الفهرس 
Extended RAS gene mutations study in colorectal cancer patients
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Abstract
Background: Colorectal cancer (CRC) is the third most prevalent malignancy worldwide. In Egypt, CRC contributes 6.5% of all cancers. Efforts have been made for better understanding of the pathophysiological and molecular mechanisms of the disease, and improvements in its clinical management. RAS family proteins play important roles in the epidermal growth factor receptor (EGFR) signaling pathway. Mutations in RAS genes (including KRAS and NRAS) often result in constitutive activation of RAS proteins and persistent downstream signaling. RAS mutation status has emerged as an important predictive marker for anti-EGFR therapy in patients with CRC because patients with mutant RAS are unlikely to benefit from treatment with the anti-EGFR antibodies. Aim of the work: Extended RAS gene mutations screening, including KRAS and NRAS genes exons 2, 3 and 4 in CRC patients using HRMA and Sanger sequencing and to correlate the tumor mutational status with the clincopathological status in the studied group of patients. Subjects and Methods: KRAS and NRAS genes were scanned for mutations in 50 FFPE CRC tissue samples using High Resolution Melting Analysis followed by mutation confirmation using Sanger sequencing. Results: Our study included 28 (56%) male patients and 22 (44%) female patients diagnosed with CRC aged from 19 to 81 years. Histopathological examination of the samples revealed 47 (94%) adenocarcinoma and 3 (6%) mucinous carcinoma. Of the examined samples, 22/37 (59.5%) patients had Lymph Node (LN) metastasis and 7/37 (19%) had distant metastasis. Screening for mutations in KRAS and NRAS genes in exons 2, 3 and 4 using HRMA followed by confirmation by Sanger sequencing showed no mutations