Colorectal Cancer (CRC)
Colorectal Cancer originates in the colon or rectum and includes molecular subtypes defined by key genomic alterations. These biomarkers influence prognosis and therapy.
Biomarkers used in this indication
Each approval combines this indication with specific biomarker criteria and a therapy. Select a therapy from the tables below to open its FDA-defined testing pathway.
Defined explicitly for Colorectal Cancer (CRC) in FDA labeling.
| Biomarker | Biomarker criteria | Therapies |
|---|---|---|
| ACVR2A, BTBD7, DIDO1, MRE11, RYR3, SEC31A and SULF2 |
| |
| BRAF |
| |
| EGFR (HER1) |
| |
| KRAS |
| |
| KRAS |
| |
| KRAS |
| |
| KRAS |
| |
| KRAS and NRAS |
|
Defined at the solid tumor level and applicable to Colorectal Cancer (CRC) and other solid tumor cancers.
Therapies with biomarker-defined approvals
Each therapy below has at least one FDA companion diagnostic approval tied to Colorectal Cancer (CRC). Select a therapy to view the specific approval and eligible tests.
BRAF (V600E)
EGFR (HER1) (protein expression); KRAS (G12A, G12D, G12R, G12C, G12S, G12V, G13D); KRAS (KRAS wild-type (absence of mutations in codons 12 and 13)); KRAS (Mutations in codons 12 and 13 of KRAS gene)
deficient mismatch repair (dMMR) proteins (MLH1, PMS2, MSH2 and MSH6); MSI-High (Microsatellite instability-High)
deficient mismatch repair (dMMR) proteins (MLH1, PMS2, MSH2 and MSH6); MSI-High (Microsatellite instability-High); TMB (TMB ≥ 10 mutations per megabase)
KRAS (G12C)
KRAS (G12C)
ACVR2A, BTBD7, DIDO1, MRE11, RYR3, SEC31A and SULF2 (Microsatellite instability-High (MSI-H)); deficient mismatch repair (dMMR) proteins (MLH1, PMS2, MSH2 and MSH6)
ACVR2A, BTBD7, DIDO1, MRE11, RYR3, SEC31A and SULF2 (Microsatellite instability-High (MSI-H)); deficient mismatch repair (dMMR) proteins (MLH1, PMS2, MSH2 and MSH6)
RET (fusions)
NTRK1, NTRK2 and NTRK3 (fusions)
EGFR (HER1) (protein expression); KRAS (G12A, G12D, G12R, G12C, G12S, G12V, G13D); KRAS (KRAS wild-type (absence of mutations in codons 12 and 13)); KRAS (Mutations in codons 12 and 13 of KRAS gene); KRAS and NRAS (wild-type (absence of mutations in exons 2, 3 and 4))
NTRK1, NTRK2 and NTRK3 (fusions)