eligibility_summary
Inclusion: consent, ≥18, ECOG 0–2, LE >12 wks, left‑sided unresectable metastatic colorectal adenocarcinoma, no prior systemic tx for mets (neo/adjuvant >6 mo ok), KRAS/NRAS WT, adequate labs: ANC ≥1.5, Plt ≥100, Hgb ≥90, CrCl >50, Tbili <1.5×ULN, AST/ALT per liver mets, tumor tissue ≤24 mo. Exclusion: RAS or BRAF V600E mut/uncertain RAS, other cancer <5 y (except BCC/cervical CIS), pregnant/lactating, HIV, active HBV/HCV, urgent surgery, investigator risk, no central venous access.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Phase III randomized trial in left‑sided RAS‑wild type metastatic colorectal cancer. Interventions: FOLFOX chemotherapy (oxaliplatin: platinum DNA crosslinker, 5‑fluorouracil: antimetabolite thymidylate synthase inhibitor, folinic acid: 5‑FU enhancer) plus either anti‑EGFR monoclonal antibodies (cetuximab, chimeric IgG, panitumumab, fully human IgG) or bevacizumab (humanized IgG anti‑VEGF‑A), assigned by molecular profiling. Mechanisms: cetuximab/panitumumab block EGFR, inhibiting ligand binding and downstream MAPK and PI3K signaling in tumor cells, bevacizumab neutralizes VEGF‑A to inhibit tumor angiogenesis, FOLFOX damages DNA and impairs synthesis in rapidly dividing cells. Targets/pathways: EGFR on colorectal cancer cells, RAS/RAF/MEK/ERK and PI3K/AKT pathways, VEGF‑driven endothelial cells/angiogenesis, DNA replication/repair machinery. Molecular testing seeks to identify alternative oncogenic drivers predicting resistance to EGFR blockade.