Evidence map›Paper›PMID 29486770›Full record

ArticleJournal of translational medicine2018

A novel DNA methylation panel accurately detects colorectal cancer independently of molecular pathway.

Micaela Freitas, Fábio Ferreira, Sónia Carvalho, Fernanda Silva, Paula Lopes, Luís Antunes, Sofia Salta, Francisca Diniz, Lúcio Lara Santos, José Flávio Videira and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

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  10. EpiPanGI Dx: A Cell-free DNA Methylation Fingerprint for the Early Detection of Gastrointestinal Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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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

12 authors at 2 institutions in 1 country.

Micaela FreitasCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Fábio FerreiraCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Sónia CarvalhoCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Fernanda SilvaDepartments of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Paula LopesCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Luís AntunesDepartments of Epidemiology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Sofia SaltaCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Francisca DinizCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.
Lúcio Lara SantosDepartments of Surgical Oncology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
José Flávio VideiraDepartments of Surgical Oncology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Rui HenriqueCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal. rmhenrique@icbas.up.pt.
Carmen JerónimoCancer Biology & Epigenetics Group-Research Center (CI-IPOP), Research Center-LAB 3, Portuguese Oncology Institute of Porto (IPO Porto), F Bdg, 1st Floor, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal. carmenjeronimo@ipoporto.min-saude.pt.ORCID 0000-0003-4186-5345
Instituto Português de Oncologia Francisco Gentil · PTUniversidade do Porto · PT

Funding

Norte2020 ESTIMA-1 NORTE-01-0145-FEDER-000027Research Center of Portuguese Oncology Institute of Porto Research Center of Portuguese Oncology Institute - Porto (PI 74-CI-IPOP-19-2016)
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is one of the most incident cancers, associated with significant morbidity and mortality, and usually classified into three main molecular pathways: chromosomal instability, microsatellite instability (MSI) and CpG island methylator phenotype (CIMP). Currently, available screening methods are either costly or of limited specificity, impairing global implementation. More cost-effective strategies, including DNA methylation-based tests, might prove advantageous. Although some are already available, its performance is suboptimal, entailing the need for better candidate biomarkers. Herein, we tested whether combined use of APC, IGF2, MGMT, RASSF1A, and SEPT9 promoter methylation might accurately detect CRC irrespective of molecular subtype.

methodsSelected genes were validated using formalin-fixed paraffin-embedded tissues from 214 CRC and 50 non-malignant colorectal mucosae (CRN). Promoter methylation levels were assessed using real-time quantitative methylation-specific PCR. MSI and CIMP status were determined. Molecular data were correlated with standard clinicopathological features. Diagnostic and prognostic performances were evaluated by receiver operator characteristics curve and survival analyses, respectively.

resultsExcept for IGF2, promoter methylation levels were significantly higher in CRC compared to CRN. A three-gene panel (MGMT, RASSF1A, SEPT9) identified malignancy with 96.6% sensitivity, 74.0% specificity and 91.5 positive predictive value (area under the curve: 0.97), independently of tumor location, stage, and molecular pathway.

conclusionsCombined promoter methylation analysis of MGMT/RASSF1A/SEPT9 displays a better performance than currently available epigenetic-based biomarkers for CRC, providing the basis for the development of a non-invasive assay to detect CRC irrespective of the molecular pathway.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorColorectal NeoplasmsCpG IslandsDNA MethylationEpigenesis, GeneticFemaleHumansMaleMicrosatellite InstabilityMiddle AgedMultivariate AnalysisPhenotypePromoter Regions, GeneticBiomarkers, TumorBiomarkersColorectal cancerDiagnosisGene promoter methylationPrognosis

Identifiers

PMID29486770
PMCPMC6389195
OpenAlexW2794821911

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.