Abstract. KRAS proteins play an important role in regulating cell functions. A series of studies has revealed that mutations of KRAS are involved in gastric carcinogenesis. However, mutation status of KRAS remains unclear in gastric cancer from Chinese Mainland. It has been proved that KRAS mutation associates with resistance to epidermal growth factor receptor (EGFR) inhibitors. In this study, KRAS mutations were detected in 52 gastric adenocarcinomas from Northern China. High-resolution melting analysis (HRMA) was used and positive samples were confirmed by direct sequencing. Of the 52 cancers, KRAS mutations were found in 5 (9.6%). All cancers with KRAS mutation were from male patients. Frequencies of KRAS mutation were 14.3% (3/21) and 6.5% (2/31) in differentiated and undifferentiated cancers; 25% (1/4) and 8.3% (4/48) in early and advanced wall penetration cancers; and were 13.3% (2/15) and 8.1% (3/37) in without and with lymph node metastasis cancers, respectively. There was no significant correlation between KRAS mutation and clinicopathological features. There were 3 mutation types in the 5 mutations, including 2 G12D, 1 G12V and 2 G13D mutations. All codon 12 mutations were found in patients with lymph node metastasis and at advanced stage, whereas all codon 13 mutations were found in patients without lymph node metastasis and at early stage. These results support KRAS mutation may only be involved in carcinogenesis of partial gastric cancers and the different mutation types of KRAS may take part in development of gastric cancer at different stages. The resistance of partial gastric cancer patients to EGFR inhibitors may be induced by KRAS mutation.
ABSTRACT. Cyclin D1 (CCND1) plays a significant role in G1-S transition of cell cycle, and phosphatase and a tensin homologue (PTEN) negatively regulate cell cycle through phosphatidylinositol 3-kinase (PI3K)/AKT signaling. CCND1 and PTEN genetic polymorphisms might induce susceptibility to the occurrence of esophageal squamous cell carcinoma (ESCC). Three hundred and four ESCC patients and 413 healthy controls from Anyang, China, were enrolled in this study. All genotyping at CCND1 (807 G/A) and PTEN (rs701848 T/C and rs2735343 C/G) were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Unconditional logistic regression model was used to analyze the correlation between the polymorphisms and the susceptibility to develop ESCC. Statistically significant differences were observed between cases and controls in
Abstract. KRAS mutation is closely associated to carcinogenesis and prognosis of non-small cell lung cancer (NSCLC). Detection of KRAS mutation can also be used to select NSCLC patients for drug targeting with EGFR tyrosine kinase inhibitors. Data regarding the status of KRAS mutation in mainland China, which would assist in these interventions, is lacking. We have detected KRAS mutation from 103 NSCLC patients in mainland China with high resolution melting analysis (HRM) on LightScanner™, and compared this method of detection with sequencing, and found HRM to have greater sensitivity. We found 6 patients (5.8%) with KRAS mutation (3 patients, G12C; 1 patient, G12S; 1 patient, G12V; 1 patient, G13D). KRAS mutation was significantly associated to gender (p=0.027) and pathology types (p=0.000), but not to smoking. The mutation frequency of KRAS in NSCLC patients in mainland China is similar to those in East Asian countries, but lower than those in Western countries. However, the spectrum of KRAS mutation in mainland China is similar to those found in the USA. The results also exhibit dependence of KRAS mutation in China on ethnicity. The clinical significance of the spectral pattern of KRAS mutations in TKI resistance or tumorigenesis among patients with NSCLC in mainland China requires further investigation.
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