Mutation Analysis of K-rasOncogenes in Gastroenterologic Cancers by the Amplified Created Restriction Sites Method

Lin, Shyr-Yi; Chen, Pao-Huei; Wang, Chung-Kwe; Liu, Jean-Dean; Siauw, Chuan-Pau; Chen, Yi Jen; Yang, Ming-Jui; Liu, Mau-Ho; Chen, Te‐Chuan; Chang, Jan‐Gowth

doi:10.1093/ajcp/100.6.686

Cited by 26 publications

(15 citation statements)

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“…No mutation was found in specimens from South Africa (20). In China, some study groups including one from Taiwan did not find KRAS mutation in gastric cancer specimens (29,30), whereas 8.5% of KRAS mutation frequency was revealed by a study group from Hong Kong region (31). We found 9.6% of KRAS mutation frequency in gastric cancers from Chinese Mainland.…”

Section: ------------------------------------------------------------mentioning

confidence: 51%

Mutation detection of KRAS by high-resolution melting analysis in Chinese with gastric cancer

Liu

Liu²,

Li³

et al. 2009

Oncol Rep

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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.

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confidence: 51%

Mutation detection of KRAS by high-resolution melting analysis in Chinese with gastric cancer

Liu

Liu²,

Li³

et al. 2009

Oncol Rep

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“…Tumor specimens were frozen immediately after surgical resection and stored in liquid nitrogen until the DNA was extracted. DNA was extracted as previously described [22]. This study was approved by the Institutional Review Board of the Changhua Christian Hospital.…”

Section: Methodsmentioning

confidence: 99%

RAS, BRAF, and TP53 Gene Mutations in Taiwanese Colorectal Cancer Patients

Chang

Yeh

et al. 2013

Onkologie

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Background: Colorectal cancer (CRC) plays an important role in cancer mortality and morbidity. This study examined colorectal tissues for RAS, BRAF, and TP53 gene mutations to assess their value as indicators of outcomes of CRC therapy. Material and Methods: DNA was extracted from tissues taken from 165 patients with CRC. RAS gene mutations (exons 2 and 3) were detected by primer extension analysis. BRAF gene mutations (V600E) were detected by high resolution melting (HRM) analysis. TP53 gene mutations (exons 5-8) were detected by direct sequencing. Results: RAS, BRAF, and TP53 mutations occurred in 36.97% (61/165), 4.24% (7/165), and 37.58% (62/165), respectively. The KRAS mutation is a predictor for poor 5-year survival (p = 0.05), and the co-presence of KRAS and TP53 mutations correlates with lymph node involvement (p = 0.029), tumor stage (p = 0.029), and poor survival (p = 0.021). Multivariate analysis adjusted for tumor size, histologic grade, lymph node metastasis, sex, and age also indicated that KRAS mutations correlate significantly with overall survival (p = 0.036). Conclusion: The KRAS mutation is not present in about one-third of CRC patients, and therefore other gene mutations need to be investigated to better understand the molecular mechanisms of CRC and its treatment.

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“…HRAS codon 12 primers and PCR conditions are shown in Table 1. KRAS codon 13 method was per Lin et al 22 HRAS codon 13 method was per O'Leary et al 23 …”

Section: Nras Mutation Screen: Denaturing High-performance Liquid Chrmentioning

confidence: 99%

RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years

Bowen

Frew

Hills

et al. 2005

Blood

220

188

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The pathogenesis of acute myeloid leukemia (AML) involves the cooperation of mutations promoting proliferation/survival and those impairing differentiation. The RAS pathway has been implicated as a key component of the proliferative drive in AML. We have screened AML patients, predominantly younger than 60 years and treated within 2 clinical trials, for NRAS (n ‫؍‬ 1106), KRAS (n ‫؍‬ 739), and HRAS (n ‫؍‬ 200) hot-spot mutations using denaturing high-performance liquid chromatography or restriction fragment length polymorphism (RFLP) analysis. NRAS mutations were confirmed in 11% of patients (126/1106) and KRAS mutations in 5% (39/739). No HRAS mutations were detected in 200 randomly selected samples. Codons most frequently mutated were N12 (43%), N13 (21%), and K12 (21%). KRAS mutations were relatively overrepresented in French-American-British (FAB) type M4 (P < .001). NRAS mutation was overrepresented in the t(3;5)(q21ϳ25;q31ϳq35) subgroup (P < .001) and underrepresented in t(15;17)(q22;q21) (P < .001). KRAS mutation was overrepresented in inv(16)(p13q22) (P ‫؍‬ .004). Twenty-three percent of KRAS mutations were within the inv(16) subgroup. RAS mutation and FLT3 ITD were rarely coexistent (14/768; P < .001). Median percentage of RAS mutant allele assayed by quantitative RFLP analysis was 28% (N12), 19% (N13), 25% (N61), and 21% (K12). RAS mutation did not influence clinical outcome (overall/ disease-free survival, complete remission, relapse rate) either for the entire cohort or within cytogenetic risk groups.

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Mutation Analysis of K-rasOncogenes in Gastroenterologic Cancers by the Amplified Created Restriction Sites Method

Cited by 26 publications

References 0 publications

Mutation detection of KRAS by high-resolution melting analysis in Chinese with gastric cancer

Mutation detection of KRAS by high-resolution melting analysis in Chinese with gastric cancer

<b><i>RAS, BRAF,</i></b> and <b><i>TP53</i></b> Gene Mutations in Taiwanese Colorectal Cancer Patients

RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years

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