Trial reportMolecular medicine (Cambridge, Mass.)2013
Low percentage of KRAS mutations revealed by locked nucleic acid polymerase chain reaction: implications for treatment of metastatic colorectal cancer.
Trial report in Molecular medicine (Cambridge, Mass.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Expanded Low Allele FrequencyClinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- Article
- Optical and theoretical study of strand recognition by nucleic acid probes.Communications chemistry · 2020Article
- Clinical Evaluation of IntelliPlex™ KRAS G12/13 Mutation Kit for Detection of KRAS Mutations in Codon 12 and 13: A Novel Multiplex Approach.Molecular diagnosis & therapy · 2019Article
- Clinico-pathological associations and concomitant mutations of the RAS/RAF pathway in metastatic colorectal cancer.Journal of translational medicine · 2019Article
- Wild‑type blocking pcr coupled with internal competitive amplified fragment improved the detection of rare mutation of KRAS.Molecular medicine reports · 2017Article
- Extreme assay sensitivity in molecular diagnostics further unveils intratumour heterogeneity in metastatic colorectal cancer as well as artifactual low-frequency mutations in the KRAS gene.British journal of cancer · 2017Article
- Current companion diagnostics in advanced colorectal cancer; getting a bigger and better piece of the pie.Journal of gastrointestinal oncology · 2017Review
- Consensus molecular subtypes and the evolution of precision medicine in colorectal cancer.Nature reviews. Cancer · 2017Review
- The influence of subclonal resistance mutations on targeted cancer therapy.Nature reviews. Clinical oncology · 2016Review
- Liquid biopsy for detection of actionable oncogenic mutations in human cancers and electric field induced release and measurement liquid biopsy (eLB).The Analyst · 2016Review
- Significance of KRAS, NRAS, BRAF and PIK3CA mutations in metastatic colorectal cancer patients receiving Bevacizumab: a single institution experience.Acta medica Lituanic · 2016Article
- Prediction of response to anti-EGFR antibody-based therapies by multigene sequencing in colorectal cancer patients.BMC cancer · 2015Article
- Eprobe-mediated screening system for somatic mutations in the KRAS locus.Oncology reports · 2015Article
- Expanded RAS: refining the patient population.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Article
- BRAF Mutations in an Italian Regional Population: Implications for the Therapy of Thyroid Cancer.International journal of endocrinology · 2015Article
- Report from the OECI Oncology Days 2014.Ecancermedicalscience · 2014Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic colorectal cancer (mCRC) is frequently characterized by the presence of mutations of the KRAS oncogene, which are generally associated with a poor response to treatment with anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibodies. With the methods currently used, a case is classified as KRAS-mutated when approximately 20% of the cells bear an activating KRAS mutation. These considerations raise the question of whether cells with a mutated KRAS can be found in mCRC cases classified as KRAS wild-type when more sensitive methods are used. In addition, the issue arises of whether these mCRC cases with low proportion of KRAS-mutated cells could account at least in part for the therapeutic failure of anti-EGFR therapies that occur in 40-60% of cases classified as KRAS wild type. In this study, we compared the classical assays with a very sensitive test, a locked nucleic acid (LNA) polymerase chain reaction (PCR), capable of detecting KRAS-mutated alleles at extremely low frequency (detection sensitivity limit 0.25% mutated DNA/wild-type DNA). By analyzing a cohort of 213 mCRC patients for KRAS mutations, we found a 20.6% discordance between the sequencing/TheraScreen methods and the LNA-PCR. Indeed, 44 mCRC patients initially considered KRAS wild type were reclassified as KRAS mutated by using the LNA-PCR test. These patients were more numerous among individuals displaying a clinical failure to anti-EGFR therapies. Failure to respond to these biological treatments occurred even in the absence of mutations in other EGFR pathway components such as BRAF.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.