Background: CC is a heterogeneuous disease with clinical, pathological and biological variability. Molecular classification could indentify prognostic subtypes. Methods: 105 patients with stage I-III were included in the study. KRAS, NRAS (Exons 2,3,4) and BRAFV600E mutations were analyzed by a PCR-based assay. MMR (MLH1 and MSH2) proteins expression were analyzed by immunohistochemistry; loss of expression of any indicated deficient (dMMR) vs proficient MMR (pMMR). CC was categorized into 5 subtypes: Traditional (T) (pMMR; wt BRAF and RAS); Alternate (A) (pMMR; wt BRAF and mutant RAS); Serrated (S) (pMMR; mutant BRAF and wt RAS); Serrated dMMR (Sd) (dMMR; mutant BRAF and wt RAS) and Familial (F) (dMMR; wt BRAF, any RAS). Non-parametric tests were used for correlation with clinico-pathological variables and Cox models for association with Disease Free Survival (DFS). Results: Mutational status: 41% KRAS, 5% NRAS and 11% BRAF mutations. MMR status: dMMR 19%; pMMR 81%. Molecular subtypes: T 35%, A 39%, S 7%, Sd 5% and F 14%. Right-sided CC 46%; high grade (HG) CC 12%. Right-sided and dMMR CC showed higher rate of BRAF mutations (21% vs 4% p = .011 and 25% vs 8% p = .034). Stage II and III CC showed higher rate of BRAF mutations vs stage I (14% and 21% vs 0%, respectively; p < .005). dMMR CC was more often right-sided (85% vs 37%, p < .001) and had more HG histology (31% vs 8%, p = .006). T subtype vs others was more likely left-sided (78% vs A 55% vs S 28% vs Sd 0% vs F 20%; p < 0.005). S dMMR and F vs A were more likely right-sided (100% and 80 % vs 45 %; p < .05). F vs T and vs A CC had more HG (33% vs 8%, p = .039; vs 7%, p = .026). Risk of progression is higher in mutated KRAS CC (Odds ratio (OR) 3,36; CI: 1,19-9,47 p = .017). RAS mutated CC showed higher risk of death (OR 5,11; CI: 1,00-25,43 p = .040). Wt KRAS and wt RAS CC showed better DFS (HR 0,31 CI 0.12-0.79 p = .015 and HR 0,39 CI 0,15–1,00 p = .051). T vs S showed better DFS (HR 0,21 IC 0,04 – 0,95 p = .044). S and A together compared to T, showed a tendency to a worse DFS (HR 2,86 IC 0,93–0,78 p = .066). Conclusions: This molecular classification identifies prognostic groups with different clinical and pathological features in early-stage CC.