Evidence map›Paper›PMID 30413173›Full record

ArticleClinical epigenetics2018

Two histologically colorectal carcinomas subsets from the serrated pathway show different methylome signatures and diagnostic biomarkers.

José García-Solano, María C Turpin, Daniel Torres-Moreno, Francisco Huertas-López, Anne Tuomisto, Markus J Mäkinen, Ana Conesa, Pablo Conesa-Zamora

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 13 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

8 authors at 4 institutions in 3 countries.

José García-SolanoDepartment of Pathology, Santa Lucía General University Hospital (HGUSL), C/Mezquita s/n, 30202, Cartagena, Spain.
María C TurpinFaculty of Experimental Sciences, Universidad Francisco de Vitoria, Carretera Pozuelo-Majadahonda km. 1.800 28223 Pozuelo de Alarcón, Madrid, Spain.
Daniel Torres-MorenoDepartment of Pathology, Santa Lucía General University Hospital (HGUSL), C/Mezquita s/n, 30202, Cartagena, Spain.
Francisco Huertas-LópezMicrobiology and Cell Sciences Department, Institute for Food and Agricultural Sciences, University of Florida, Gainesville, FL, USA.
Anne TuomistoCancer and Translational Medicine Research Institute, Department of Pathology, and Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.
Markus J MäkinenCancer and Translational Medicine Research Institute, Department of Pathology, and Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.
Ana ConesaMicrobiology and Cell Sciences Department, Institute for Food and Agricultural Sciences, University of Florida, Gainesville, FL, USA.
Pablo Conesa-ZamoraFacultad de Ciencias de la Salud, Catholic University of Murcia (UCAM), Murcia, Spain. pablo.conesa@carm.es.ORCID http://orcid.org/0000-0003-0190-3044
Santa Lucía University General Hospital · ESOulu University Hospital · FIUniversity of Florida · USUniversidad Francisco de Vitoria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAltered methylation patterns are driving forces in colorectal carcinogenesis. The serrated adenocarcinoma (SAC) and sporadic colorectal carcinoma showing histological and molecular features of microsatellite instability (hmMSI-H) are two endpoints of the so-called serrated pathological route sharing some characteristics but displaying a totally different immune response and clinical outcome. However, there are no studies comparing the methylome of these two subtypes of colorectal carcinomas. The methylation status of 450,000 CpG sites using the Infinium Human Methylation 450 BeadChip array was investigated in 48 colorectal specimens, including 39 SACs and 9 matched hmMSI-H.

resultsMicroarray data comparing SAC and hmMSI-H showed an enrichment in functions related to morphogenesis, neurogenesis, cytoskeleton, metabolism, vesicle transport and immune response and also significant differential methylation of 1540 genes, including CD14 and HLA-DOA which were more methylated in hmMSI-H than in SAC and subsequently validated at the CpG, mRNA and protein level using pyrosequencing, quantitative polymerase chain reaction (qPCR) and immunohistochemistry.

conclusionsThese results demonstrate particular epigenetic regulation patterns in SAC which may help to define key molecules responsible for the characteristic weak immune response of SAC and identify potential targets for treating SAC, which lacks molecular targeted therapy.

Indexed as

DNA MethylationAgedAged, 80 and overBiomarkers, TumorColorectal NeoplasmsCpG IslandsEpigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMicrosatellite InstabilityMiddle AgedOligonucleotide Array Sequence AnalysisBiomarkers, TumorCD14Colon carcinogenesisColorectal cancerEpigeneticsHLA-DOAImmune responseMethylomeMicrosatellite instabilitySerrated

Identifiers

PMID30413173
PMCPMC6230233
OpenAlexW2899737058

What OpenQuestion holds

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LicenceCC BY
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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.