Abstract
ObjectivesKRAS, NRAS, and BRAF mutations are commonly present in colorectal cancer (CRC). We estimated the frequency of KRAS, NRAS, and BRAF mutations and assessed their impact on survival and other clinical variables among Saudi patients.DesignRetrospective cohort study design.SettingsOncology department of a tertiary hospital in Riyadh, Saudi Arabia. We gathered information from 2016 to 2018.ParticipantsCohort of 248 CRC patients to assess the demographic data, pathological tumour features, response to treatment modalities, disease progression, and metastasis.Statistical analysis usedCorrelation analysis using the chi-square test. Survival analysis using a Kaplan Meier method. Cox regression analysis to calculate the hazard ratios.ResultsDemographic data revealed that 84% of patients were diagnosed with CRC above the age of 50 years. Only 27% of patients presented with distant metastasis. KRAS mutations were the most prevalent (49.6%), followed by NRAS mutations (2%) and BRAF mutations (0.4%). Wild type tumours were found among 44.4% of patients. KRAS mutation showed no significant correlation with the site, type, pathological grade, and stage of the tumour.The mean survival time was shorter among patients with KRAS mutations than among patients with wild type KRAS tumours (54.46 vs. 58.02 months). Adjusted analysis showed that the survival time was significantly affected by patients’ age at diagnosis (P = 0.04). Male patients had an increased risk of mortality by 77% (hazard ratio: 1.77).ConclusionsSaudi CRC patients had a high frequency of KRAS mutations and a low frequency of BRAF mutations. The KRAS mutation status did not affect the patients’ survival.
Highlights
According to the Saudi Cancer Registry, colorectal cancer (CRC) is the most commonly diagnosed cancer among males and the third commonest among females [1]
KRAS, NRAS, and BRAF mutations are commonly present in colorectal cancer (CRC)
Saudi CRC patients had a high frequency of KRAS mutations and a low frequency of BRAF mutations
Summary
According to the Saudi Cancer Registry, colorectal cancer (CRC) is the most commonly diagnosed cancer among males and the third commonest among females [1]. Despite advancements made in CRC diagnosis and multimodal treatment, it remains the third commonest cause of cancer-related deaths worldwide; accounting for over half a million deaths annually [2,3]. CRC is a heterogeneous disease that arises from multiple cellular and genetic alterations. Advanced characterisation of the genetic alterations in CRC has suggested that the epidermal growth factor receptor (EGFR) and the downstream RAS–RAF–BRAF–MAPK pathways play a significant role in disease development [5]. RAS is a family of genes that encode for guanosine triphosphatases. The first identified RAS genes were HRAS, KRAS, and NRAS. RAS can subsequently activate other proteins that regulate transcription factors involved in cell cycle progression, apoptosis, differentiation, and proliferation [6]
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