Evidence map›Paper›PMID 31724937›Full record

ArticleBioMedicine2019

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer.

Kosar Babaei, Roya Khaksar, Tahereh Zeinali, Hossein Hemmati, Ahmadreza Bandegi, Pirouz Samidoust, Mohammad Taghi Ashoobi, Hooman Hashemian, Kourosh Delpasand, Fereshteh Talebinasab and 4 more

Open access · diamondAbstract read
In one paragraph

Article in BioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. 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

14 authors at 4 institutions in 1 country.

Kosar BabaeiDepartment of Biology, Islamic Azad University of Tonekabon Branch, Tonekabon, Iran.
Roya KhaksarGastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran.
Tahereh ZeinaliGastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran.
Hossein HemmatiRazi Clinical Research Development Unit, Guilan University of Medical Sciences, Rasht, Iran.
Ahmadreza BandegiDepartment of Biochemistry, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Pirouz SamidoustRazi Clinical Research Development Unit, Guilan University of Medical Sciences, Rasht, Iran.
Mohammad Taghi AshoobiDepartment of Surgery, Poursina Hospital, Guilan University of Medical Sciences, Rasht, Iran.
Hooman HashemianPediatric Diseases Research Center,Guilan University of Medical ciences, Rasht, Iran.
Kourosh DelpasandSchool of Medicine, Kurdistan University of Mdical Ciences, Sanandaj, Iran.
Fereshteh TalebinasabDepartment of Biochemistry, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Hoora NaebiDepartment of Biochemistry, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Seyed Hossein MirpourDepartment of Hematology and Oncology, Razi hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Arman KeymoradzadehGastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran.
Seyedeh Elham NorollahiGastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran.
Guilan University of Medical Sciences · IRSemnan University of Medical Sciences · IRIslamic Azad University Tonekabon · IRUniversity of Guilan · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

Indexed as

CarcinogenesisEpigeneticsFluctuationsTumorigenesis

Identifiers

PMID31724937
PMCPMC6855188
OpenAlexW2986166718

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.