Objective: Despite the recent advances in therapeutic armamnet colorectal cancer (CRC) remains one of the leading cancer deaths worlwide. CRC has a heterogenous molecular background with known prognostic and predictive markers, but the whole picture is rather complex with many unexplored connections. Method: We performed multiple immunohistochemical stainings on tissue microarrays (TMA) made of 95 CRC cases to study the correlations between EGFR-RAS, cell cycling, apoptosis, cell adhesion and tumor invasion pathways. We evaluated digitized slides using matrix scores considering both the frequency and positivity of cells and statistical analysis followed. Results: We found strong linear correlation between positivity and (p-1068, p-1173) phosphorylation of the EGFR receptor and p53 positivity detected with different clones. Furthermore, phospho-NF-KB p65 positivity was strongly linked to Survivin-expression. Conclusion: Activation of EGFR-related pathways including NF-kB is a key factor in CRC-growth. The strong link between cancer promoting EGFR signaling and the mutational lack of the p53 driven apoptosis suggests a deadly cooperation, which can be further aggravated by forced tumor survival through survivin. Correlation of these markers potentially predict poor disease outcome but can be specifically targeted by the upcoming new molecules of tailored therapy. Objective: KRAS mutational status is important in colorectal carcinoma (CRC). It is unclear, however, which is the most informative tissue source for study in CRC cases showing more than one tumor mass. To explore this issue we determined KRAS status in a series of primary (PT) and metastatic CRCs.