Published online Jan 15, 2016. doi: 10.4251/wjgo.v8.i1.128
Peer-review started: July 10, 2015
First decision: September 30, 2015
Revised: October 22, 2015
Accepted: November 23, 2015
Article in press: November 25, 2015
Published online: January 15, 2016
Processing time: 195 Days and 11.2 Hours
AIM: To investigate the impact of RAS and BRAF mutations on the pattern of metastatic disease and carcinoembryonic antigen (CEA) production.
METHODS: In this retrospective study, we investigated the impact of RAS and BRAF mutational status on pattern of metastatic disease and CEA production. Only patients presenting with a newly diagnosed metastatic colorectal cancer (CRC) were included. Patients’ characteristics, primary tumor location, site of metastatic disease and CEA at presentation were compared between those with and without RAS and BRAF mutations.
RESULTS: Among 174 patients, mutations in KRAS, NRAS and BRAF were detected in 47%, 3% and 6% respectively. RAS mutations (KRAS and NRAS) were more likely to be found in African American patients (87% vs 13%; P value = 0.0158). RAS mutations were associated with a higher likelihood of a normal CEA (< 5 ng/mL) at presentation. BRAF mutations were more likely to occur in females. We were not able to confirm any association between mutational status and site of metastatic disease at initial diagnosis.
CONCLUSION: No association was found between RAS and BRAF mutations and sites of metastatic disease at the time of initial diagnosis in our cohort. Patients with RAS mutations were more likely to present with CEA levels < 5 ng/mL. These findings may have clinical implications on surveillance strategies for RAS mutant patients with earlier stages of CRC.
Core tip: We investigated the impact of RAS and BRAF mutations on pattern of colorectal cancer (CRC) metastases and carcinoembryonic antigen (CEA) production. Patients with RAS mutations were more likely to present with CEA levels < 5 ng/mL. No association was found between RAS and BRAF mutations and sites of metastatic disease at the time of initial diagnosis in our cohort. Our study is the first study to link low CEA production with a RAS mutant status at the time of initial presentation of metastatic CRC. These findings may have clinical implications on surveillance strategies for RAS mutant patients with earlier stages of CRC.