Evidence map›Paper›PMID 27145369›Full record

ArticleOncotarget2016

Assessment of epigenetic alterations in early colorectal lesions containing BRAF mutations.

Takeshi Sawada, Eiichiro Yamamoto, Hiro-O Yamano, Masanori Nojima, Taku Harada, Reo Maruyama, Masami Ashida, Hironori Aoki, Hiro-O Matsushita, Kenjiro Yoshikawa and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
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

18 authors at 5 institutions in 1 country.

Takeshi SawadaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Eiichiro YamamotoDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiro-O YamanoDepartment of Gastroenterology, Akita Red Cross Hospital, Akita, Japan.
Masanori NojimaCenter for Translational Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Taku HaradaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Reo MaruyamaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masami AshidaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hironori AokiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiro-O MatsushitaDepartment of Gastroenterology, Akita Red Cross Hospital, Akita, Japan.
Kenjiro YoshikawaDepartment of Gastroenterology, Akita Red Cross Hospital, Akita, Japan.
Eiji HaradaDepartment of Gastroenterology, Akita Red Cross Hospital, Akita, Japan.
Yoshihito TanakaDepartment of Gastroenterology, Akita Red Cross Hospital, Akita, Japan.
Shigenori WakitaDivision of Cardiovascular Medicine, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Japan.
Takeshi NiinumaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masahiro KaiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Makoto EizukaDepartment of Molecular Diagnostic Pathology, Iwate Medical University School of Medicine, Morioka, Japan.
Tamotsu SugaiDepartment of Molecular Diagnostic Pathology, Iwate Medical University School of Medicine, Morioka, Japan.
Hiromu SuzukiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sapporo Medical University · JPAkita Red Cross Hospital · JPIwate Medical University · JPKanazawa University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To clarify the molecular and clinicopathological characteristics of colorectal serrated lesions, we assessed the DNA methylation of cancer-associated genes in a cohort of BRAF-mutant precancerous lesions from 94 individuals. We then compared those results with the lesions' clinicopathological features, especially colorectal subsites. The lesions included hyperplastic polyps (n = 16), traditional serrated adenomas (TSAs) (n = 15), TSAs with sessile serrated adenomas (SSAs) (n = 6), SSAs (n = 49) and SSAs with dysplasia (n = 16). The prevalence of lesions exhibiting the CpG island methylator phenotype (CIMP) was lower in the sigmoid colon and rectum than in other bowel subsites, including the cecum, ascending, transverse and descending colon. In addition, several cancer-associated genes showed higher methylation levels within lesions in the proximal to sigmoid colon than in the sigmoid colon and rectum. These results indicate that the methylation status of lesions with BRAF mutation is strongly associated with their location, histological findings and neoplastic pathways. By contrast, no difference in aberrant DNA methylation was observed in normal-appearing background colonic mucosa along the bowel subsites, which may indicate the absence of an epigenetic field defect.

Indexed as

AdenomaAdultAgedColorectal NeoplasmsCpG IslandsDNA MethylationEpigenesis, GeneticFemaleHumansMaleMiddle AgedMutationProto-Oncogene Proteins B-rafBRAF protein, humanProto-Oncogene Proteins B-rafBRAFcolorectal cancerCpG island methylator phenotypemethylationserrated lesion

Identifiers

PMID27145369
PMCPMC5085213
OpenAlexW2342913962

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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.