Parameter
| Biomarker | MSI (microsatellite instability) /dMMR (mismatch repair deficiency) | Full name | Microsatellite Instability / Mismatch Repair Deficiency | Molecular Type | Genomic features (DNA) |
|---|---|---|---|---|---|
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, and prediction | ||
| Disease | Gastric Cancer | Disease Subtypes | / | ||
| Organ | Stomach | Test Sample / Technology Platform | Tumor tissue (IHC for MMR protein, PCR for microsatellite loci, and NGS for TMB/MSI) | ||
| Pathobiological Mechanisms | Mutations or methylation of DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2) lead to dMMR, which in turn causes microsatellite sequence instability (MSI-H). Due to the accumulation of mutations, tumor cells produce a large number of neoantigens, which are easily recognized by the immune system and have a high response rate to ICIs treatment | ||||
| Clinical Availability Status | Clinically available (immunotherapy screening) : guidelines recommend ICIs treatment, and immunotherapy is recommended for MSI-H/dMMR patients | ||||
| Notes and Dynamics | As a "dominant population" marker for immunotherapy, MSI-H/dMMR patients have an objective response rate (ORR) of 30%-50% after ICIs treatment, which is significantly better than that of the general gastric cancer population. It can be used as a core indicator for first-line immunotherapy screening and is associated with a good prognosis | ||||