Furthermore, high tumor budding was associated with mutations in TP53 (P=0.03) and inversely associated with mutations in the mTOR pathway (PIK3CA and AKT, P=0.02).
Our results showed that 21 of 34 tumors with high-grade TB had KRAS mutations (P=.001) and KRAS G12D and PIK3CA exon 9 variants were significantly associated with high-grade TB (P=.002 and .006, respectively); furthermore, tumors with KRAS mutations in exons 3 and 4 tended to have lymphovascular tumor emboli and perineural invasion (P=.044 and .049, respectively).