The detection of K-ras mutations in colorectal cancer using the amplification-refractory mutation system

Fox, Jayne C.; England, J.; White, Peter S.; Ellison, Gillian; Callaghan, Kay; Charlesworth, N. R.; Hehir, J.; McCarthy, Thomas L.; Smith-Ravin, Juliette; Talbot, Ian C.; Snary, David; Northover, J. M. A.; Newton, Clive R.; Little, Stephen F.

doi:10.1038/bjc.1998.212

Cited by 33 publications

(22 citation statements)

References 58 publications

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“…We have chosen ARMS because this technique has already been successfully applied elsewhere, such as for detection of mutations in hemochromatosis [Andre et al, 1998] or in cystic fibrosis [Ferrie et al, 1992] and is now commonly used in routine diagnosis in many laboratories. The suitability of ARMS PCR is demonstrated in many applications performed in different ways such as prenatal screening for cystic fibrosis [Bradley et al, 1998], gene therapy for the discrimination between expression of endogenous CFTR and introduced transgene [Thorpe and Porteous, 1999], detection of the most common G6PD gene mutations [Du et al, 1999], diagnosis of autosomal recessive spinal muscular atrophy [RavardGoulvestre et al, 1999], and detection of KRAS2 mutations in colorectal cancer [Fox et al, 1998]. A recent study [Tonks et al, 1999] has compared three methods: sequence specific oligotyping (SSO), reverse dot blot, and ARMS PCR for molecular typing of HLA class I.…”

Section: Discussionmentioning

confidence: 99%

High incidence of N and K-Ras activating mutations in multiple myeloma and primary plasma cell leukemia at diagnosis

Bézieau¹,

Devilder²,

et al. 2001

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Using allele-specific amplification method (ARMS), a highly sensitive one-stage allele-specific PCR, we have evaluated the incidence of NRAS and KRAS2 activating mutations (codons 12, 13, and 61) in 62 patients with either monoclonal gammopathy of undetermined significance (MGUS) or multiple myeloma (MM), primary plasma-cell leukemia (P-PCL), and also in human myeloma cell lines (HMCL). NRAS and/or KRAS2 mutations were found in 54.5% of MM at diagnosis (but in 81% at the time of relapse), in 50% of P-PCL, and in 50% of 16 HMCL. In contrast, the occurrence of such mutations was very low in MGUS and indolent MM (12.50%). Of note, KRAS2 mutations were always more frequent than NRAS. The validity of the technique was assessed by direct sequencing of cell lines and of some patients. Multiple mutations found in two patients were confirmed by subcloning exon PCR amplification products, testing clones with our method, and sequencing them. Thus, these early mutations could play a major role in the oncogenesis of MM and P-PCL.

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Section: Discussionmentioning

confidence: 99%

High incidence of N and K-Ras activating mutations in multiple myeloma and primary plasma cell leukemia at diagnosis

Bézieau¹,

Devilder²,

et al. 2001

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“…All patients had a histologically confirmed diagnosis of mCRC, and the mutational status of KRAS exon 2 (codons 12 and 13) was wild type as evaluated by one of the following methods: cycleave primer chain reaction method (13,14), direct sequencing or amplification refractory mutation system-Scorpion (ARMS/S) assay (15 …”

Section: Methodsmentioning

confidence: 99%

A short interval between bevacizumab and anti-epithelial growth factor receptor therapy interferes with efficacy of subsequent anti-EGFR therapy for refractory colorectal cancer

Taniguchi

Komori

Kadowaki

et al. 2016

Jpn. J. Clin. Oncol.

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Background: Both bevacizumab and anti-epithelial growth factor receptor (EGFR) agents (e.g. cetuximab and panitumumab) are sequentially used for metastatic colorectal cancer (mCRC). Their coadministration as a first-line treatment does not improve outcome, indicating that there are negative interactions between these agents. A long-term pharmacokinetics study demonstrated serum persistence of bevacizumab following termination of bevacizumab 6 months after the last administration. This prompted us to investigate the impact of short intervals between bevacizumab and anti-EGFR antibody on the efficacy of subsequent anti-EGFR therapy. Methods: We retrospectively reviewed consecutive patients with KRAS exon 2 wild-type mCRC who underwent anti-EGFR therapy after the failure of fluoropyrimidines, oxaliplatin and irinotecan. We divided patients into two groups (Group A: the interval between bevacizumab and anti-EGFR agent< 6 months; Group B: the interval >6 months). Results: Of the 114 included patients (median age, 63 years), 78 (68%) were male. Most patients (88%) were treated with cetuximab plus irinotecan. Groups A and B consisted of 74 and 40 patients, respectively. There were no significant differences in patient characteristics. Group B patients had significantly longer progression-free survival (4.2 vs. 6.6 months; HR, 0.65; 95% CI, 0.43-0.98; P = 0.038) and longer overall survival (11.6 vs. 14.3 months; HR, 0.63; 95% CI, 0.41-0.98, P = 0.039). The response rate was 24.3% in Group A and 47.5% in Group B (P = 0.012). Conclusion: A short interval between bevacizumab and anti-EGFR antibody treatment may interfere with the efficacy of subsequent anti-EGFR therapy.

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“…Among them, 128 patients enrolled in this retrospective study fulfilled the following criteria ( [15,16] , or the amplification refractory mutation system-Scorpion assay [17] .…”

Section: Study Populationmentioning

confidence: 99%

Efficacy of Second-Line Bevacizumab-Containing Chemotherapy for Patients with Metastatic Colorectal Cancer following First-Line Treatment with an Anti-Epidermal Growth Factor Receptor Antibody

Hasegawa¹,

Taniguchi²,

Mitani³

et al. 2017

Oncology

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Objective: Anti-epidermal growth factor receptor (EGFR) antibodies and bevacizumab are commonly used, sequentially, as palliative chemotherapies for patients with metastatic colorectal cancer. However, little is known about the efficacy of second-line treatments containing bevacizumab after first-line treatment with an anti-EGFR antibody. Methods: We retrospectively reviewed 128 patients who received second-line bevacizumab-containing chemotherapy and evaluated the effect of prior use of anti-EGFR antibody on the efficacy of the second-line treatment. Results: As first-line treatments, 35 of these patients received only cytotoxic chemotherapy (cohort A), 58 received bevacizumab-containing chemotherapy (cohort B), and 35 received anti-EGFR-containing chemotherapy (cohort C). The median progression-free survival (PFS) with the second-line bevacizumab-containing therapy was 8.3 months in cohort C, 6.9 months in cohort A (hazard ratio [HR], 1.43; 95% confidence interval [CI], 0.83-2.51), and 5.6 months in cohort B (HR, 1.95; 95% CI, 1.18-3.22). Multivariate analysis showed that PFS in cohort C was the same as that in cohort A, but better than that in cohort B. The overall response rate in cohort C (25.7%) was also similar to that in cohort A (20.0%), but better than that in cohort B (10.3%). Conclusions: Prior use of anti-EGFR antibody did not adversely affect the efficacy of subsequent bevacizumab-containing chemotherapy.

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The detection of K-ras mutations in colorectal cancer using the amplification-refractory mutation system

Cited by 33 publications

References 58 publications

High incidence of N and K-Ras activating mutations in multiple myeloma and primary plasma cell leukemia at diagnosis

High incidence of N and K-Ras activating mutations in multiple myeloma and primary plasma cell leukemia at diagnosis

A short interval between bevacizumab and anti-epithelial growth factor receptor therapy interferes with efficacy of subsequent anti-EGFR therapy for refractory colorectal cancer

Efficacy of Second-Line Bevacizumab-Containing Chemotherapy for Patients with Metastatic Colorectal Cancer following First-Line Treatment with an Anti-Epidermal Growth Factor Receptor Antibody

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