options, monitoring plans, genetic counseling if a germline mutation is possible, and second opinions or clinical-trial opportunities before making treatment decisions.