Evidence map›Paper›PMID 28378457›Full record

ArticleCancer medicine2017

DNA methylation epigenotype and clinical features of NRAS-mutation(+) colorectal cancer.

Kiyoko Takane, Kiwamu Akagi, Masaki Fukuyo, Koichi Yagi, Tadatoshi Takayama, Atsushi Kaneda

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Kiyoko TakaneDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kiwamu AkagiDivision of Molecular Diagnosis and Cancer Prevention, Saitama Cancer Center, Saitama, Japan.
Masaki FukuyoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Koichi YagiDepartment of Gastrointestinal Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tadatoshi TakayamaDepartment of Digestive Surgery and Pathology, Nihon University School of Medicine, Tokyo, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0002-6980-5515
Chiba University · JPNihon University · JPSaitama Cancer Center · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sporadic colorectal cancer (CRC) is classified into several molecular subtypes. We previously established two groups of DNA methylation markers through genome-wide DNA methylation analysis to classify CRC into distinct subgroups: high-, intermediate-, and low-methylation epigenotypes (HME, IME, and LME, respectively). HME CRC, also called CpG island methylator phenotype (CIMP)-high CRC, shows methylation of both Group 1 markers (CIMP markers) and Group 2 markers, while IME/CIMP-low CRC shows methylation of Group 2, but not of Group 1 markers, and LME CRC shows no methylation of either Group 1 or Group 2 markers. While BRAF- and KRAS-mutation(+) CRC strongly correlated with HME and IME, respectively, clinicopathological features of NRAS-mutation(+) CRC, including association with DNA methylation, remain unclear. To characterize NRAS-mutation(+) CRC, the methylation levels of 19 methylation marker genes (6 Group 1 and 13 Group 2) were analyzed in 61 NRAS-mutation(+) and 144 NRAS-mutation(-) CRC cases by pyrosequencing, and their correlation with clinicopathological features was investigated. Different from KRAS-mutation(+) CRC, NRAS-mutation(+) CRC significantly correlated with LME. NRAS-mutation(+) CRC showed significantly better prognosis than KRAS-mutation(+) CRC (P = 3 × 10

Indexed as

DNA MethylationMutationAgedAged, 80 and overAge FactorsColorectal NeoplasmsCpG IslandsEpigenesis, GeneticFemaleGTP PhosphohydrolasesHumansMaleMembrane ProteinsMiddle AgedNeoplasm InvasivenessPrognosisGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins p21(ras)BRAF mutationcolorectal cancerDNA methylationKRAS mutationNRAS mutation

Identifiers

PMID28378457
PMCPMC5430106
OpenAlexW2604376384

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Registered trials

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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.