Different survival rates of patients with colorectal cancer have been investigated in several studies [20–22, 28–31]. The results are sometimes conflicting because of the different pathogenetic mechanism of tumorigenesis between sporadic and familiar types of colorectal syndrome (HNPCC in particular). These differences are probably due to different clinical pathological characteristics of neoplasia and genetic alterations. Two major mechanisms of genomic instability have been identified in sporadic colorectal cancer progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes, such as Ki-ras, and inactivation of tumor-suppressor genes, such as TP53 and APC [32–34]. The second, known as microsatellite instability (MSI), was described in association with hereditary nonpolyposis colorectal cancer [35–37].
The aim of our retrospective cohort study was to compare the survival between patients with sporadic and hereditary colorectal cancer after surgical resection. A Finnish study  and a recent Lithuanian study  reported an improved prognosis for HNPCC patients compared to sporadic colorectal cancer patients, but an Italian study could not confirm this result . The localization of tumor is an important prognostic factor for survival. In our study right localization (from cecum to splenic flexure) is significantly more represented in the HNPCC group with respect to the sporadic colorectal cancer group (p < 0.0001). This different anatomical distribution between HNPCC and sporadic CRC, confirmed in literature [34, 35], is one of the Amsterdam criteria for the diagnosis of HNPCC and determines a better prognosis, being less aggressive.
We have considered survival, stratified by site, in the two groups and we demonstrated that survival for rectal cancer does not differ statistically, so the presence of rectal cancer with a known worse prognosis and high rate of recurrence does not influence survival of sCRC or HNPCC (p = 0.45). The statistically significant difference of survival was for colon cancer (right location), independent of stage at diagnosis, between sporadic and HNPCC cancer (p < 0.0001).
Furthermore, in order to have a better definition of population in the study, we considered several clinical features such as the presence of synchronous or metachronous tumors. None of these features were represented sufficiently enough in either of the groups as to influence survival rates.
The 5 years cumulative survival in HNPCC and in sporadic colorectal cancer was 94.2% versus 75.3% respectively. This difference was statistically significant (p < 0.0001). These results do not confirm the observations previously reported by Bertario et al  where 5 years cumulative survival in HNPCC, FAP and sporadic colorectal cancer groups was not statistically different. Otherwise, our results conflicts with those of Barnetson et al , in which survival was not significantly different among carriers and non-carriers of MMR mutations in a series of early colorectal cancer patients. However, after stratification for Dukes' stage survival remained statistically significant, better for HNPCC versus sporadic colorectal cancer (p < 0.0001). In our study the stage distribution was not significantly different between the two groups (sCRC versus HNPCC), 61.6% vs. 70% and 38.4% vs. 30% respectively (p = 0.29), demonstrating that it did not influence the overall survival between the two groups.
Myrhoj et al  reported an improved prognosis of cancer in patients with HNPCC versus sporadic CRC, but in the HNPCC series included a high proportion of localized tumors and this indicated that the good prognosis was based on a more favourable stage at diagnosis. Several studies described a trend toward prolonged survival and better prognosis in patients with mutations or MSI in HNPCC, revealing the presence of distinct biological features of colon cancer in families with or without mutations , though, as above mentioned, it was not observed by other authors . In our study 15 HNPCC patients had positive MSI mutational analysis; overall survival of this series of patients was 100%.