Evidence map›Paper›PMID 25093594›Full record

ArticlePloS one2014

Distinct molecular features of different macroscopic subtypes of colorectal neoplasms.

Kenichi Konda, Kazuo Konishi, Toshiko Yamochi, Yoichi M Ito, Hisako Nozawa, Masayuki Tojo, Kensuke Shinmura, Mari Kogo, Atsushi Katagiri, Yutaro Kubota and 9 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 23 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

19 authors at 3 institutions in 1 country.

Kenichi KondaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Kazuo KonishiDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Toshiko YamochiDepartment of Pathology, Showa University School of Medicine, Tokyo, Japan.
Yoichi M ItoDepartment of Biostatistics, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hisako NozawaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Masayuki TojoDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Kensuke ShinmuraDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Mari KogoDepartment of Hospital Pharmaceutics, Showa University School of Pharmacy, Tokyo, Japan.
Atsushi KatagiriDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Yutaro KubotaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Takashi MuramotoDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Yuichiro YanoDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Yoshiya KobayashiDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Toshihiro KiharaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Teppei TagawaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Reiko MakinoClinical Collaborating laboratory, Showa University School of Medicine, Tokyo, Japan.
Masafumi TakimotoDepartment of Pathology, Showa University School of Medicine, Tokyo, Japan.
Michio ImawariDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Hitoshi YoshidaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Showa University · JPHokkaido University · JPShowa University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal adenoma develops into cancer with the accumulation of genetic and epigenetic changes. We studied the underlying molecular and clinicopathological features to better understand the heterogeneity of colorectal neoplasms (CRNs).

methodsWe evaluated both genetic (mutations of KRAS, BRAF, TP53, and PIK3CA, and microsatellite instability [MSI]) and epigenetic (methylation status of nine genes or sequences, including the CpG island methylator phenotype [CIMP] markers) alterations in 158 CRNs including 56 polypoid neoplasms (PNs), 25 granular type laterally spreading tumors (LST-Gs), 48 non-granular type LSTs (LST-NGs), 19 depressed neoplasms (DNs) and 10 small flat-elevated neoplasms (S-FNs) on the basis of macroscopic appearance.

resultsS-FNs showed few molecular changes except SFRP1 methylation. Significant differences in the frequency of KRAS mutations were observed among subtypes (68% for LST-Gs, 36% for PNs, 16% for DNs and 6% for LST-NGs) (P<0.001). By contrast, the frequency of TP53 mutation was higher in DNs than PNs or LST-Gs (32% vs. 5% or 0%, respectively) (P<0.007). We also observed significant differences in the frequency of CIMP between LST-Gs and LST-NGs or PNs (32% vs. 6% or 5%, respectively) (P<0.005). Moreover, the methylation level of LINE-1 was significantly lower in DNs or LST-Gs than in PNs (58.3% or 60.5% vs. 63.2%, P<0.05). PIK3CA mutations were detected only in LSTs. Finally, multivariate analyses showed that macroscopic morphologies were significantly associated with an increased risk of molecular changes (PN or LST-G for KRAS mutation, odds ratio [OR] 9.11; LST-NG or DN for TP53 mutation, OR 5.30; LST-G for PIK3CA mutation, OR 26.53; LST-G or DN for LINE-1 hypomethylation, OR 3.41).

conclusionWe demonstrated that CRNs could be classified into five macroscopic subtypes according to clinicopathological and molecular differences, suggesting that different mechanisms are involved in the pathogenesis of colorectal tumorigenesis.

Indexed as

DNA Mutational AnalysisAdenomaAdultAgedAged, 80 and overClass I Phosphatidylinositol 3-KinasesCohort StudiesColorectal NeoplasmsDNA MethylationFemaleHumansMaleMicrosatellite InstabilityMiddle AgedMutationPhosphatidylinositol 3-KinasesBRAF protein, humanClass I Phosphatidylinositol 3-KinasesKRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25093594
PMCPMC4122357
OpenAlexW2067160997

What OpenQuestion holds

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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.